Renin-angiotensin system, natriuretic peptides, obesity, metabolic syndrome, and hypertension: an integrated view in humans
ABSTRACT The obesity pandemic is closely related to hypertension and metabolic syndrome. Visceral adipose tissue plays a key role in the metabolic and cardiovascular complications of being overweight. The pathophysiological link between visceral adiposity and cardiometabolic complications focuses on insulin sensitivity, sympathetic nervous system, renin-angiotensin-aldosterone system (RAAS) and, only recently, on cardiac natriuretic peptide system (CNPS). RAAS and CNPS are endogenous antagonistic systems on sodium balance, cardiovascular system, and metabolism. The circulating RAAS is dysregulated in obese patients, and adipose tissue has a full local renin-angiotensin system that is active at local and systemic level. Adipocyte biology and metabolism are influenced by local renin-angiotensin system, with angiotensin II acting as a 'growth factor' for adipocytes. CNPS induces natriuresis and diuresis, reduces blood pressure, and, moreover, has powerful lipolytic and lipomobilizing activity in humans but not in rodents. In obesity, lower plasmatic natriuretic peptides levels with increasing BMI, waist circumference, and metabolic syndrome have been documented. Thus, reduced CNPS effects coupled with increased RAAS activity have a central role in obesity and its deadly complications. We propose herein an integrated view of the dysregulation of these two antagonistic systems in human obesity complicated with hypertension, metabolic syndrome, and increased cardiovascular risk.
- SourceAvailable from: Xingjiang Xiong[Show abstract] [Hide abstract]
ABSTRACT: Objectives. To assess the clinical evidence of Chinese herbal medicine (CHM) for obesity-related hypertension. Search Strategy. Electronic databases were searched until January, 2013. Inclusion Criteria. We included randomized clinical trials (RCTs) testing CHM against nondrug therapy and conventional western medicine, or combined with conventional western medicine against conventional western medicine. Data Extraction and Analyses. Study selection, data extraction, quality assessment, and data analyses were conducted according to Cochrane standards. Results. 11 trials were included. Methodological quality was evaluated as low. 1 trial investigated the efficacy of CHM plus nondrug therapy versus nondrug therapy. Positive results in diastolic blood pressure (DBP) (WMD: -5.40 [-5.88, -4.92]; P < 0.00001) were found in combination group. 1 trial investigated the efficacy of CHM versus conventional western medicine. Positive results in systolic blood pressure (SBP) (WMD: -1.39 [-2.11, -0.67]; P = 0.0002) were found in CHM. 9 trials investigated the efficacy of CHM plus conventional western medicine versus conventional western medicine. Positive results in SBP (WMD: -6.71 [-11.08, -1.25]; P = 0.02) were found in combination group. The safety of CHM is unknown. Conclusions. No definite conclusion could be got due to poor methodological quality. Rigorously designed trials are warranted to confirm these results.Evidence-based Complementary and Alternative Medicine 06/2013; 2013:757540. DOI:10.1155/2013/757540 · 1.88 Impact Factor
- Cardiomyopathies - From Basic Research to Clinical Management, 02/2012; , ISBN: 978-953-307-834-2
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ABSTRACT: We compared the effects of tempol (300 μmol kg(-1) plus 300 μmol kg(-1) h(-1), n=14) and candesartan (10 μg kg(-1) plus 10 μg kg(-1) h(-1), n=14) on renal haemodynamics, excretory function, and responses to electrical stimulation of the renal nerves (RNS) in lean and obese rabbits under pentobarbitone anaesthesia. Depressor responses to tempol (-16 ± 2 mmHg) and candesartan (-12 ± 1 mmHg) were similar. Candesartan, but not tempol, significantly increased basal renal blood flow (RBF; +36 ± 7%). Tempol, but not candesartan, significantly reduced glomerular filtration rate (GFR; -30 ± 10%) and sodium excretion (U(Na)V; -44 ± 14%). RNS induced frequency-dependent reductions in RBF (-20 ± 3% at 1 Hz), GFR (-28 ± 6% at 1 Hz) and U(Na)V (-55 ± 6% at 1 Hz). Candesartan blunted these responses. Tempol did not significantly alter RBF and GFR responses to RNS but blunted the U(Na)V response. Responses to RNS, and the effects of tempol and candesartan, were similar in lean compared with obese rabbits. Unlike candesartan, tempol did not induce renal vasodilatation, maintain GFR and U(Na)V during reductions in arterial pressure, or blunt neurally-mediated vasoconstriction. In conclusion, unlike the AT(1)-receptor antagonist candesartan, tempol does not blunt the effects of RNS on renal haemodynamic function. Furthermore, under the current experimental conditions superoxide appears to make little contribution to the actions of endogenous angiotensin II on baseline renal haemodynamics or excretory function, or their responses to RNS.Autonomic neuroscience: basic & clinical 02/2012; 168(1-2):48-57. DOI:10.1016/j.autneu.2012.01.007 · 1.37 Impact Factor