Aldosterone angiotensin affecting

The hypotensive response to captopril is accompanied by a fall in plasma aldosterone and angiotensin II levels and an increase in plasma renin activity. Serum potassium levels are not affected unless potassium supplements or potassium-sparing diuretics are used concomitantly this can result in severe hyperkalemia. 

Of 12 patients with ascites due to cirrhosis of the liver, who received subcutaneous octreotide 300 micrograms bd for 11 days, 11 had increased renal plasma flow and 10 had a reduced GFR (44). Creatinine concentrations did not change. The effects of octreotide on the kidneys have been variably reported in previous studies. In patients with cirrhosis the effects are likely to be affected by the activated renin-angiotensin-aldosterone system. 

Beta-adrenoceptor blockers. The realisation that the coiuse of chronic heart failure can be adversely affected by activation of the renin-angiotensin-aldosterone and sympathetic nervous systems led to exploration of possible benefit from P-adrenoceptors in a condition where, paradoxically, such drugs can have an adverse effect. Clinical trials have, indeed, shown that bisoprolol, carvedilol or metoprolol lower mortality and decrease hospitalisation when added to diuretics, digoxin and an ACE inhibitor (see below). 

Many factors contribute to ventricular remodehng, including neurohormonal factors (e.g., activation of the renin-angiotensin-aldosterone and sympathetic nervous systems), hemodynamic factors, mechanical factors, and changes in gene expression. This process affects both cardiomyocytes (cardiomyocyte hypertrophy, loss of cardiomyocytes) and the extracellular matrix (increased interstitial fibrosis), thereby promoting both systohc and diastohc dysfunction. ... 

Blood pressure is also regulated via the hormonal feedback loop shown in Figure II-1-3. The system is affected only by decreases in mean blood pressure (hypotension), which result in decreased renal blood flow. Decreased renal pressure causes the release of renin, which promotes formation of the angiotensins. Angiotensin II increases aldosterone release from the adrenal cortex, which, via its mineralocorticoid actions to retain sodium and water, increases blood volume. Increased venous return results in an increase in cardiac output. Angiotensin II also causes vasoconstriction, resulting in an increase in TPR. 

Because the control mechanisms that attempt to maintain blood pressure constant are intact in patients with pheochromocytoma (they are reset in patients with ordinary hypertension), a number of compensatory changes are observed in pheochromocytoma patients tsee Figure 6 ). These include reduced renin, angiotensin, and aldosterone levels in the blood. With the reduced aldosterone effect on the kidney, more salt and water is excreted, reducing blood volume. Since the red cell mass is not affected, hematocrit is often increased. If the tumor releases only norepinephrine, a compensatory bradycardia may also be present, but most patients release enough epinephrine to maintain heart rate at a normal or even increased level. 

In addition, due to their effects on aldosterone, the ACE inhibitors and angiotensin II antagonists may increase potassium concentrations and can therefore have additive hyperkalaemic effects with other drugs that cause elevated potassium levels. Furthermore, drugs that affect renal function may potentiate the adverse effects of ACE inhibitors and angiotensin II antagonists on the kidneys. 

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