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Aldosterone System (aldosterone + system)
Selected AbstractsTHE ,BODY FLUID PRESSURE CONTROL SYSTEM' RELIES ON THE RENIN,ANGIOTENSIN,ALDOSTERONE SYSTEM: BALANCE STUDIES IN FREELY MOVING DOGSCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 5-6 2005Erdmann Seeliger SUMMARY 1.,The physiological role of the ,renal body fluid pressure control system', including the intrarenal mechanism of ,pressure natriuresis', is uncertain. 2.,Balance studies in freely moving dogs address the following questions: (i) what is the physiological contribution of pressure natriuresis to the control of total body sodium (TBS); (ii) to what extent is long-term mean arterial blood pressure (MABP) determined by TBS and total body water (TBW); and (iii) during Na accumulation, is Na stored in an osmotically inactive form? 3.,Diurnal time-courses of Na excretion (UNaV) and MABP reveal no correlation. Spontaneous MABP changes do not affect UNaV. The long-term 20% reduction of renal perfusion pressure (RPP) results in Na retention via pressure-dependent stimulation of the renin,angiotensin,aldosterone system (RAAS), not via a pressure natriuresis mechanism. Prevention of pressure natriuresis does not result in ongoing Na retention when the RAAS is operative. The long-term 20% elevation of RPP induced by sustained TBS elevation facilitates Na excretion via pressure natriuresis, but does not restore TBS to normal. 4.,Changes in TBW correlate well with changes in TBS (r2 = 0.79). This correlation is even closer when concomitant changes in total body potassium are also considered (r2 = 0.91). 5.,With normal or elevated TBW, long-term MABP changes correlate well with TBW changes (r2 = 0.69). At lowered TBW, no correlation is found. 6.,In conclusion, the physiological role of pressure natriuresis is limited. Pressure natriuresis does not appear to be operative when RPP is changed from ,20 to +10% and neurohumoral control of UNaV is unimpeded. Within this range, pressure-dependent changes in the RAAS mediate the effects of changes in RPP on UNaV. Pressure natriuresis may constitute a compensating mechanism under pathophysiological conditions of substantial elevation of RPP. A large portion of the long-term changes in MABP are attributable to changes in TBW. The notion of osmotically inactive Na storage during Na accumulation appears to be invalid. [source] Role of aldosterone and angiotensin II in insulin resistance: an updateCLINICAL ENDOCRINOLOGY, Issue 1 2009Guido Lastra-Lastra Summary The role of the Renin,Angiotensin,Aldosterone system (RAAS) on the development of insulin resistance and cardiovascular disease is an area of growing interest. Most of the deleterious actions of the RAAS on insulin sensitivity appear to be mediated through activation of the Angiotensin II (Ang II) Receptor type 1 (AT1R) and increased production of mineralocorticoids. The underlying mechanisms leading to impaired insulin sensitivity remain to be fully elucidated, but involve increased production of reactive oxygen species and oxidative stress. Both experimental and clinical studies also implicate aldosterone in the development of insulin resistance, hypertension, endothelial dysfunction, cardiovascular tissue fibrosis, remodelling, inflammation and oxidative stress. There is abundant evidence linking aldosterone, through non-genomic actions, to defective intracellular insulin signalling, impaired glucose homeostasis and systemic insulin resistance not only in skeletal muscle and liver but also in cardiovascular tissue. Blockade of the different components of the RAAS, in particular Ang II and AT1R, results in attenuation of insulin resistance, glucose homeostasis, as well as decreased cardiovascular disease morbidity and mortality. These beneficial effects go beyond to those expected with isolated control of hypertension. This review focuses on the role of Ang II and aldosterone in the pathogenesis of insulin resistance, as well as in clinical relevance of RAAS blockade in the prevention and treatment of the metabolic syndrome and cardiovascular disease. [source] The role of renin,angiotensin,aldosterone system-based therapy in diabetes prevention and cardiovascular and renal protectionDIABETES OBESITY & METABOLISM, Issue 12 2008Hussam Abuissa Hypertension increases the risk of type 2 diabetes mellitus (T2DM) and cardiovascular disease. In addition to lowering blood pressure, blockade of the renin,angiotensin,aldosterone system (RAAS) reduces the risk of new-onset T2DM and offers renal protection. Using a MEDLINE search, we identified multiple trials that reported the incidence of T2DM in patients taking inhibitors of RAAS. In this review, we will discuss the RAAS as a potential target in diabetes prevention and the mechanisms through which inhibitors of this system achieve such an important effect. We will also shed light on the beneficial cardiovascular and renal effects of RAAS blockade. Although multiple studies have demonstrated that inhibitors of RAAS, especially angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, can reduce the incidence of T2DM, randomized controlled studies are still needed to further elucidate their exact role in diabetes prevention. [source] Effects of raloxifene on the renin,angiotensin,aldosterone system and blood pressure in hypertensive and normotensive osteoporotic postmenopausal womenGERIATRICS & GERONTOLOGY INTERNATIONAL, Issue 1 2010Hiroyuki Sumino Aim: An increase in blood pressure after menopause has been documented. The renin,angiotensin,aldosterone system (RAAS) plays a central role in the regulation of blood pressure and in the pathophysiology of hypertension. This study investigated the effects of raloxifene, a selective estrogen receptor modulator, on components of the RAAS and blood pressure in hypertensive and normotensive osteoporotic postmenopausal women. Methods: A total of 41 hypertensive or normotensive postmenopausal women with osteoporosis or osteopenia were divided into four groups. Eleven hypertensive and eight normotensive women received raloxifene hydrochloride (60 mg/day) p.o. for 6 months, and 12 hypertensive and 10 normotensive women did not receive raloxifene hydrochloride for 6 months. In all of the hypertensive women, blood pressure had been controlled prior to the start of the study using a variety of antihypertensive drugs other than angiotensin-converting enzyme (ACE) inhibitors, angiotensin (Ang)II type 1 receptor antagonists or diuretics. Plasma renin activity (PRA), serum ACE activity, plasma AngI, AngII and aldosterone concentrations, and blood pressure were measured before and 6 months after the start of the study. Results: No significant changes in PRA, ACE activity, or the AngI, AngII or aldosterone levels were observed in any of the groups. In all the groups, blood pressure remained unchanged. Conclusion: Raloxifene may have no significant effect on the RAAS or blood pressure in hypertensive and normotensive osteoporotic postmenopausal women. [source] Selective aldosterone blocker, eplerenone, attenuates hepatocellular carcinoma growth and angiogenesis in miceHEPATOLOGY RESEARCH, Issue 5 2010Kosuke Kaji Aim:, The renin,angiotensin,aldosterone system (RAAS) has become known as a prerequisite for tumor angiogenesis, including hepatocellular carcinoma (HCC). Although angiotensin II is known to play an important role in tumor growth and angiogenesis, the role of aldosterone (Ald) is still obscure. The aim of our current study was to elucidate the effect of eplerenone, a clinically used selective Ald blocker (SAB), on murine HCC development especially in conjunction with angiogenesis. Methods:, To create an allograft model, we injected 1 × 106 of BNL-HCC cells into the flanks of BALB/c mice. After the tumor was established, SAB was administrated at dose of 100 mg/kg per day. Results:, Administration of SAB significantly suppressed HCC development along with inhibition of angiogenesis and expression of the vascular endothelial growth factor (VEGF), a potent angiogenic factor. SAB treatment resulted in a marked increase of apoptosis in the tumor, whereas tumor cell proliferation was not altered. Our in vitro study showed that SAB significantly suppressed the Ald-induced endothelial proliferation and tubular formation through inhibition of phosphorylation of the extracellular signal-regulated kinase 1/2. On the contrary, neither Ald nor SAB affected the proliferation of HCC cells in vitro. Conclusion:, Ald plays a pivotal role in HCC development through VEGF-mediated tumor angiogenesis, and SAB may be a potential new strategy in HCC therapy in the future. [source] Obesity,hypertension: an ongoing pandemicINTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 2 2007E. A. Francischetti Summary Considerable evidence has suggested that excessive weight gain is the most common cause of arterial hypertension. This association has been observed in several populations, in different regions of the world. Obesity,hypertension, a term that underscores the link between these two deleterious conditions, is an important public health challenge, because of its high frequency and concomitant risk of cardiovascular and kidney diseases. The obesity,hypertension pandemic imposes a considerable economic burden on societies, directly reflecting on healthcare system costs. Increased renal sodium reabsorption and blood volume expansion are central features in the development of obesity,hypertension. Overweight is also associated with increased sympathetic activity. Leptin, a protein expressed in and secreted by adipocytes, is the main factor linking obesity, increased sympathetic nervous system activity and hypertension. The renin,angiotensin,aldosterone system has also been causally implicated in obesity,hypertension, because angiotensinogen is expressed in and secreted by adipose tissue. Hypoadiponectinemia, high circulating levels of free fatty acids and increased vascular production of endothelin-1 (ET-1) have been reported as potential mechanisms for obesity,hypertension. Lifestyle changes are effective in obesity,hypertension control, though pharmacological treatment is frequently necessary. Despite the consistency of the mechanistic approach in explaining the causal relation between hypertension and obesity, there is yet no evidence that one class of drug is superior to the others in controlling obesity,hypertension. In this review, we present the current knowledge and research in obesity,hypertension, exploring the epidemiologic evidence of the association, its probable pathophysiological mechanisms and treatment issues. [source] Update on the Management of Hypertension: Recent Clinical Trials and the JNC 7JOURNAL OF CLINICAL HYPERTENSION, Issue 2004Marvin Moser MD Editor in Chief The following issues are highlighted: Emphasis is placed on the importance of systolic blood pressure elevations in estimating risk and in determining prognosis. A review of placebo-controlled clinical trials indicates that cardiovascular events are statistically significantly reduced with diuretic- or , blocker-based treatment regimens. The question of whether blood pressure lowering alone or specific medications make the difference in outcome is discussed. Based on the results of numerous trials, it is apparent that blood pressure lowering itself is probably of greater importance in reducing cardiovascular events than the specific medication used. Meta-analyses suggest, however, that the use of an agent that blocks the renin-angiotensin aldosterone system is probably more effective in diabetics and in patients with nephropathy than a regimen based on calcium channel blocker therapy. The Antihypertensive and Lipid-Lowering treatment to Prevent Heart Attack Trial (ALLHAT) reported no overall difference in coronary heart disease outcome among patients treated with a diuretic-based compared to a calcium channel blocker- or an angiotensin-converting enzyme inhibitor-based treatment program. However, patients in the diuretic group experienced fewer episodes of heart failure than in the calcium channel blocker group and fewer episodes of heart failure and strokes than those in the angiotensin-converting enzyme inhibitor group. Results were similar in diabetics and nondiabetics. Possible reasons for this outcome are discussed. The Australian National Blood Pressure 2 study, which was unblinded, reported a marginally significantly better outcome only in male patients receiving an angiotensin-converting enzyme inhibitor-based regimen compared to those receiving a diuretic-based program. Finally, the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) is reviewed. Highlights of this report include the new designation of prehypertension, i.e., blood pressures of 120,139 mm Hg/80,89 mm Hg. The JNC 7 suggested that diuretics should be the first-step drug of choice in most patients, but listed numerous specific reasons why other agents should be used in special situations. The report stressed that the majority of patients will require two or more medications to achieve goal blood pressure. [source] Folding in solution of the C-catalytic protein fragment of angiotensin-converting enzymeJOURNAL OF PEPTIDE SCIENCE, Issue 8 2009Sotirios-Spyridon M. Vamvakas Abstract Angiotensin-converting enzyme (ACE) is a key molecule of the renin,angiotensin,aldosterone system which is responsible for the control of blood pressure. For over 30 years it has become the target for fighting off hypertension. Many inhibitors of the enzyme have been synthesized and used widely in medicine despite the lack of ACE structure. The last 5 years the crystal structure of ACE separate domains has been revealed, but in order to understand how the enzyme works it is necessary to study its structure in solution. We present here the cloning, overexpression in Escherichia coli, purification and structural study of the Ala959 to Ser1066 region (ACE_C) that corresponds to the C-catalytic domain of human somatic angiotensin-I-converting enzyme. ACE_C was purified under denatured conditions and the yield was 6 mg/l of culture. Circular dichroism (CD) spectroscopy indicated that 1,1,1-trifluoroethanol (TFE) is necessary for the correct folding of the protein fragment. The described procedure can be used for the production of an isotopically labelled ACE959,1066 protein fragment in order to study its structure in solution by NMR spectroscopy. Copyright © 2009 European Peptide Society and John Wiley & Sons, Ltd. [source] The emerging role of ACE2 in physiology and disease,THE JOURNAL OF PATHOLOGY, Issue 1 2007I Hamming Abstract The renin,angiotensin,aldosterone system (RAAS) is a key regulator of systemic blood pressure and renal function and a key player in renal and cardiovascular disease. However, its (patho)physiological roles and its architecture are more complex than initially anticipated. Novel RAAS components that may add to our understanding have been discovered in recent years. In particular, the human homologue of ACE (ACE2) has added a higher level of complexity to the RAAS. In a short period of time, ACE2 has been cloned, purified, knocked-out, knocked-in; inhibitors have been developed; its 3D structure determined; and new functions have been identified. ACE2 is now implicated in cardiovascular and renal (patho)physiology, diabetes, pregnancy, lung disease and, remarkably, ACE2 serves as a receptor for SARS and NL63 coronaviruses. This review covers available information on the genetic, structural and functional properties of ACE2. Its role in a variety of (patho)physiological conditions and therapeutic options of modulation are discussed. Copyright © 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. [source] Modulation of body fluids and angiotensin II receptors in a rat model of intra-uterine growth restrictionTHE JOURNAL OF PHYSIOLOGY, Issue 3 2005Sophie Bédard We previously reported that sodium restriction during pregnancy reduces plasma volume expansion and promotes intra-uterine growth restriction (IUGR) in rats while it activates the renin,angiotensin,aldosterone system (RAAS). In the present study, we proceeded to determine whether expression of the two angiotensin II (ANGII) receptor subtypes (AT1 and AT2) change in relation to maternal water,electrolyte homeostasis and fetal growth. To this end, pregnant (gestation day 15) and non-pregnant Sprague-Dawley rats were randomly assigned to two groups fed either normal, or Na+ -restricted diets for 7 days. At the end of the treatment period, plasma aldosterone and renin activity as well as plasma and urine electrolytes were measured. Determinations for AT1 and AT2 mRNA and protein were made by RNase protection assay and photoaffinity labelling, respectively, using a number of tissues implicated in volume regulation and fetal growth. In non-pregnant rats, Na+ restriction decreases Na+ excretion without altering plasma volume, plasma Na+ concentration or the expression of AT1 and AT2 mRNA or protein in the tissues examined. In normally fed pregnant rats when compared to non-pregnant controls, AT1 mRNA increases in the hypothalamus as well as pituitary and declines in uterine arteries, while AT1 protein decreases in the kidney and AT2 mRNA declines in the adrenal cortex. In pregnant rats, Na+ restriction induces a decrease in plasma Na+, an increase in plasma urea, as well as a decline in renal urea and creatinine clearance rates. Protein levels for both AT1 and AT2 in the pituitary and AT2 mRNA in the adrenal cortex are lower in the Na+ -restricted pregnant group when compared to normally fed pregnant animals. Na+ restriction also induces a decrease in AT1 protein in the placenta. In conclusion, these results suggest that pregnancy may increase sensitivity to Na+ depletion by the tissue-specific modulation of ANGII receptors. Finally, these receptors may be implicated in the IUGR response to low Na+. [source] AT1 -receptor blockade and sympathetic neurotransmission in cardiovascular diseaseAUTONOMIC & AUTACOID PHARMACOLOGY, Issue 5-6 2003A. Nap Summary 1 The present survey is dealing with the interactions between the renin,angiotensin,aldosterone system (RAAS) and the sympathetic nervous system (SNS) in various organs and tissues, with an emphasis on the angiotensin AT-receptors located at the sympathetic nerve endings. 2 Angiotensin II, the main effector of the RAAS is known to stimulate sympathetic nerve traffic and its sequelae in numerous organs and tissues, such as the central nervous system, the adrenal medulla, the sympathetic ganglia and the sympathetic nerve endings. These stimulatory effects are mediated by AT1 -receptors and counteracted by AT1 -receptor antagonists. 3 Sympatho-inhibition at the level of the sympathetic nerve ending appears to be a class effect of the AT1 -receptor blockers, mediated by presynaptic AT1 -receptors. With respect to the ratio pre-/postsynaptic AT1 -receptor antagonism important quantitative differences between the various compounds were found. 4 Both the pre- and postjunctional receptors at the sympathetic nerve endings belong to the AT1 -receptor population. However, the presynaptic receptors belong to the AT1B -subtype, whereas the postjunctional receptors probably belong to a different AT1 -receptor subpopulation. 5 Sympatho-inhibition is a class effect of the AT1 -receptor antagonists. In conditions in which the SNS plays a pathophysiological role, such as hypertension and congestive heart failure, this property may well be of therapeutic relevance. [source] Maternal pseudo primary hyperaldosteronism in twin-to-twin transfusion syndromeBJOG : AN INTERNATIONAL JOURNAL OF OBSTETRICS & GYNAECOLOGY, Issue 1 2007IL Gussi Objective, To monitor changes in the maternal renin,angiotensin,aldosterone system following laser therapy and amnioreduction in severe twin-to-twin transfusion syndrome (TTTS). Design, Observational prospective study. Setting, Single university hospital in Poissy, France. Population, Sixty cases of TTTS at 16,26 weeks of gestation. Method, Maternal blood sampling before, 6 and 24 hours following the procedure. Main outcome measures, Plasma levels of aldosterone, renin, angiotensin II (AII), atrial natriuretic peptide (ANP), vasopressin, sodium, potassium and plasma proteins together with full blood count were measured before, 6 and 24 hours following the procedure. Results, TTTS is associated with maternal hyperaldosteronism dissociated from renin,angiotensin changes. Correcting TTTS by placental surgery and amnioreduction triggers incomplete correction of hyperaldosteronism, as early as 6 hours following the procedure, without changes in AII but an increase in the levels of ANP in plasma. Electrolyte concentrations remained stable despite haemodilution, while vasoactive hormone levels such as that of vasopressin remained unchanged. Conclusion, Mechanisms involved in marked fluid retention in TTTS are rapidly corrected by laser therapy followed by amnioreduction while maintaining electrolyte homeostasis. [source] CHARACTERIZATION OF THE ACUTE CARDIOVASCULAR EFFECTS OF INTRAVENOUSLY ADMINISTERED INSULIN-LIKE GROWTH FACTOR-I IN CONSCIOUS SPRAGUE-DAWLEY RATSCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 12 2006Nga Cao SUMMARY 1Insulin-like growth factor (IGF)-I has acute effects on cardiovascular function, including a well-characterized vasodilator response in isolated arteries. In addition to increasing the release of nitric oxide, IGF-I also has effects on a variety of other signalling pathways that affect vascular tone, in particular interactions with the sympathetic nervous system and the renin,angiotensin,aldosterone system. We sought to characterize the effects of intravenous IGF-I on blood pressure and on responses to noradrenaline (NA), angiotensin II, acetylcholine and dobutamine. 2Administration of IGF-I administration caused small decreases in mean arterial pressure (5.4 ± 1.5%) and responsiveness to the prazosin-sensitive vasoconstrictor effects of NA (a 2.1 ± 0.6-fold increase in ED50; n = 40; P < 0.01) and both effects were maximal at 200 µg/kg IGF-I. In addition, IGF-I significantly increased pulse pressure increases induced by low doses of dobutamine (from an increase in pulse pressure of 9.9 ± 1.2 to 13.4 ± 1.9 mmHg; n = 39; P < 0.05). Administration of IGF-I had no significant effect on responses to AngII or ACh. 3Intravenous administration of IGF-I receptor antisense oligonucleotides (400 µg/kg) abolished the effects of IGF-I on NA-induced vasoconstriction (n = 11; P < 0.05), whereas administration of a mismatch oligonucleotide did not. 4These data indicate that the maximal effects of exogenously administered IGF-I include modest direct vasodilation and inhibition of constrictor responses to NA and an increase in the effect of dobutamine on pulse pressure. The magnitude of these effects was less than what previous in vitro studies and those performed in anaesthetized animals may have indicated likely. 5The modest magnitude of the dilator effects of IGF-I observed in conscious rats in vivo in the present study suggests that IGF-I is unlikely to be a major player in regulating vascular tone in normotensive animals. [source] THE ,BODY FLUID PRESSURE CONTROL SYSTEM' RELIES ON THE RENIN,ANGIOTENSIN,ALDOSTERONE SYSTEM: BALANCE STUDIES IN FREELY MOVING DOGSCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 5-6 2005Erdmann Seeliger SUMMARY 1.,The physiological role of the ,renal body fluid pressure control system', including the intrarenal mechanism of ,pressure natriuresis', is uncertain. 2.,Balance studies in freely moving dogs address the following questions: (i) what is the physiological contribution of pressure natriuresis to the control of total body sodium (TBS); (ii) to what extent is long-term mean arterial blood pressure (MABP) determined by TBS and total body water (TBW); and (iii) during Na accumulation, is Na stored in an osmotically inactive form? 3.,Diurnal time-courses of Na excretion (UNaV) and MABP reveal no correlation. Spontaneous MABP changes do not affect UNaV. The long-term 20% reduction of renal perfusion pressure (RPP) results in Na retention via pressure-dependent stimulation of the renin,angiotensin,aldosterone system (RAAS), not via a pressure natriuresis mechanism. Prevention of pressure natriuresis does not result in ongoing Na retention when the RAAS is operative. The long-term 20% elevation of RPP induced by sustained TBS elevation facilitates Na excretion via pressure natriuresis, but does not restore TBS to normal. 4.,Changes in TBW correlate well with changes in TBS (r2 = 0.79). This correlation is even closer when concomitant changes in total body potassium are also considered (r2 = 0.91). 5.,With normal or elevated TBW, long-term MABP changes correlate well with TBW changes (r2 = 0.69). At lowered TBW, no correlation is found. 6.,In conclusion, the physiological role of pressure natriuresis is limited. Pressure natriuresis does not appear to be operative when RPP is changed from ,20 to +10% and neurohumoral control of UNaV is unimpeded. Within this range, pressure-dependent changes in the RAAS mediate the effects of changes in RPP on UNaV. Pressure natriuresis may constitute a compensating mechanism under pathophysiological conditions of substantial elevation of RPP. A large portion of the long-term changes in MABP are attributable to changes in TBW. The notion of osmotically inactive Na storage during Na accumulation appears to be invalid. [source] Renin Inhibitors in Chronic Heart Failure: The Aliskiren Observation of Heart Failure Treatment Study in ContextCLINICAL CARDIOLOGY, Issue 9 2010FESC, FRACP, Henry Krum PhD Renin-angiotensin aldosterone system (RAAS) activation is a key neurohormonal contributor to the progression of chronic heart failure. Strategies that block this activation have consistently demonstrated major beneficial impacts on morbidity and mortality in this setting. Direct renin inhibitors (DRIs) present a novel opportunity to block at an additional or alternative step in this pathway, that being conversion of angiotensinogen to angiotensin I. Theoretical benefits of blocking at the level of renin include: inhibition of the reflex activation of plasma renin activity induced by conventional downstream RAAS blockers. Minimization of angiotensin II and/or aldosterone escape and blocking upstream at the rate-limiting step of angiotensin I production. Preclinical and early-phase clinical studies have largely supported this hypothesis. In the Aliskiren Observation of Heart Failure Treatment study, patients with systolic chronic heart failure receiving background angiotensin converting enzyme (ACE) inhibitors or angiotensin receptor blockers and ,-blockers benefited from aliskiren in reduction vs placebo of plasma levels of brain natriuretic peptide, the primary efficacy endpoint of that study. Large-scale outcome trials are, however, required to definitively determine the benefits of a DRI strategy additional to, or as an alternative to, conventional approaches such as ACE inhibitors in the systolic chronic heart failure setting. Copyright © 2010 Wiley Periodicals, Inc. The authors have no funding, financial relationships, or conflicts of interest to disclose. [source] Human in vivo study of the renin,angiotensin,aldosterone system and the sympathetic activity after 8 weeks daily intake of fermented milkCLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 2 2010Lotte Usinger Summary Objective:, Milk fermented by lactic acid bacteria is suggested to have antihypertensive effect in humans. In vitro and animal studies have established an angiotensin-converting enzyme (ACE) inhibitor effect of peptides in fermented milk. However, other modes of action must be considered, because until today no human studies have confirmed an ACE inhibition in relation to the intake of fermented milk. Materials and methods:, We undertook a double-blinded randomized placebo-controlled study including 94 borderline-hypertensive persons to study the effect on human physiology of Lactobacillus helveticus fermented milk. The subjects were randomized into three groups: Cardi04-300 ml, Cardi04-150 ml or placebo. All components of the renin,angiotensin,aldosterone system were measured several times. Sympathetic activity was estimated by plasma noradrenaline and cardiovascular response to head-up tilt at baseline and after 8 weeks of intervention. Results:, No ACE inhibition of the fermented milk was demonstrated, as none of the components of the renin,angiotensin,aldosteron system changed. Plasma noradrenaline response to tilt test after intervention stayed unchanged between groups (P = 0·38), but declined in the group Cardi04-300 from 2·01 ± 0·93 nmol l,1 at baseline to 1·49 ± 0·74 nmol l,1 after 8 weeks (P = 0·002). There was no change in 24-h ambulatory blood pressure or heart rate between groups. Conclusions:, Despite a known ACE inhibitory effect in vitro and in animals, milk fermented with Lb. helveticus did not inhibit ACE in humans. Our results suggest that the intake of fermented milk decreases sympathetic activity, although not to an extent mediating reductions of blood pressure and heart rate in borderline-hypertensive subjects. [source] | |||||||||||||||||||||||||