Renin release inhibition

As an autacoid, adenosine possesses negative chronotropic and inotropic effects, is a vasodilator in almost all vascnlar beds, inhibits nenrotransmitter release in the CNS, canses sedation, displays anticonvnlsant activity, regulates renin release, inhibits platelet aggregation, modulates lymphocyte function, induces bronchospasm, and inhibits hpolysis. 

By themselves, potassium-sparing agents are relatively weak antihypertensives. In general, there are four ways to reduce the activity of the RAS. The first way is the use of p-blockers to reduce renin release from the juxtaglomerular (JG). The second way, the direct inhibition of the activity of renin, although being actively investigated has not been successful in the clinical arena thus far. The third way is to inhibit the activity of the... 

The exact hypotensive mechanism of /1-blockers is not known but may involve decreased cardiac output through negative chronotropic and inotropic effects on the heart and inhibition of renin release from the kidney. 

Alpha receptors There are two major groups of alpha receptors, and a. Activation of postsynaptic receptors increases the intracellular concentration of calcium by activation of a phospholipase G in the cell membrane via G protein, receptor is responsible for inhibition of renin release from the kidney and for central a-adrenergically mediated blood pressure depression. 

The release of renin is altered by a wide variety of pharmacologic agents. Renin release is stimulated by vasodilators (hydralazine, minoxidil, nitroprusside), 13-adrenoceptor agonists, cx-adrenoceptor antagonists, phosphodiesterase inhibitors (eg, theophylline, milrinone, rolipram), and most diuretics and anesthetics. This stimulation can be accounted for by the control mechanisms just described. Drugs that inhibit renin release are discussed below. 

Kidney a2 inhibition of renin release and modulation of tubular function Mostly a2A Limited... 

Adipocytes (inhibit lipoiysis) Intestinal secretions (inhibit) Platelet aggregation (stimulate) Kidney (renin release)... 

Inhibition of ACE prevents formation of angiotensin II, which is a powerful vasoconstrictor (see Eigure 4.5). This results in vasodilation and fall in peripheral vascular resistance and therefore reduction in blood pressure. Reduction in blood pressure also improves cardiac output. In addition, ACE inhibitors suppress aldosterone secretion producing a reduction in salt and water retention and improve renal blood flow, which in turn inhibits renin release. 

By extracting water from intracellular compartments, osmotic diuretics expand the extracellular fluid volume, decrease blood viscosity, and inhibit renin release. These effects increase RBF, and the increase in renal medullary blood flow removes NaCl and urea from the renal medulla, thus reducing medullary tonicity. Under some circumstances, prostaglandins may contribute to the renal vasodilation and medullary washout induced by osmotic diuretics. A reduction in medullary tonicity causes a decrease in the extraction of water from the DTL, which limits the concentration of NaCl in the tubular fluid entering the ATL. This latter effect diminishes the passive reabsorption of NaCl in the ATL. In addition, osmotic diuretics may also interfere with transport processes in the TAL. 

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