Renin-angiotensin-aldosterone mechanism fluid volume

The renin-angiotensin-aldosterone mechanism also responds to changes in fluid volume ... 

The low fluid volume triggers the renin-angiotensin-aldosterone mechanism. 

Physiologically, in both normal and hypertensive individuals, blood pressure is maintained by moment-to-moment regulation of cardiac output and peripheral vascular resistance, exerted at three anatomic sites (Figure 11-1) arterioles, postcapillary venules (capacitance vessels), and heart. A fourth anatomic control site, the kidney, contributes to maintenance of blood pressure by regulating the volume of intravascular fluid. Baroreflexes, mediated by autonomic nerves, act in combination with humoral mechanisms, including the renin-angiotensin-aldosterone system, to coordinate function at these four control sites and to maintain normal blood pressure. Finally, local release of vasoactive substances from vascular endothelium may also be involved in the regulation of vascular resistance. For example, endothelin-1 (see Chapter 17) constricts and nitric oxide (see Chapter 19) dilates blood vessels. 

Diuretics are drugs that increase the rate of urine flow clinically useful diuretics also increase the rate of excretion of Na+ (natiiuresis) and an accompanying anion, usually CD. Most clinical applications of diuretics aim to reduce extracellular fluid volume by decreasing total-body NaCl content. Although continued administration of a diuretic causes a sustained net deficit in total-body Na+, the time course of natriuresis is finite because renal compensatory mechanisms bring Na+ excretion in line with Na+ intake, a phenomenon known as diuretic braking. Compensatory mechanisms include activation of the sympathetic nervous system, activation of the renin-angiotensin-aldosterone axis, decreased arterial blood pressure (which reduces pressure natriuresis), hypertrophy of renal epithelial cells, increased expression of renal epithelial transporters, and perhaps alterations in natriuretic hormones such as atrial natriuretic peptide. 

The low perfusion pressme to the kidneys triggers feedback mechanisms such as the renin-angiotensin-aldosterone system to stimulate vasoconstriction and reabsorption of sodium and water in an attempt to increase fluid volume. 

From the point of view of potassium balance, there is increased renal excretion of potassium, loss of potassium in the vomitus and no potassium being delivered for absorption in the alimentary tract. All these factors contribute to a severe depletion of the body s total potassium content. Yet another factor contributes to potassium loss. A drop in volume of the circulating blood leads to aldosterone secretion via the renin-angiotensin mechanism which, in turn, promotes sodium reabsorption in the renal tubule this contributes further to excessive renal loss of potassium and hydrogen ions. The acidity of the urine is inappropriate as a response to metabolic alkalosis, but the preservation of electrolyte and fluid volume takes precedence over the acid-base disturbance. These various efiects all combine to yield a positive feedback system driving the metabolic alkalosis which, if not treated, reaches lethal levels in a few days. 

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