Role of adrenal renin-angiotensin system in the control of aldosterone secretion in sodium-restricted rats

Abstract

This study examined the effect of the pharmacological manipulation of adrenal renin-angiotensin system (RAS) on aldosterone secretion from in situ perfused adrenals of rats kept on a normal diet and sodium restricted for 14 days. Neither the angiotensin-converting enzyme inhibitor captopril nor the nonselective angiotensin II receptor antagonist saralasin and the AT(1) receptor-selective antagonist losartan affected basal aldosterone output in normally fed rats. In contrast, they concentration dependently decreased aldosterone secretion in sodium-restricted animals, with maximal effective concentration ranging from 10(-7) to 10(-6) M. Captopril (10(-6) M), saralasin (10(-6) M), and losartan (10(-7) M) counteracted aldosterone response to 10 mM K(+) in sodium-restricted rats but not in normally fed animals. Collectively, these findings provide evidence that adrenal RAS plays a role in the regulation of aldosterone secretion, but only under conditions of prolonged stimulation of zona glomerulosa probably leading to overexpression of adrenal RAS.

Urinary Biomarkers for Screening for Renal Scarring in Children with Febrile Urinary Tract Infection: Pilot Study

“…16e18 The importance of tissue RAS in the kidneys, brain, heart, adrenal glands and blood vessels has also been reported. 19,20 Among them the kidneys are unique because all of the RAS components are present. The AGT gene and its protein expression have been shown in the proximal renal tubules, and renin, or a protein with renin-like activity, has been confirmed in cultured proximal tubule cells.…”

Kidney-specific enhancement of ANG II stimulates endogenous intrarenal angiotensinogen in gene-targeted mice

“…Emerging evidence has demonstrated the importance of the tissue RAS in the brain (1), heart (7), adrenal glands (34), vasculature (5,13,15,36), and kidneys (37). The RAS has been acknowledged as an endocrine, paracrine, autocrine, and intracrine system and thus it has been difficult to delineate the quantitative contributions of systemically delivered vs. locally formed ANG peptides to the levels existing in any given tissue (37).…”

Effect of enalapril injected in the early period of postnatal ontogeny on structure of adrenal glands in mature hypertensive NISAG rats

“…The experiments on regenerating adrenocortical tissue demonstrated the inhibitory action of enalapril on proliferation and steroidogenesis in the zona glomerulosa [12]. Similarly, captopril (another ACE inhibitor) decreases the level of aldosterone in the zona glomerulosa only in the animals with enhanced synthesis of this enzyme [8]. It can be hypothesized that administration of enalapril to prepubertal animals (during the development of blood pressure regulation systems) to a some extent decelerates hyperplasic processes in the zona glomerulosa of NISAG rats not only during treatment, but also at later terms.…”