Journal of the renin-angiotensin-aldosterone system : JRAAS
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J Renin Angiotensin Aldosterone Syst · Mar 2012
Nephron-specific expression of components of the renin-angiotensin-aldosterone system in the mouse kidney.
The renin-angiotensin-aldosterone system (RAAS) plays an integral role in the regulation of blood pressure, electrolyte and fluid homeostasis in mammals. The capability of the different nephron segments to form components of the RAAS is only partially known. This study therefore aimed to characterize the nephron-specific expression of RAAS components within the mouse kidney. ⋯ Our data demonstrate a nephron-specific distribution of RAAS components. All components of the local RAAS - except ACE - are present in proximal convoluted tubules, emphasizing their involvement in sodium and water handling.
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J Renin Angiotensin Aldosterone Syst · Jun 2010
Renin-angiotensin-aldosterone system gene polymorphisms in coronary artery bypass graft surgery patients.
Candidates for coronary artery bypass grafting (CABG) represent a group of patients with well documented, severe coronary artery disease (CAD). Genetic polymorphisms of renin-angiotensin-aldosterone system (RAAS) components have been associated with CAD. We examined the association of polymorphisms of angiotensin-converting enzyme (ACE), angiotensinogen (AGT), and angiotensin II type 1 receptor (AT(1) receptor) with severe CAD in CABG patients. ⋯ There is no association of the analysed RAAS polymorphisms with severe CAD in CABG patients. However, within these patients, an association was found between AGT 235TT genotype and hypertension.
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J Renin Angiotensin Aldosterone Syst · Jun 2008
Rho-kinase inhibitor and nicotinamide adenine dinucleotide phosphate oxidase inhibitor prevent impairment of endothelium-dependent cerebral vasodilation by acute cigarette smoking in rats.
We previously reported that acute cigarette smoking can cause a dysfunction of endothelium-dependent vasodilation in cerebral vessels, and that blocking the angiotensin II (Ang II) type 1 (AT1) receptor with valsartan prevented this impairment. Our aim was to investigate the effects of a Rho-kinase inhibitor (fasudil) and a Nicotinamide Adenine Dinucleotide PHosphate (NADPH) oxidase inhibitor (apocynin) on smoking-induced endothelial dysfunction in cerebral arterioles. ⋯ Thus, inhibition of Rho-kinase and NADPH oxidase activities may prevent the above smoking-induced impairment of endothelium-dependent vasodilation.