Aldosterone Essay Example | Topics and Well Written Essays - 1000 words

Aldosterone - Essay Example The scheme of renin-angiotensin-aldosterone system is shown at the Fig. 2. The renin is enzyme catalysing the reaction of the transformation of angiotensinogen into angiotensin I. Angiotensin I is converted into angiotensin II and the last one is partially converted into angiotensin III (Wehling, 1995). Both angiotensin II and III stimulate the synthesis of aldosterone by the adrenal glomerulosa layer . They bind to G-protein coupled receptors and stimulate the activity of phospholipase C and adenylate cyclase. This results in the increase of conversion of cholesterol to pregnenolone and corticosterone to aldosterone (Horton, 1994; Fuller, 2006). Aldosterone controls electrolyte excretion and intravascular fluid volume. It acts on the mineralocorticoid receptors of the distal renal tubules and cortical collecting ducts of the kidneys. Aldosterone regulates such physiological mechanisms as resorption and excretion of the electrolytes, particularly its action increases sodium resorption and potassium excretion. Sodium and water reabsorption is regulated by opening Na+ channels in the apical membranes of the tubular epithelium (Fuller, 2006; Rosansky, 2006). Correspondingly, opening K+ channels leads to increased potassium conductance from the cell and potassium excretion. These processes are regulated by the Na+/K+-ATPase (see Fig. 3). Aldosterone receptors are localised intracellularly. Their stimulation leads to DNA-binding and to the changes in the transcription of genes (Fig. 4). Fig. 4 Mechanisms of aldosterone action. There is interestingly that aldosterone do not only participate in the regulation of blood pressure but it also influences on the function of mononuclear leukocytes (Chai, 2005; Wehling, 1995). Thus the role of aldosterone in the regulation of blood pressure is related to its ability to increase sodium level in the blood, and, respectively change the tonus of vasculature and by the increase of circulating volume of blood (Hamilton, 2006; Rosansky, 2006). Many pathological conditions can cause hyperaldosteronism (Horton, 1994), which is characterised by the hypertension. Thus primary aldosteronism can be caused by solitary aldosterone-producing adrenal adenoma or mono- or bilateral hyperplasia of the zona glomerulosa. The patients suffering with aldosteronism have hypertension and hypokalemic alkalosis whereas hypernatremia is not common. Aldosterone deficiency causes hyponatriemia, hypovolemia, and hyperkalemia (Horton, 1994). There are many diseases characterising with the decrease of aldosterone biosynthesis, e.g adrenoleukodystrophy, adrenal hypoplasia, infections and excessive haemorrhages. Nevertheless, the most frequent cause of hypoaldosteronism is adrenal insufficiency, i.e. both aldosterone and cortisol secretion are affected. Thus fulminating sepsis, autoimmunic disorders and haemorrhagic