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Sodium Excretion (sodium + excretion)
Kinds of Sodium Excretion Selected AbstractsUridine adenosine tetraphosphate affects contractility of mouse aorta and decreases blood pressure in conscious rats and miceACTA PHYSIOLOGICA, Issue 2 2010P. B. Hansen Abstract Aim:, In the anaesthetized rat, uridine adenosine tetraphosphate (Up4A) is a circulating, endothelium-derived vasoconstrictor presumably operating as such in un-anaesthetized animals. The present study investigated the in vivo effects of Up4A in conscious mice and rats, and its direct vascular effects in the mouse aorta in vitro. Methods:,In vivo, Up4A was given as step-up infusion at rates of 8,512 nmol min,1 kg,1 for 30 min periods in chronically catheterized rodents. In vitro, the effect of Up4A on rings of mouse aortae mounted in a myograph was tested. Results:, High doses of Up4A (mice: 512 nmol min,1 kg,1; rats: 128 nmol min,1 kg,1) caused hypotension (99 ± 4 to 64 ± 7 mmHg and 114 ± 3 to 108 ± 3 mmHg, respectively, both P < 0.01). In rats, Up4A significantly decreased sodium excretion by >75% and potassium excretion by ,60% without significant changes in urine flow. Exposure of phenylephrine-contracted rings to increasing concentrations of Up4A elicited contraction at 10,7 and 10,6 mol L,1 (18 ± 2% and 76 ± 16% respectively); unexpectedly, 10,5 mol L,1 caused a biphasic response with a contraction (19 ± 6%) followed by a relaxation (,46 ± 6%). No relaxation was observed when the concentration was increased further. Bolus exposure to 10,5 mol L,1 of Up4A caused contraction (+80 ± 2%). Added successively to untreated vessels, increasing concentrations of Up4A (10,7,10,5 mol L,1) induced a biphasic response of contraction followed by relaxation. Conclusion:, Up4A has direct biphasic effects on vascular smooth muscle of the mouse aorta but vasoconstriction dominates at low concentrations. In conscious rodents, step-up infusions of Up4A elicit hypotension and electrolyte retention. [source] Blood volume, blood pressure and total body sodium: internal signalling and output controlACTA PHYSIOLOGICA, Issue 1 2009P. Bie Abstract Total body sodium and arterial blood pressure (ABP) are mutually dependent variables regulated by complex control systems. This review addresses the role of ABP in the normal control of sodium excretion (NaEx), and the physiological control of renin secretion. NaEx is a pivotal determinant of ABP, and under experimental conditions, ABP is a powerful, independent controller of NaEx. Blood volume is a function of dietary salt intake; however, ABP is not, at least not in steady states. A transient increase in ABP after a step-up in sodium intake could provide a causal relationship between ABP and the regulation of NaEx via a hypothetical integrative control system. However, recent data show that subtle sodium loading (simulating salty meals) causes robust natriuresis without changes in ABP. Changes in ABP are not necessary for natriuresis. Normal sodium excretion is not regulated by pressure. Plasma renin is log-linearly related to salt intake, and normally, decreases in renin secretion are a precondition of natriuresis after increases in total body sodium. Renin secretion is controlled by renal ABP, renal nerve activity and the tubular chloride concentrations at the macula densa (MD). Renal nerve activity is related to blood volume, also at constant ABP, and elevates renin secretion by means of ,1 -adrenoceptors. Recent results indicate that renal denervation reduces ABP and renin activity, and that sodium loading may decrease renin without changes in ABP, glomerular filtration rate or ,1 -mediated nerve activity. The latter indicates an essential role of the MD mechanism and/or a fourth mediator of the physiological control of renin secretion. [source] Volume natriuresis vs. pressure natriuresisACTA PHYSIOLOGICA, Issue 4 2004P. Bie Abstract Body fluid regulation depends on regulation of renal excretion. This includes a fast vasopressin-mediated water-retaining mechanism, and slower, complex sodium-retaining systems dominated by the renin,angiotensin aldosterone cascade. The sensory mechanisms of sodium control are not identified; effectors may include renal arterial pressure, renal reflexes, extrarenal hormones and other regulatory factors. Since the pioneering work of Guyton more than three decades ago, pressure natriuresis has been in focus. Dissociations between sodium excretion and blood pressure are explained as conditions where regulatory performance exceeds the precision of the measurements. It is inherent to the concept, however, that sudden transition from low to high sodium intake elicits an arterial pressure increase, which is reversed by the pressure natriuresis mechanism. However, such transitions elicit parallel changes in extracellular fluid volume thereby activating volume receptors. Recently we studied the orchestration of sodium homeostasis by chronic and acute sodium loading in normal humans and trained dogs. Small increases in arterial blood pressure are easily generated by acute sodium loading, and dogs appear more sensitive than humans. However, with suitable loading procedures it is possible , also acutely , to augment renal sodium excretion by at least one order of magnitude without any change in arterial pressure whatsoever. Although pressure natriuresis is a powerful mechanism capable of overriding any other controller, it seems possible that it is not operative under normal conditions. Consequently, it is suggested that physiological control of sodium excretion is neurohumoral based on extracellular volume with neural control of renin system activity as an essential component. [source] Intrauterine growth restriction reduces nephron number and renal excretory function in newborn piglets,ACTA PHYSIOLOGICA, Issue 2 2002R. Bauer ABSTRACT To examine the effects of intrauterine growth restriction on nephron number, renal circulation, and renal excretory functions in newborns, studies were conducted on 1-day-old anaesthetized piglets, divided into normal weight (n = 6) and intrauterine growth restricted (n = 6) piglets. Renal blood flow was measured by coloured microspheres, glomerular filtration rate was measured by inulin clearance, and osmotic clearance and fractional sodium excretion were calculated. In addition, an estimation of the nephron number was performed by counting representative glomerular numbers in microscopic sections. Newborn intrauterine growth restricted piglets exhibited a reduced glomerular filtration rate and osmotic clearance (P < 0.05), whereas renal blood flow and the filtration fraction as well as fractional sodium excretion were similar in normal weight and intrauterine growth restricted piglets. The nephron number was markedly reduced in intrauterine growth restricted piglets even if the nephron number was related to body weight (P < 0.01). There was a positive correlation between nephron number and glomerular filtration rate (r = 0.69, P < 0.05). Reduced glomerular filtration rate of newborn intrauterine growth restricted piglets is associated with a reduced nephron number. Thus, at birth, compensatory response of renal function due to nephron deficit does not exist in intrauterine growth restricted piglets. [source] Mechanisms of renal hyporesponsiveness to ANP in heart failureEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 9 2003A. Charloux Abstract The atrial natriuretic peptide (ANP) plays an important role in chronic heart failure (CHF), delaying the progression of the disease. However, despite high ANP levels, natriuresis falls when CHF progresses from a compensated to a decompensated state, suggesting emergence of renal resistance to ANP. Several mechanisms have been proposed to explain renal hyporesponsiveness, including decreased renal ANP availability, down-regulation of natriuretic peptide receptors and altered ANP intracellular transduction signal. It has been demonstrated that the activity of neutral endopeptidase (NEP) is increased in CHF, and that its inhibition enhances renal cGMP production and renal sodium excretion. In vitro as well as in vivo studies have provided strong evidence of an increased degradation of intracellular cGMP by phosphodiesterase in CHF. In experimental models, ANP-dependent natriuresis is improved by phosphodiesterase inhibitors, which may arise as new therapeutic agents in CHF. Sodium-retaining systems likely contribute to renal hyporesponsiveness to ANP through different mechanisms. Among these systems, the renin-angiotensin-aldosterone system has received particular attention, as angiotensin II and ANP have renal actions at the same sites and inhibition of angiotensin-converting enzyme and angiotensin-receptor blockade improve ANP hyporesponsiveness. Less is known about the interactions between the sympathetic nervous system, endothelin or vasopressin and ANP, which may also blunt ANP-induced natriuresis. To summarize, renal hyporesponsiveness to ANP is probably multifactorial. New treatments designed to restore renal ANP efficiency should limit sodium retention in CHF patients and thus delay the progression to overt heart failure. [source] Central nitric oxide blocks vasopressin, oxytocin and atrial natriuretic peptide release and antidiuretic and natriuretic responses induced by central angiotensin II in conscious ratsEXPERIMENTAL PHYSIOLOGY, Issue 5 2007Wagner Luis Reis The presence of nitric oxide synthase (NOS), the enzyme that catalyses the formation of nitric oxide (NO), in the circumventricular organs and magnocellular neurones suggests an important role of NO in the modulation of vasopressin (AVP) and oxytocin (OT) release. Intracerebroventricular (i.c.v.) injection of angiotensin II (Ang II) stimulates the release of AVP, OT and atrial natriuretic peptide (ANP), with the resultant antidiuretic and natriuretic effects. This study investigated the interaction between nitrergic and angiotensinergic pathways on the release of AVP, OT and ANP and on urinary volume and sodium excretion in water-loaded rats. Unanaesthetized, freely moving, male Wistar rats received two water loads followed by an injection into the lateral ventricle of an inhibitor of NOS (l -NAME), a NO donor [3-morpholinylsydnoneimine chloride (SIN-1) or S -nitroso- N -acetyl penicillamine (SNAP)] or vehicle (isotonic saline) and, 20 min after, they received a second i.c.v. injection of Ang II or vehicle. Injections of l -NAME or Ang II produced an increase in plasma levels of AVP, OT and ANP, a reduction in urinary volume and an increase in sodium excretion. Pretreatment with l -NAME enhanced the Ang II-induced increase in AVP, OT and ANP release, as well as the antidiuresis and natriuresis. Injection of SIN-1 or SNAP did not modify hormonal plasma levels and urinary parameters. In contrast SNAP blocked the AVP, OT and ANP release, as well as antidiuretic and natriuretic responses induced by ANG-II. Thus, the central nitrergic system can act to inhibit AVP, OT and ANP secretion and the antidiuretic and natriuretic effects in response to Ang II. [source] Renal Response to Arginine Vasopressin During the Oestrous Cycle in the Rat: Comparison of Glucose and Saline Infusion Using Physiological Doses of VasopressinEXPERIMENTAL PHYSIOLOGY, Issue 1 2002David E. Hartley The renal response to arginine vasopressin in the rat has been shown to depend on reproductive status. However there is no consensus as to when the kidney is most responsive. The varying results could depend on the protocol and the dose of hormone used. A study has been performed, with physiological doses of vasopressin, comparing the responses during infusion of hypotonic saline and glucose. After an equilibration period of 150 min, conscious rats were infused on each of the four days of the oestrous cycle with either isotonic saline (0.077 M) or 0.14 M glucose for a control period of 45 min. Vasopressin was then infused at 10-40 fmol min,1 for 1 h, followed by a recovery period of 90 min. Timed urine samples were collected for determination of volume, sodium concentration and osmolality. During the control period urine flow was greatest at oestrus and dioestrus day 2 and sodium excretion on dioestrus day 2 irrespective of the infusate. Vasopressin concentrations achieved lay within the physiological range and no difference was observed between the different days for a given dose. Infusion of vasopressin in both saline and glucose produced a dose-dependent antidiuresis, the greatest responses being seen of pro-oestrus and dioestrus day 2. It was only with the highest rate of infusion that a significant increase in sodium excretion was seen on each day of the cycle and the greatest responses were seen on pro-oestrus and dioestrus day 1 for both infusates. Thus the kidney shows the greatest response to physiological doses of vasopressin at pro-oestrus and dioestrus day 1 irrespective of the infusate employed. [source] The effect of single oral low-dose losartan on posture-related sodium handling in post-TIPS ascites-free cirrhosis,HEPATOLOGY, Issue 3 2006George Therapondos Post-TIPS ascites-free patients with cirrhosis and previous refractory ascites demonstrate subtle sodium retention when challenged with a high sodium load. This is also observed in pre-ascitic patients with cirrhosis. This phenomenon is dependent on an intrarenal angiotensin II (ANG II) mechanism related to the assumption of erect posture. We investigated whether similar mechanisms were involved in post-TIPS ascites-free patients, by studying 10 patients with functioning TIPS and no ascites. We measured the effect of changing from supine to erect posture on sodium excretion at baseline and after single oral low dose losartan (7.5 mg) which has been shown to blunt proximal and distal tubular sodium reabsorption in pre-ascites. At baseline, the assumption of erect posture produced a reduction in sodium excretion (from 0.30 ± 0.06 to 0.13 ± 0.02 mmol/min, P = .05), which was mainly due to an increase in proximal tubular reabsorption of sodium (PTRNa) (69.7 ± 3.1% to 81.1 ± 1.8%, P = .003). The administration of losartan resulted in a blunting of PTRNa (supine 69.7 ± 3.1% to 63.9 ± 3.9%, P = .01 and erect 81.1 ± 1.8% to 73.8 ± 2.4%, P = .01), accompanied by an increased distal tubular reabsorption of sodium in both postures, with no overall improvement in sodium excretion on standing. In conclusion, post-TIPS ascites-free patients with cirrhosis exhibit erect posture-induced sodium retention. We speculate that (1) this effect is partly mediated by the effect of ANG II on PTRNa and (2) that the inability of low dose losartan to block the erect posture-induced sodium retention may be related to the erect posture-induced rise in aldosterone which is unmodified by losartan. (HEPATOLOGY 2006;44:640,649.) [source] The mechanism of improved sodium homeostasis of low-dose losartan in preascitic cirrhosisHEPATOLOGY, Issue 6 2002Florence Wong 200 Elizabeth St. Renal sodium retention on standing is one aspect of the abnormal renal sodium handling in preascitic, well-compensated patients with cirrhosis. Recently, it has been shown that low doses (7.5 mg) of the angiotensin II (Ang II) receptor antagonist, losartan, can reverse renal sodium retention on high, 200-mmol sodium/d diet in these patients and restore them to sodium balance. Therefore, the effect of 7.5 mg of losartan on sodium excretion, when changing from supine to erect posture for 2 hours, was examined in 10 well-compensated patients with cirrhosis and 9 age- and sex-matched controls on the same sodium diet, under strictly controlled metabolic conditions. In contrast to control subjects, in whom sodium excretion was unaffected, single 7.5-mg doses of losartan again restored the preascitic patients with cirrhosis to sodium balance. In addition, it blunted the fall in erect posture, induced renal sodium excretion by a reduction in proximal and distal tubular reabsorption of sodium. These changes occurred without any significant changes in blood volumes, systemic and renal hemodynamics, or glomerular filtration rate (GFR) and filtered sodium load compared with controls, and despite activation of the systemic renin-angiotensin-aldosterone system, which was still within normal levels. In conclusion, the beneficial natriuretic effects of low-dose losartan on erect posture , induced sodium retention in preascitic cirrhosis supports the suggestion that the pathophysiology of sodium retention in preascites is in part caused by an intrarenal tubular effect of Ang II in that posture. [source] Long-term evolution of the acute tubular necrosis (ATN) induced by glycerol: role of myofibroblasts and macrophagesINTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY, Issue 4 2002Telma J. Soares Summary. Late structural changes such as interstitial fibrosis in the renal cortex and tubular atrophy have been detected after severe acute tubular necrosis (ATN). The aim of this study was to investigate the expression of fibronectin, ,-smooth muscle actin and macrophages during the evolution of the ATN induced by glycerol and their relationship with the late structural changes observed in the kidneys of these animals. Forty-nine male Wistar rats were injected with a 50% glycerol solution, 8 mL/kg (4 mL/kg applied i.m. to each hind leg) and 14 with 0.15 m NaCl solution. Before glycerol injection on day 1, water was removed for 17 h. Blood and urine samples were collected 1 day after the injection to quantify sodium and creatinine. The animals were killed 5, 30 and 60 days after the injections and the kidneys removed for histological and immunohistochemical studies. The results of the histological and immunohistochemical studies were scored according to the extent of lesion or staining in the cortical tubulointerstitium, respectively. The percentage of tubulointerstitial lesions was determined by morphometry. Glycerol-injected rats presented a transitory increase in plasma creatinine levels and in fractional sodium excretion. The immunohistochemical studies showed increased fibronectin, ,-smooth muscle actin (,-SM-actin), TGF-, and ED-1 (macrophages) staining in the renal cortex from rats killed 5, 30 and 60 days after glycerol injection (P < 0.05) compared to control. The animals killed on day 30 and 60 also presented chronic lesions (fibrosis, tubular dilatation and atrophy) in the renal cortex, despite the recovery of renal function. Macrophages, TGF-, and myofibroblasts may have contributed to the development of renal fibrosis in these rats. [source] Different protective actions of losartan and tempol on the renal inflammatory response to acute sodium overloadJOURNAL OF CELLULAR PHYSIOLOGY, Issue 1 2010María I. Rosón The aim of this work was to study the role of local intrarenal angiotensin II (Ang II) and the oxidative stress in the up-regulation of pro-inflammatory cytokines expression observed in rats submitted to an acute sodium overload. Sprague,Dawley rats were infused for 2,h with isotonic saline solution (Control group) and with hypertonic saline solution alone (Na group), plus the AT1 receptor antagonist losartan (10,mg,kg,1 in bolus) (Na,Los group), or plus the superoxide dismutase mimetic tempol (0.5,mg,min,1,kg,1) (Na,Temp group). Mean arterial pressure, glomerular filtration rate, and fractional sodium excretion (FENa) were measured. Ang II, NF-,B, hypoxia inducible factor-1, (HIF-1,), transforming growth factor ,1 (TGF-,1), smooth muscle actin (,-SMA), endothelial nitric oxide synthase (eNOS), and RANTES renal expression was evaluated by immunohistochemistry. Ang II, NF-,B, and TGF-,1 and RANTES early inflammatory markers were overexpressed in Na group, accompanied by enhanced HIF-1, immunostaining, lower eNOS expression, and unmodified ,-SMA. Losartan and tempol increased FENa in sodium overload group. Although losartan reduced Ang II and NF-,B staining and increased eNOS expression, it did not restore HIF-1, expression and did not prevent inflammation. Conversely, tempol increased eNOS and natriuresis, restored HIF-1, expression, and prevented inflammation. Early inflammatory markers observed in rats with acute sodium overload is associated with the imbalance between HIF-1, and eNOS expression. While both losartan and tempol increased natriuresis and eNOS expression, only tempol was effective in restoring HIF-1, expression and down-regulating TGF-,1 and RANTES expression. The protective role of tempol, but not of losartan, in the inflammatory response may be associated with its greater antioxidant effects. J. Cell. Physiol. 224:41,48, 2010 © 2010 Wiley-Liss, Inc. [source] Adduction of amiloride hydrochloride in urea through a modified technique for the dissolution enhancementJOURNAL OF PHARMACEUTICAL SCIENCES, Issue 3 2008Seema Thakral Abstract Amiloride hydrochloride is a potassium-sparing diuretic since it favors sodium excretion and potassium reabsorption. In the present study, urea, a well-known adductor for linear compounds was successfully employed for inclusion of amiloride hydrochloride,a substituted cyclic organic compound through a modified technique. Formation of urea inclusion compounds was confirmed by FTIR, DSC and XRD. The minimum amount of rapidly adductible endocyte (RAE) required for adduction of amiloride hydrochloride in urea was estimated by a modified Zimmerschied calorimetric method. Urea,AH,RAE inclusion compounds containing varying proportions of guests were prepared and their thermal behavior studied by DSC. The inclusion compounds were also found to exhibit high content uniformity and markedly improved dissolution profile as demonstrated by increased dissolution efficiency. Studies reveal the possibility of exploiting co-inclusion of the drug in urea host lattice for the dissolution enhancement. © 2007 Wiley-Liss, Inc. and the American Pharmacists Association J Pharm Sci 97:1191,1201, 2008 [source] The effects of midodrine on the natriuretic response to furosemide in cirrhotics with ascitesALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 8 2010V. L. Misra Aliment Pharmacol Ther 2010; 32: 1044,1050 Summary Background, Resistance to loop diuretics is common in patients with ascites. Diminished glomerular filtration rate (GFR) is thought to mediate resistance to loop diuretics. Midodrine, a commonly used alpha-1 agonist, has been shown to improve GFR in non-azotemic patients with cirrhosis. Aim, To conduct a randomized, double-blind, placebo-controlled, cross-over study to test the hypothesis that midodrine significantly increases natriuretic response of IV furosemide in non-azotemic cirrhotics with ascites. Methods, All subjects participated in both phases, which were (i) furosemide IV infusion + oral midodrine 15 mg administered 30 min before furosemide (ii) furosemide IV infusion + oral placebo administered 30 min before furosemide. Primary outcomes were 6-h urine sodium excretion and 6-h total urine volume. Results, A total of 15 patients (men: 8; age: 52.7 ± 7.6 years; serum creatinine: 1.06 ± 0.2 mg/dL) were studied. Total 6-h urine sodium excretion was 109 ± 42 mmol in the furosemide + midodrine treatment phase and was not significantly different from that in the furosemide + placebo treatment phase (126 ± 69 mmol, P = 0.6). Similarly, mean 6-h total urine volume was not significantly different between two groups (1770 ± 262 mL vs. 1962 ± 170 mL, P = 0.25). Conclusions, Oral midodrine does not increase the natriuretic response to furosemide in non-azotemic cirrhotic patients with ascites. Orally administered midodrine does not increase natriuretic response to furosemide in non-azotemic cirrhotic patients with ascites. [source] Renal impairment in deoxycorticosterone acetate-salt hypertensive ratsNEPHROLOGY, Issue 4 2000Catherine Dallemagne Summary: This study has compared renal function in deoxycorticosterone (DOCA)-salt hypertensive Wistar rats (uninephrectomy followed by administration of DOCA 25 mg subcutaneously every fourth day and 1% NaCl in the drinking water) with various control rats using the isolated perfused kidney preparation. The systolic blood pressure of DOCA-salt hypertensive rats was 180 ± 10 mmHg (uninephrectomy controls: 136 ± 9 mmHg) while normalization of calcium intake (DOCA-Ca rats, 1% CaCl2 in water) attenuated this increase (systolic blood pressure, 146 ± 5 mmHg). Renal mass corrected for body weight increased by 25% after uninephrectomy, 55% in uninephrectomized rats given NaCl, 152% in DOCA-salt rats and 147% in DOCA-Ca rats. At a renal perfusion pressure of 135 mmHg, isolated perfused kidneys from DOCA-salt rats showed decreases of 48% in glomerular filtration rate and 69% in sodium excretion with an increase of 44% in renal vascular resistance compared with uninephrectomized rats. There were no significant differences in renal function between DOCA-salt and DOCA-Ca rats. Histological assessment of renal pathology showed proximal tubular hypertrophy and hyperplasia, marked focal distal tubular atrophy, interstitial fibrosis and glomerular hypercellularity in DOCA rats compared with UNX rats. Lesions were less obvious in UNX-salt or DOCA-Ca rats. The lack of direct correlation between alterations in function and pathology may be explained by the compensatory effect of remaining healthy or hypertrophied nephrons. Thus, the DOCA-salt model of hypertension in rats is associated with marked structural kidney damage and severely decreased kidney function. Marked attenuation of systemic hypertension by normalizing calcium intake in DOCA-salt rats did not prevent impairment of kidney function. [source] Changes in renal hemodynamics and urodynamics in rats with chronic hyperoxaluria and after acute oxalate infusion: Role of free radicalsNEUROUROLOGY AND URODYNAMICS, Issue 2 2003Ho-Shiang Huang Abstract Aims The aim of this study was to evaluate possible changes in renal hemodynamic and urodynamic parameters in rats with chronic hyperoxaluria and after acute oxalate challenge. We also evaluated the possible association between free radical (FR) production, hyperoxaluria, and calcium oxalate (CaOx) calculi formation. Methods Chronic hyperoxaluria was induced by adding 0.75% ethylene glycol (EG) to the drinking water of male Wistar rats. After 7, 21, and 42 days of treatment, urinary biochemistry, oxalate levels, and lipid peroxides were measured. Kidney calculi were examined by polarizing microscopy. In the second part of the experiments, 1, 10, 20, and 30 mg kg,1 hr,1 oxalate was infused, by means of an intrarenal arterial catheter (IRA), into normal rats sequentially. Superoxide dismutase (SOD) infusion by means of IRA, in addition to oxalate, was also performed to check its influence on the altered renal function after oxalate infusion. In both the acute and chronic groups, renal blood flow (RBF), cortical microvascular blood flow (CMVBF), glomerular filtration rate (GFR), urine flow (UV), and urinary sodium excretion (UNaV) were measured, and chemiluminescence (CL) was examined in the renal venous blood. Results Levels of urinary lipid peroxides and enzymuria had increased since day 7, and increased the size of numbers of CaOx crystals in the kidney were noted beginning on day 21, but elevated CL was detectable only on day 7 after 0.75% EG treatment. Decreased UV and UNaV were noted in the 42-day EG group, although the 24-hr creatinine clearance values were normal in all experimental groups. On the other hand, RBF, GFR, and CMVBF were attenuated with elevated FR when the oxalate concentration was higher than 10 mg kg,1 hr,1 in the acute oxalate infusion group. With SOD pretreatment, the decreased RBF, GFR, and CMVBF could be reversed at 10 mg kg,1 hr,1 of oxalate, and be partially reversed at 20. FR also could be reduced significantly at 10 and 20 mg kg,1 hr,1 of oxalate. Conclusions Decreased urine flow and sodium excretion were the main renal functions affected by chronic hyperoxaluria. However, that only the 42-day EG group had a decreased tubular function cannot be fully explained by the persistent tubular enzymuria and increased lipid peroxides that began on day 7 after EG treatment. With acute oxalate infusion, the major insult to renal function was renal hemodynamics. Pretreated SOD could reverse the attenuated hemodynamics and reduce the elevated FR partly, which suggested that FR is responsible for oxalate toxicity. Neurourol. Urodynam. 22:176,182, 2003. © 2003 Wiley-Liss, Inc. [source] Role of cardiac-renal neural reflex in regulating sodium excretion during water immersion in conscious dogsTHE JOURNAL OF PHYSIOLOGY, Issue 1 2002Kenju Miki The present study was undertaken to determine the role of cardiopulmonary mechanoreceptors in inducing the sustained reduction of renal sympathetic nerve activity (RSNA) and concomitant changes in sodium excretion occurring during water immersion (WI) in intact dogs. Seven cardiac-denervated dogs were chronically instrumented for measuring RSNA, systemic arterial (Pa), central venous (Pcv) and left atrial pressures (Pla). WI initially decreased RSNA in cardiac denervated dogs by 10.0 ± 5.5 %; thereafter the RSNA fell to a nadir of 18.5 ± 5.6 % (P < 0.05) at 40,80 min of WI and then returned toward the pre-immersion level. Renal sodium excretion increased significantly by 211 ± 69 % (P < 0.05) only during the first 20,40 min of WI. WI increased Pa, Pcv and Pla in a step manner from 94 ± 3 to 108 ± 3 mmHg (P < 0.05), from 1.4 ± 0.5 to 12.3 ± 1.0 mmHg (P < 0.05) and from 4.9 ± 0.6 to 15.4 ± 1.2 mmHg (P < 0.05), respectively. These responses in RSNA and sodium excretion to WI in the cardiac-denervated dogs were significantly (P < 0.05) attenuated compared with those in a previous group of intact dogs. These data suggest that the attenuated responses of neural and excretory response to WI observed in cardiac-denervated dogs can be attributed to an interruption of afferent input originating from the cardiopulmonary mechanoreceptors to the central nervous system. [source] Biological Activity of Endogenous Atrial Natriuretic Peptide During Cardiopulmonary BypassARTIFICIAL ORGANS, Issue 10 2000Nobuhiko Hayashida Abstract: To evaluate the effect of cardiopulmonary bypass (CPB) on atrial natriuretic peptide (ANP) biological activity in patients undergoing cardiac operations, we conducted a prospective study. Ten patients undergoing mitral valve surgery were enrolled. Plasma levels of ANP and cyclic guanosine monophosphate (cGMP), hemodynamic variables, and renal function parameters were assessed perioperatively. The molar ratio of cGMP to ANP (as a marker for ANP biological activity) decreased significantly (p < 0.05) during CPB despite similar plasma ANP levels. The ratio correlated inversely with the duration of CPB (r = ,0.85, p = 0.002). The ratio also correlated with fractional sodium excretion (r = 0.65, p = 0.04) and correlated inversely with pulmonary vascular resistance (r = ,0.79, p = 0.009) and atrial filling pressure (r = ,0.84, p = 0.003) postoperatively. CPB decreased the molar ratio of cGMP to ANP, which may represent ANP biological activity, such as vasodilation and natriuresis. The phenomenon may contribute to water,sodium retention and pulmonary hypertension after cardiac surgery. [source] Urinary sodium excretion, dietary sources of sodium intake and knowledge and practices around salt use in a group of healthy Australian womenAUSTRALIAN AND NEW ZEALAND JOURNAL OF PUBLIC HEALTH, Issue 4 2010Karen Charlton Abstract Objective: Strategies that aim to facilitate reduction of the salt content of foods in Australia are hampered by sparse and outdated data on habitual salt intakes. This study assessed habitual sodium intake through urinary excretion analyses, and identified food sources of dietary sodium, as well as knowledge and practices related to salt use in healthy women. Methods: Cross-sectional, convenient sample of 76 women aged 20 to 55 years, Wollongong, NSW. Data included a 24 hour urine sample, three-day food diary and a self-administered questionnaire. Results: Mean Na excretion equated to a NaCl (salt) intake of 6.41 (SD=2.61) g/day; 43% had values <6 g/day. Food groups contributing to dietary sodium were: bread and cereals (27%); dressings/sauces (20%); meat/egg-based dishes (18%); snacks/desserts/extras (11%); and milk and dairy products (11%). Approximately half the sample reported using salt in cooking or at the table. Dietary practices reflected a high awareness of salt-related health issues and a good knowledge of food sources of sodium. Conclusion: These findings from a sample of healthy women in the Illawarra indicate that dietary sodium intakes are lower in this group than previously reported in Australia. However, personal food choices and high levels of awareness of the salt reduction messages are not enough to achieve more stringent dietary targets of <4 g salt per day. Implications: Urinary Na excretion data are required from a larger nationally representative sample to confirm habitual salt intakes. The bread and cereals food group are an obvious target for sodium reduction strategies in manufactured foods. [source] The abuse of diuretics as performance-enhancing drugs and masking agents in sport doping: pharmacology, toxicology and analysisBRITISH JOURNAL OF PHARMACOLOGY, Issue 1 2010Amy B Cadwallader Diuretics are drugs that increase the rate of urine flow and sodium excretion to adjust the volume and composition of body fluids. There are several major categories of this drug class and the compounds vary greatly in structure, physicochemical properties, effects on urinary composition and renal haemodynamics, and site and mechanism of action. Diuretics are often abused by athletes to excrete water for rapid weight loss and to mask the presence of other banned substances. Because of their abuse by athletes, diuretics have been included on The World Anti-Doping Agency's (WADA) list of prohibited substances; the use of diuretics is banned both in competition and out of competition and diuretics are routinely screened for by anti-doping laboratories. This review provides an overview of the pharmacology and toxicology of diuretics and discusses their application in sports. The most common analytical strategies currently followed by the anti-doping laboratories accredited by the WADA are discussed along with the challenges laboratories face for the analysis of this diverse class of drugs. [source] Indomethacin decreases particulate guanylyl cyclase activity in rat kidneyCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 4 2004JongUn Lee SUMMARY 1.,Effects of non-steroidal anti-inflammatory drugs on the local atrial natriuretic peptide (ANP) and nitric oxide (NO) systems in the kidney were investigated. 2.,Male Sprague-Dawley rats were treated with indomethacin (5 mg/kg, every 12 h, i.p.) for 2 days. The expression of ANP and natriuretic peptide receptor-A (NPR-A) mRNA was determined in the kidney, as was that of endothelial NO synthase (NOS) proteins. Particulate and soluble guanylyl cyclase activities were determined separately. 3.,Following treatment with indomethacin, urinary sodium excretion decreased significantly. Although the renal expression of ANP was not changed significantly, that of NPR-A decreased significantly. The expression of NOS increased significantly. Particulate guanylyl cyclase activity was decreased, whereas the activity of soluble guanylyl cyclase was increased. The catalytic activity of Na+/K+ -ATPase was increased, with no significant changes in its expression. The expression of the type 3 Na/H exchanger and Na,K,2CL cotransporters increased significantly. 4.,The indomethacin-induced decrease in urinary sodium excretion may be attributed, at least in part, to decreased activity of the local ANP/cGMP system. The increased activity of the NO/cGMP system may be a compensatory response to the diminished activity of the prostaglandin system. [source] Neural Regulation Of Renal Blood Flow: A Re-ExaminationCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 12 2000Simon C Malpas SUMMARY 1. The importance of renal sympathetic nerve activity (RSNA) in the regulation of renal function is well established. However, it is less clear how the renal vasculature responds to the different mean levels and patterns of RSNA. While many studies have indicated that small to moderate changes in RSNA preferentially regulate renin secretion or sodium excretion and only large changes in RSNA regulate renal blood flow (RBF), other experimental evidence suggests that small changes in RSNA can influence RBF 2. When RSNA has been directly measured in conjunction with RBF, it appears that a range of afferent stimuli can induce reflex changes in RBF. However, many studies in a variety of species have measured RBF only during stimuli designed to reflexly increase or decrease sympathetic activity, but have not recorded RSNA. While this approach can be informative, it is not definitive because the ability of the vasculature to respond to RSNA may, in part, reflect the resting level of RSNA and, therefore, the vasoconstrictive state of the vasculature under the control conditions. 3. Further understanding of the control of RBF by RSNA has come from studies that have analysed the underlying rhythms in sympathetic nerve activity and their effect on the cardiovascular system. These studies show that the frequency,response characteristic of the renal vasculature is such that higher frequency oscillations in RSNA (above 0.6 Hz) contribute to setting the mean level of RBF. In comparison, lower frequency oscillations in RSNA can induce cyclic vasoconstriction and dilation in the renal vasculature, thus inducing oscillations in RBF. 4. In summary, the present review discusses the neural control of RBF, summarizing evidence in support of the hypothesis that RBF is under the influence of RSNA across the full range of RSNA. [source] | |||||||||||||