Cardiovascular system aldosterone

Atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP) are members of a family of so-called natriuretic peptides, synthesized predominantly in the cardiac atrium, ventricle, and vascular endothelial cells, respectively (G13, Y2). ANP is a 28-amino-acid polypeptide hormone released into the circulation in response to atrial stretch (L3). ANP acts (Fig. 8) on the kidney to increase sodium excretion and glomerular filtration rate (GFR), to antagonize renal vasoconstriction, and to inhibit renin secretion (Ml). In the cardiovascular system, ANP antagonizes vasoconstriction and shifts fluid from the intravascular to the interstitial compartment (G14). In the adrenal cortex, ANP is a powerful inhibitor of aldosterone synthesis (E6, N3). At the hypothalamic level, ANP inhibits vasopressin secretion (S3). It has been shown that some of the effects of ANP are mediated via a newly discovered hormone, called adreno-medullin, controlling fluid and electrolyte homeostasis (S8). The diuretic and blood pressure-lowering effect of ANP may be partially due to adrenomedullin (V5). 

CARDIOVASCULAR SYSTEM The most striking cardiovascular effects of corticosteroids result from mineralocorticoid-induced changes in renal Na+ excretion, as is evident in primary aldosteronism. The resultant hypertension can lead to a diverse group of adverse effects on the cardiovascular system (see Chapter 32). Consistent with the known actions of mineralocorticoids in the kidney, restriction of dietary Na can lower the blood pressure considerably in mineralocorticoid excess. 

A number of mechanisms has been postulated to explain the effects of Cd on the cardiovascular system, e.g. interference with catecholamine metabolism (inhibition of MAO-activity), direct action on vascular walls changing peripheral compliance or modifying responses to endogeneous pressor substances, modification of cardiac performance and involvement of the renin-angiotensin-aldosteron system, possibly triggered by changes in sodium reabsorption. 

Interestingly, suppressing the Renin-Angioten-sin-Aldosteron System (RAAS) using ACE-I or ARB will reduce the risk for HF in patient with diabetes, even if they do not have hypertension. These drugs have been shown to be beneficial for patients with diabetic nephropathy, and via the same mechanism to also reduce the HF risk. There is abundant support in the literature for the usefulness of RAAS suppression in diabetes combined with cardiovascular disease. 

Autonomic and hormonal control of cardiovascular function. Note that two feedback loops are present the autonomic nervous system loop and the hormonal loop. The sympathetic nervous system directly influences four major variables peripheral vascular resistance, heart rate, force, and venous tone. It also directly modulates renin production (not shown). The parasympathetic nervous system directly influences heart rate. In addition to its role in stimulating aldosterone secretion, angiotensin II directly increases peripheral vascular resistance and facilitates sympathetic effects (not shown). The net feedback effect of each loop is to compensate for changes in arterial blood pressure. Thus, decreased blood pressure due to blood loss would evoke increased sympathetic outflow and renin release. Conversely, elevated pressure due to the administration of a vasoconstrictor drug would cause reduced sympathetic outflow, reduced renin release, and increased parasympathetic (vagal) outflow. 

Dzau V. The cardiovascular continuum and renin-angiotensin-aldosterone system blockade. J Hypertens Suppl. 2005 23 S9-S17. 

Bristow MR, Port JD, Kelly RA. Inhibitors of the renin-angiotensin-aldosterone system. In Braunwald E, Libby P Zipes DD, Zipes DP eds. Heart Disease A Textbook of Cardiovascular Medicine. Philadelphia WB Saunders, 2001 582-583. 

Spironolactone induced a marked and statistically significant inhibitory effect on the cardiovascular reactivity to both the adrenergic and the rennin-angiotensin-aldosterone systems. This may play a major role in the vascular and antihypertensive properties of the drug [68],... 

Angiotensin II is involved in the renin-angiotensin-aldosterone system, which regulates blood pressure, sodium and water homoeostasis by the kidneys, and cardiovascular function. Angiotensin II stimulates the synthesis and secretion of aldosterone and raises blood pressure via a direct vasoconstrictor effect. 

Cardiovascular Paradoxical severe hypertension occurred in three patients with advanced chronic kidney disease and bilateral renal artery stenosis. After the introduction of ramipril, an initial fall in blood pressure was followed by a paradoxical increase in blood pressure. This was postulated to be caused by activation of the renin-angiotensin-aldosterone system, as a result of renal artery stenosis and renal dysfunction [55 ]. 

Cardiovascular As was reported in SEDA-32 (p. 817), ILLUMINATE, an outcome study that recruited around 15 000 statin-eligible patients with coronary heart disease or type 2 diabetes mellitus was terminated after a median follow-up of only 550 days, because of a small but significant increase in major cardiovascular events in those taking torcetrapib - - atorvastatin compared with those taking atorvastatin alone (49 versus 35 cardiovascular deaths) [69. This occurred despite a 72% increase in HDL cholesterol and a 25% reduction in LDL cholesterol compared with the statin alone. This was almost certainly correctly attributed to activation of the renin-angiotensin-aldosterone system, resulting in increments in blood pressure and aldosterone and reduced potassium. 

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