Angiotensin aldosterone secretion

Stimulates Renin-angiotensin-aldosterone release ADH secretion Sympathetic response —> vasoconstriction Inhibits ANP secretion Stimulates ANP secretion Arteriole vasodilation Inhibits ADH secretion Renin-angiotensin-aldosterone secretion... 

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. 

In the presence of renin, an enzyme produced by specialized cells in the kidney, angiotensinogen is split to form angiotensin I. This prohormone is then acted upon by angiotensin-converting enzyme (ACE) as the blood passes through the lungs to form Ag II. Angiotensin II acts directly on the adrenal cortex to promote aldosterone secretion. 

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. 

Nesiritide is manufactured using recombinant techniques and is identical to the endogenous B-type natriuretic peptide secreted by the ventricular myocardium in response to volume overload. Consequently, nesiritide mimics the vasodilatory and natriuretic actions of the endogenous peptide, resulting in venous and arterial vasodilation increases in cardiac output natriuresis and diuresis and decreased cardiac filling pressures, sympathetic nervous system activity, and renin-angiotensin-aldosterone system activity. 

I to angiotensin II, a potent vasoconstrictor and stimulator of aldosterone secretion. ACE inhibitors also block the degradation of bradykinin and stimulate the synthesis of other vasodilating substances including prostaglandin E2 and prostacyclin. The fact that ACE inhibitors lower BP in patients with normal plasma renin activity suggests that bradykinin and perhaps tissue production of ACE are important in hypertension. 

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. 

The novel endocrine glands are the skin, gastrointestinal tract, adipose tissue, kidney (juxtaglomerular apparatus in the cortex which secretes renin that indirectly controls aldosterone secretion, via angiotensin-11), pineal gland, which secretes melatonin, and the heart (cardiac myocytes in the atria, which secrete atrial natriuretic peptide). 

Angiotensin-II-receptor antagonists These block the binding of this messenger to its receptors on the two target tissues, i.e. smooth muscle in the arterioles and the aldosterone-secreting cells in the adrenal cortex. 

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. 

I. Replacement therapy. The adrenal cortex (AC) produces the glucocorticoid cortisol (hydrocortisone) and the mine-ralocorticoid aldosterone. Both steroid hormones are vitally important in adaptation responses to stress situations, such as disease, trauma, or surgery. Cortisol secretion is stimulated by hypophyseal ACTH, aldosterone secretion by angiotensin 11 in particular (p. 124). In AC failure (primary AC insuffiency ... 

Angiotensin II receptor antagonists (AIIRAs) block the vasoconstrictor and aldosterone-secreting effects of angiotensin II by selectively blocking the binding of angiotensin II to the AT- receptor found in many tissues. 

Angiotensin II stimulates aldosterone synthesis and secretion from the glomerulosa cells of the adrenal cortex. The aldosterone secretion induced by angiotensin II in humans is not accompanied by an increase in glucocorticoid plasma levels. Chronic administration of angiotensin II will maintain elevated aldosterone secretion for several days to weeks unless hypokalemia ensues. 

Mechanism of Action AnACE inhibitor that suppresses the renin-angiotensin-aldos-terone system and prevents conversion of angiotensin I to angiotensin 11, a potent vasoconstrictor may also inhibit angiotensin II at local vascular and renal sites. Decreases plasma angiotensin II, increases plasma renin activity, and decreases aldosterone secretion. Therapeutic Effect Reduces peripheral arterial resistance, pulmonary capillary wedge pressure improves cardiac output and exercise tolerance. Pharmacokinetics ... 

Mechanism of Action An angiotensin II receptor antagonist that blocks the vasoconstrictor and aldosterone-secreting effects of angiofensin II, inhibiting the binding of angiofensinlltotheATi receptors TherapeuticEffect Causes vasodilation, decreases peripheral resistance, and decreases BP. 

Mechanism of Action An ACE inhibitor that suppresses the renin-angiotensin-aldosterone system. Decreases plasma angiotensin II, increases plasma renin activity, and decreases aldosterone secretion. Therapeutic Effect Reduces peripheral arterial resistance and BP. 

ACE). Hence, angiotensin II production is inhibited. Decrease in angiotensin II results in dilatation of peripheral vessels leading to a reduction in systemic vascular resistance and a decreased aldosterone secretion. They can be administered safely in patients of hypertension with diabetes mellitus or bronchial asthma. ACE inhibitors are efficacious drugs, are well tolerated and are useful antihypertensive drugs. ACE inhibitors are also used in coronary artery... 

Autonomic and hormonal control of cardiovascular function. Note that two feedback loops are present the autonomic nervous system loop and the hormonal loop. The sympathetic nervous system directly influences four major variables peripheral vascular resistance, heart rate, force, and venous tone. It also directly modulates renin production (not shown). The parasympathetic nervous system directly influences heart rate. In addition to its role in stimulating aldosterone secretion, angiotensin II directly increases peripheral vascular resistance and facilitates sympathetic effects (not shown). The net feedback effect of each loop is to compensate for changes in arterial blood pressure. Thus, decreased blood pressure due to blood loss would evoke increased sympathetic outflow and renin release. Conversely, elevated pressure due to the administration of a vasoconstrictor drug would cause reduced sympathetic outflow, reduced renin release, and increased parasympathetic (vagal) outflow. 

Captopril, many others Inhibit angiotensin converting enzyme Reduce angiotensin II levels reduce vasoconstriction and aldosterone secretion increase bradykinin Hypertension heart failure, diabetes Oral Toxicity Cough, angioedema teratogenic... 

Without ACTH, aldosterone secretion falls to about half the normal rate, indicating that other factors, eg, angiotensin, are able to maintain and perhaps regulate its secretion (see Chapter 17). Independent variations between cortisol and aldosterone secretion can also be demonstrated by means of lesions in the nervous system such as decerebration, which decreases the secretion of cortisol while increasing the secretion of aldosterone. 

These preparations cause alterations in the renin-angiotensin-aldosterone system. Plasma renin activity has been found to increase, and there is an increase in aldosterone secretion. 

Mechanism of Action Inhibit angiotensin-converting enzyme (ACE), resulting in decreased plasma angiotensin II which leads to decreased vasopressor activity and decreased aldosterone secretion ... 

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