Renin release regulation

While the rate limiting step of the cascade is the renin release, the biological active component is the octapeptide angiotensin n. It is an essential regulator of fluid and electrolyte balance as well as blood pressure. It exerts its actions on various structures like blood vessels, adrenal cortex, kidney and central nervous system. Although at least two different receptor subtypes for angiotensin II have been identified (ATi and AT2) the ATi-subtype is responsible for most of the cardiovascular effects of the agonist. 

The major eicosanoid products of the renal cortex are PGE2 and PGI2. Both compounds increase renin release normally, however, renin release is more directly under Bi adrenoceptor control. The glomeruli synthesize small amounts of TXA2 but this potent vasoconstrictor does not appear to be responsible for regulating glomerular function in healthy humans. 

Regulation of renin release. Numbers 1-7 indicate the steps involved in the secretion of renin by the juxtaglomerular apparatus and its action. , Stimulatory, inhibitory f increa.sed production. 

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. 

Although a change in NaCl transport is a key modulator, regulation of the macula densa pathway pathway depends more on the luminal concentration of Ct than Na. Physiological changes in Ct concentrations (e.g., from 20 to 60 mEq/L) at the macula densa profoundly affect macula densa—mediated renin release. 

The pathophysiological effects of PG cannot readily be isolated from those of many other hormones and factors which regulate the haemodynamic, tubular and endocrine functions of the kidneys. It is clear that renal PG play a central role in water metabolism and renin release, whereas the effect of PG on transepithelial transport and the pathogenetic potential of other eicosanoids, such as leukotrienes, have not been fully explored. In addition, recent studies have supported the concept that enhanced generation of the vasoconstrictor, TXA2, is prominent in many experimental models of... 

Mills [28] has reviewed the intricacies of the regulation of renin release. Molecular details are not available. 

In an attempt to conserve sodium, the kidney secretes renin increased plasma renin activity increases the release of aldosterone, which regulates the absorption of potassium and leads to kafluresis and hypokalemia. Hypokalemia is responsible in part for decreased glucose intolerance (82). Hyponatremia, postural hypotension, and pre-renal azotemia are considered of tittle consequence. Hypemricemia and hypercalcemia are not unusual, but are not considered harmful. However, hypokalemia, progressive decreased glucose tolerance, and increased semm cholesterol [57-88-5] levels are considered... 

The zona glomerulosa is responsible for the production of the mineralocorticoids aldosterone, deoxycorticosterone, and 18-hydroxy-deoxycorticosterone. Aldosterone promotes renal sodium retention and excretion of potassium. Its synthesis and release are regulated by renin in response to decreased vascular volume and renal perfusion. Adrenal aldosterone production is regulated by the renin-angiotensin-aldosterone system. 

Describe factors that regulate the release of renin... 

---