PHARMACOLOGICAL EVIDENCE FOR RAAS INHIBITION ACE inhibitors and ARBs inhibit the RAAS in distinct ways. ACE inhibitors prevent the enzyme ACE from converting angiotensin I into angiotensin II (Table 1) [7, 8]. Angiotensin II is a vasoconstrictor that causes a host of deleterious effects, including vascular damage at the endothelial and structural levels [9]. Angiotensin II is an important cause...

This article discusses the pathophysiology of sodium and water retention in edematous disorders with a particular focus on cardiac failure, cirrhosis, and pregnancy. The body fluid volume hypothesis, which emphasizes the dominant role of arterial baroreceptors in renal sodium and water excretion, is reviewed. With arterial underfilling, either due to a decrease in cardiac output or peripheral a...

Unlike healthy subjects, overt congestive heart failure cannot "escape" the sodium- and water-retaining actions of mineralocorticoid excess. It is undefined whether escape occurs in asymptomatic left ventricular dysfunction (ALVD), which is characterized by preserved sodium homeostasis, natriuretic peptide activation, and normal circulating aldosterone. We hypothesized that, in ALVD, mineraloco...

Aldosterone is one of the most essential hormones synthesized by adrenal gland because it regulates water and electrolyte balance. G protein–coupled estrogen receptor (GPER) a newly discovered aldosterone receptor, which proposed to mediate non-genomic pathways while hormone simultaneously interacts with mineralocorticoid receptor. In contrast its cardio-protective role in postmenopausal women ...

Circulation Research is available at http://circres.ahajournals.org DOI: 10.1161/CIRCRESAHA.116.303587 Abstract: Blockers of the renin–angiotensin–aldosterone system (RAAS), that is, renin inhibitors, angiotensin (Ang)-converting enzyme (ACE) inhibitors, Ang II type 1 receptor antagonists, and mineralocorticoid receptor antagonists, are a cornerstone in the treatment of hypertension. How exactl...

Insulin-resistant, obese Zucker rats have blunted pressure natriuresis and are mildly hypertensive. This may involve inappropriate regulation of the renin-angiotensin-aldosterone system. To evaluate mechanisms underlying this defect, we employed the model of aldosterone escape. Male lean (L) and obese (O) Zucker rats were infused with aldosterone (2.8 mug/g body wt(3/4)) via osmotic minipump wh...

Chronic left ventricular overload and left heart failure were produced by an aortic-left atrial shunt and superimposed aortic constriction. With the shunt alone, plasma renin activity and sodium balance were normal. Superimposed aortic constriction produced a further elevation in left ventricular end diastolic pressure (LVEDP), increased plasma renin activity and sodium retention occurred. Seve...

THIS THESIS IS BASED UPON THE FOLLOWING ORIGINAL PAPERS: 1. Schjoedt KJ, Andersen S, Rossing P, Tarnow L, Parving H-H. Aldosterone escape during blockade of the reninangiotensin-aldosterone system in diabetic nephropathy is associated with enhanced decline in glomerular filtration rate. Diabetologia, 2004;47:1936-1939 2. Schjoedt KJ, Jacobsen P, Rossing K, Boomsma F, Parving H-H. Dual blockade ...