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Dietary Salt Intake (dietary + salt_intake)
Selected AbstractsBlood 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] Angiotensin II-based hypertension and the sympathetic nervous system: the role of dose and increased dietary salt in rabbitsEXPERIMENTAL PHYSIOLOGY, Issue 5 2007Fiona D. McBryde There is accumulating evidence that angiotensin II may exert its hypertensive effect through increasing sympathetic drive. However, this action may be dependent on the dose of angiotensin II as well as salt intake. We determined the effect of different doses of angiotensin II and different levels of salt intake on neurogenic pressor activity. We also examined the effect of renal denervation. New Zealand White rabbits were instrumented to continuously measure arterial pressure. The depressor response to the ganglionic blocker pentolinium tartrate (5 mg kg,1) was used to assess pressor sympathetic drive on days 0, 7 and 21 of a 20 or 50 ng kg,1 min,1 continuous i.v. angiotensin II infusion. A 50 ng kg,1 min,1 infusion caused an immediate increase in pressure (23 ± 5 mmHg), whereas a 20 ng kg,1 min,1 infusion caused a slow increase in pressure, peaking by day 12 (17 ± 4 mmHg). The ganglionic blockade profiles indicated sympathoinhibition in the 50 ng kg,1 min,1 group by day 7 and sympathoinhibition in the 20 ng kg,1 min,1 group at day 21, corresponding to the development of hypertension. Animals receiving increased dietary salt (0.9% NaCl in drinking water), however, showed a similar slow increase in pressure with 20 ng kg,1 min,1 angiotensin II (16 ± 5 mmHg) but no sympathoinhibition at day 21. Bilateral renal denervation delayed the onset but not the extent of hypertension in this group. We conclude that different doses of angiotensin II produce distinct profiles of hypertension and associated changes in pressor sympathetic drive and that increased dietary salt intake disrupts the normal sympathoinhibitory response to angiotensin II-based hypertension. [source] Dietary NaCl Does Not Affect Blood Pressure in Healthy CatsJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 4 2004Nicole Luckschander The purpose of this study was to assess the effects of dietary salt intake on systolic blood pressure, water intake, urine output, and urine concentration in cats. Ten healthy young adult cats (mean age 2.5 years) were randomly divided into 2 groups and fed either a control diet (0.46% Na and 1.33% Cl on a dry matter [DM] basis) or a diet with a moderately increased salt content (1.02% Na and 2.02% Cl on a DM basis) for 2 weeks. After a 1-week wash-out period, each group was switched to the opposite diet for 2 weeks. During each 2-week study period, food and water intake, urine volume, urine specific gravity, and urine osmolality were measured daily. Systolic blood pressure (calculated as the mean of 5 readings measured with a Doppler flow detector) was assessed twice daily. No significant effect of diet composition was found on systolic blood pressure, and blood pressure measurements remained within reference limits throughout the study in all 10 cats. However, animals fed the higher salt diet had significantly increased water intake and urine osmolality, and significantly decreased urine specific gravity in comparison to animals fed the control diet. Examination of results of this preliminary study suggests that feeding a diet with moderately increased salt content increases water intake and causes diuresis without increasing systolic blood pressure in healthy adult young cats. [source] Hydrogen Peroxide-Dependent Arteriolar Dilation in Contracting Muscle of Rats Fed Normal and High Salt DietsMICROCIRCULATION, Issue 8 2007Paul J. Marvar ABSTRACT Objective: High dietary salt intake decreases the arteriolar dilation associated with skeletal muscle contraction. Because hydrogen peroxide (H2O2) can be released from contracting muscle fibers, this study was designed to assess the possible contribution of H2O2 to skeletal muscle functional hyperemia and its sensitivity to dietary salt. Methods: The authors investigated the effect of catalase treatment on arteriolar dilation and hyperemia in contracting spinotrapezius muscle of rats fed a normal salt (0.45%, NS) or high salt (4%, HS) diet for 4 weeks. Catalase-sensitive 2,,7,-dichlorofluorescein (DCF) fluorescence was measured as an index of H2O2 formation, and the mechanism of arteriolar dilation to H2O2 was probed in each group using pharmacological inhibitors. Results: DCF fluorescence increased with muscle contraction, but not if catalase was present. Catalase also reduced arteriolar dilation and hyperemia during contraction in both dietary groups. Exogenous H2O2 dilated arterioles in both groups, with greater responses in HS rats. Guanylate cyclase inhibition did not affect arteriolar responses to H2O2 in either group, but KCa or KATP channel inhibition equally reduced these responses, and KATP channel inhibition equally reduced functional hyperemia in both groups. Conclusions: These results indicate that locally produced H2O2 contributes to arteriolar dilation and hyperemia in contracting skeletal muscle, and that the effect of H2O2 on arteriolar tone in this vascular bed is mediated largely through K+ channel activation. High dietary salt intake does not reduce the contribution of H2O2 to active hyperemia, or alter the mechanism through which H2O2 relaxes arteriolar smooth muscle. [source] | |||||||||||||