Renin angiotensin produced

Hyperaldosteronism is a syndrome caused by excessive secretion of aldosterone. It is characterized by renal loss of potassium. Sodium reabsorption in the kidney is increased and accompanied by an increase in extracellular fluid. Clinically, an increased blood pressure (hypertension) is observed. Primary hyperaldosteronism is caused by aldosterone-producing, benign adrenal tumors (Conn s syndrome). Secondary hyperaldosteronism is caused by activation of the renin-angiotensin-aldosterone system. Various dtugs, in particular diuretics, cause or exaggerate secondary peadosteronism. 

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. 

Although the kidneys are not considered endocrine glands per se, they are involved in hormone production. Erythropoietin is a peptide hormone that stimulates red blood cell production in bone marrow. Its primary source is the kidneys. Erythropoietin is secreted in response to renal hypoxia. Chronic renal disease may impair the secretion of erythropoietin, leading to development of anemia. The kidneys also produce enzymes. The enzyme renin is part of the renin-angiotensin-aldosterone system. As will be discussed, these substances play an important role in the regulation of plasma volume and therefore blood pressure. Other renal enzymes are needed for the conversion of vitamin D into its active form, 1,25-d i hyd ro xyv itamin D3, which is involved with calcium balance. 

Structure and physiology of the kidney glomerular filtration tubular activity selective reabsorption and secretion, often using specific carrier mechanisms carbonic anhydrase and acid-base balance. The kidney also produces, and is sensitive to, hormones actions of the hormones ADH, aldosterone and PTH the kidney as a secretory organ erythropoietin, the renin-angiotensin system vitamin D3. 

Once vasodilatation was considered to be a good strategy, as it improves HF symptoms. However later studies showed that the disease itself was not influenced. The accent of HF treatment has moved to progression prevention with rigorous suppression of the renin angiotensin aldosterone system. Therapy with /3-blockers was also proven to be effective for the reduction of mortality. These treatments should be started early and the evaluation of their effectiveness in individual patients is difficult. As brain natriuretic peptide (BNP) is produced by the heart and more BNP is released in heart failure, the measurement of BNP in the blood has become popular as surrogate marker for the severity of heart failure and for the response of treatment for heart failure. 

Inhibition of the renin-angiotensin system with ACE inhibitors or ARBs may be incomplete because the drugs disrupt the negative feedback action of Ang II on renin secretion and thereby increase plasma renin activity. Other antihypertensive drugs, notably hydrochlorothiazide and other diuretics, also increase plasma renin activity. Aliskiren not only decreases baseline plasma renin activity in hypertensive subjects but also eliminates the rise produced by ACE inhibitors, ARBs, and diuretics and thereby results in a greater antihypertensive effect (Figure... 

Receptor sites for angiotensin II, the main active peptide of the renin-angiotensin system, have been found in the ovaries (Lightman et al., 1989). Ovarian renin-angiotensin may also have an autocrine role in angiogenesis, steroidogenesis and oocyte maturation. Inhibin is produced by the ovarian follicle and corpus luteum (Tsonis et al.,... 

Aldosterone, which is classified as a mineralo-corticoid, is produced under the control of the renin-angiotensin hormone system (Box 22-D), which is stimulated when sodium ion receptors in the kidneys... 

Fluid depletion may also be a serious problem during diuretic therapy. A decrease in blood volume may cause a reflex increase in cardiac output and peripheral vascular resistance because of activation of the baroreflex (see Chapter 18). This occurrence may produce an excessive demand on the myocardium, especially in patients with cardiac disease. Decreased blood volume may also activate the renin-angiotensin system, thereby causing further peripheral vasoconstriction and increased cardiac workload. Again, the effects of fluid depletion may be especially serious in patients with certain types of heart failure. 

The renin-angiotensin system involves several endogenous components that help regulate vascular tone in various organs and tissues.25,84,109 In systemic circulation, the renin-angiotensin system acts by a sequence of events summarized in Figure 21-2. Renin is an enzyme produced primarily in the kidneys. When blood pressure falls, renin is released from the kidneys into the systemic circulation. Angiotensinogen is a peptide that is produced by the liver and circulates... 

Mineralocorticoids are involved in controlling electtolyte and fluid levels.9,44 The primary mineralo-corticoid produced by the adrenal cortex is aldosterone. Aldosterone increases the reabsorption of sodium from the renal tubules. By increasing sodium reabsorption, aldosterone facilitates the reabsorption of water. Aldosterone also inhibits the renal reabsorption of potassium, thus increasing potassium excretion. Mineralocorticoid release is regulated by fluid and electrolyte levels in the body and by other hormones, such as the renin-angiotensin system. 

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