Aldosterone Blood volume

Aldosterone A hormone produced in and secreted by the zona glomerulosa of the adrenal cortex. Aldosterone acts on the kidneys to reabsorb sodium and excrete potassium. It is also a part of the renin-angiotensin-aldosterone system, which regulates blood pressure and blood volume. 

Renin-angiotensin-aldosterone system (RAAS) The hormonal system controlled mainly by the kidneys and adrenal glands that regulates blood pressure, blood volume, and electrolyte balance. 

Aldosterone acts on the distal tubule of the nephron to increase sodium reabsorption. The mechanism of action involves an increase in the number of sodium-permeable channels on the luminal surface of the distal tubule and an increase in the activity of the Na+-K+ ATPase pump on the basilar surface of the tubule. Sodium diffuses down its concentration gradient out of the lumen and into the tubular cells. The pump then actively removes the sodium from cells of the distal tubule and into the extracellular fluid so that it may diffuse into the surrounding capillaries and return to the circulation. Due to its osmotic effects, the retention of sodium is accompanied by the retention of water. In other words, wherever sodium goes, water follows. As a result, aldosterone is very important in regulation of blood volume and blood pressure. The retention of sodium and water expands the blood volume and, consequently, increases mean arterial pressure. 

A decrease in blood volume or blood pressure may result in a decrease in the blood flow to the kidney. The kidney monitors renal blood flow by way of stretch receptors in the vessel walls. A decrease in renal blood flow stimulates the release of renin. The subsequent secretion of aldosterone causes retention of sodium and water and, therefore, an increase in blood volume and blood pressure back to normal. An increase in renal blood flow tends to cause the opposite effect. 

T Renin — T angiotensin II —> T aldosterone -4 T Na+ reabsorption Net effects 4 urine output T blood volume T mean arterial pressure... 

There is another system involved in blood pressure regulation the renin-angiotensin-aldosterone system (Fig. 2). The arterial blood pressure in the kidney influences intrarenal baroreceptors which together with the sodium load at the macula densa lead to renin liberation, angiotensin formation and aldosterone secretion, which by influencing the sodium balance changes the blood volume and influences the arterial blood pressure. 

Angiotensin II has two effects first, as a vasoconstrictor acting via receptors on vascular smooth muscle cells, and second, it stimulates the adrenal cortex gland to produce aldosterone (a mineralocorticoid steroid hormone, see Chapter 4). Aldosterone promotes the reabsorption of sodium from the renal tubule into the bloodstream and the resulting increase in osmolality (osmotic potential) of the blood causes water reabsorption in the nephrons. The outcome is an increase in blood volume and, therefore, pressure which inhibits (by negative feedback) further renin secretion from the JGA. 

Reabsorption of water is a fundamental function of the kidney because loss of fluid volume and reduction in blood pressure (hypotension) would have devastating consequences on all other tissues, possibly leading to severe metabolic disruption or even death. Blood pressure is monitored by the kidney and regulated by secretion of a proteolytic enzyme called renin, which initiates a cascade involving angiotensin and aldosterone to restore blood volume. 

Angiotensin 11 can raise blood pressure in different ways, including (1) vasoconstriction in both the arterial and venous limbs of the circulation (2) stimulation of aldosterone secretion, leading to increased renal reabsorption of NaCl and water, hence an increased blood volume (3) a central increase in sympathotonus and, peripherally, enhancement of the release and effects of norepinephrine. 

Secondary hypotension is a sign of an underlying disease that should be treated first. If stroke volume is too low, as in heart failure, a cardiac glycoside can be given to increase myocardial contractility and stroke volume. When stroke volume is decreased due to insufficient blood volume, plasma substitutes will be helpful in treating blood loss, whereas aldosterone deficiency requires administration of a mineralocor-ticoid (e.g., fludrocortisone). The latter is the drug of choice for orthostatic hypotension due to autonomic failure. A parasympatholytic (or electrical pacemaker) can restore cardiac rate in bradycardia. 

Mineralocorticoids are corticosteroids that help maintain blood volume and control renal excretion of electrolytes. Example aldosterone. 

Angiotensin II has a variety of effects. By constricting blood vessels it raises blood pressure, and by stimulating thirst centers in the brain it increases blood volume. Both angiotensins II and III also act on the adrenal gland to promote the synthesis and release of aldosterone. Most of the effects of angiotension II are mediated by 359-residue seven-helix G-protein linked receptors which activate phospholipase C.p q qr Like other steroid hormones aldosterone acts,via mineralocorticoid receptors, to control transcription of a certain set of proteins. The end effect is to increase the transport of Na+ across the renal tubules and back into the blood. Thus, aldosterone acts to decrease the loss of Na+ from the body. It promotes retention of water and raises... 

Fluid retention A fall in cardiac output decreases blood flow to the kidney, prompting the release of renin, with a resulting increase in the synthesis of angiotensin II and aldosterone (see p. 181). This results in increased peripheral resistance and retention of sodium and water. Blood volume increases, and more blood is returned to the heart. If the heart is unable to pump this extra volume, venous pressure increases and peripheral edema and pulmonary edema occur (Figure 16.4). These compensatory responses increase the work of the heart and, therefore, can contribute to the further decline in cardiac function. 

Mineralocorticoids help control the body s water volume and concentration of electrolytes, especially sodium and potassium. Aldosterone acts on kidney tubule cells, causing a reabsorption of sodium, bicarbonate, and water. Conversely, aldosterone decreases reabsorption of potassium, which is then lost in the urine. [Note Elevated aldosterone levels may cause alkalosis and hypokalemia, whereas retention of sodium and water leads to an increase in blood volume and blood pressure (see p. 180). Hyperaldosteronism is treated with spironolactone (see p. 232).]... 

Counterregulation in acute hypotension due to vasodilators (B). Increased sympathetic drive raises heart rate (reflex tachycardia) and cardiac output and thus helps to elevate blood pressure. The patients experience palpitations. Activation of the renin-angiotensin-aldosterone (RAA) system serves to increase blood volume, hence cardiac output. Fluid retention leads to an increase in body weight and, possibly, edemas. 

Ultimately, decompensation of the water and electrolyte balance is the result of (1.) splanchnic and peripheral arterial vasodilation, (2.) subsequent marked reduction in the effective arterial blood volume, (3.) increase in renin, aldosterone, vasopressin and noradrenaline, 4.) renal vasoconstriction with retention of sodium and water, and (5.) inadequate compensation of the plasma volume as a result of progressive hypalbuminaemia. 

All routine activities which can be carried out in a supine position should indeed be performed in this way (see below). As a result, renal perfusion is improved, the sympathicotonus lessened and the tubular absorption of sodium decreased. The breakdown of aldosterone is increased by > 30%, and its half-life returns more or less to normal. The central blood volume is enhanced. Removal of ascitic fluid via the subdiaphragmatic and mediastinal lymph vessels is facilitated. 

It was concluded from these and other studies in hypophysectomized animals that ACTH had no effect on aldosterone release. The volume-sensitive renal mechanism appears to be mainly responsible for postoperative aldosterone changes (S4), but it would now appear that ACTH also plays a part in regulating aldosterone secretion (S4). Removal of the pituitary leads to an immediate fall in aldosterone levels in adrenal venous blood (H9). A linear dose response relationship exists between the infusion rate of ACTH and aldosterone secretion rates (H9). Volume receptors in the right atrium and in the vascular tree respond to minor reductions in blood volume and play an important part in stimulating the aldosterone response (Bl, FI). Patients with suppression of cortisol production due to prolonged administration of steroids continue to secrete aldosterone and are able to increase their output after stress indicating the presence of another trophic factor as well as ACTH (T3). 

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