Aldosterone secretion

Glonidine. Clonidine decreases blood pressure, heart rate, cardiac output, stroke volume, and total peripheral resistance. It activates central a2 adrenoceptors ia the brainstem vasomotor center and produces a prolonged hypotensive response. Clonidine, most efficaciously used concomitantly with a diuretic in long-term treatment, decreases renin and aldosterone secretion. 

Evidence has been put forward that 6-methoxy-l-methyl-l,2,3,4-tetrahydro-j3-carboline may be a component of animal tissues and may be identical with adrenoglomerulotrophine, a factor controlling aldosterone secretion, which is found in the pineal gland where it occurs together with 5-hydroxytryptamine... 

Induces dyskinesia/vasodilatation, schizophrenia/4- coordination Vaso constriction/cell proliferation/aldosterone secretion Vaso constriction/cell proliferation/bronchoconstriction 4-memory, sedation/vasodilatation/4 GI motility A blood pressure/4- GI secretion Vagal effects/A blood pressure/tachycardia... 

In the periphery, dopamine receptor levels are generally lower than those observed in brain, particularly in comparison to striatal dopamine receptor levels. Due to these low levels, knowledge of receptor distribution in the periphery is not yet comprehensive. Nevertheless, Dl-like receptors have been reported in the parathyroid gland and in the tubular cells of the kidney. D2-like dopamine receptors have also been observed in the kidney. In addition, dopamine D2 and D4 receptors have been found in the adrenal cortex, where they modulate aldosterone secretion. The... 

Cyclic GMP is made from GTP by the enzyme gua-nylyl cyclase, which exists in soluble and membrane-bound forms. Each of these isozymes has unique physiologic properties. The atriopeptins, a family of peptides produced in cardiac atrial tissues, cause natriuresis, diuresis, vasodilation, and inhibition of aldosterone secretion. These peptides (eg, atrial natriuretic factor) bind to and activate the membrane-bound form of guanylyl cyclase. This results in an increase of cGMP by as much as 50-fold in some cases, and this is thought to mediate the effects mentioned above. Other evidence links cGMP to vasodilation. A series of compounds, including nitroprusside, nitroglycerin, nitric oxide, sodium nitrite, and sodium azide, all cause smooth muscle re-... 

As nephron mass decreases, both the distal tubular secretion and GI excretion are increased because of aldosterone stimulation. Functioning nephrons increase FEK up to 100% and GI excretion increases as much as 30% to 70% in CKD,30 as a result of aldosterone secretion in response to increased potassium levels.30 This maintains serum potassium concentrations within the normal range through stages 1 to 4 CKD. Hyperkalemia begins to develop when GFR falls below 20% of normal, when nephron mass and renal potassium secretion is so low that the capacity of the GI tract to excrete potassium has been exceeded.30... 

N3. Naruse, M., Obana, K Naruse, K., Yamaguchi, H Demura, H., Inagami, T., and Shizume, K., Atrial natriuretic polypeptide inhibits cortisol secretion as well as aldosterone secretion in vitro from human adrenal tissue. J. Clin. Endocrinol. Metab. 64, 10-16 (1987). 

The mechanism by which potassium regulates aldosterone secretion is unclear however, this ion appears to have a direct effect on the adrenal cortex. An increase in the level of potassium in the blood stimulates the release of aldosterone. The effect of aldosterone on the kidney then decreases the level of potassium back to normal. 

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. 

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. 

Endothelin eta Human cDNA Acute pancreatitis, artherosderosis, cancer, hypertension, congestive heart failure, diabetes, obesity, inflammation, myocardial ischemia, prostatic hypertrophy, pulmonary fibrosis, stroke, ulcer, pain Vasoconstriction, bronchoconstriction, positive cardiac inotropy, proliferative responses, aldosterone secretion, neuroprotection... 

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). 

Stimulation of aldosterone secretion from the adrenal cortex, which increases Na ion reabsorption in the tubules of the kidney. Via an osmotic effect, this increases water uptake from the glomerular filtrate, which increases... 

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. 

In heart failure, cardiac output rises again because ventricular afterload diminishes due to a fall in peripheral resistance. Venous congestion abates as a result of (1) increased cardiac output and (2) reduction in venous return (decreased aldosterone secretion, decreased tonus of venous capacitance vessels). 

The diuretic effect of spironolactone develops fully only with continuous administration for several days. Two possible explanations are (1) the conversion of spironolactone into and accumulation of the more slowly eliminated metabolite canrenone (2) an inhibition of aldosterone-stimulated protein synthesis would become noticeable only if existing proteins had become nonfunctional and needed to be replaced by de novo synthesis. A particular adverse effect results from interference with gonadal hormones, as evidenced by the development of gynecomastia (enlargement of male breast). Clinical uses include conditions of increased aldosterone secretion, e.g., liver cirrhosis with ascites. 

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. 

For replacement of deficient aldosterone secretion, the fiuorinated steroid derivative fludrocortisone is used, usually in a dose of 100-200 pg per day. Replacement therapy is normally judged by monitoring blood pressure (lying and standing) and plasma electrolytes. 

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. 

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