Schematic view of a (granular) juxtaglomerular cell showing secretion mechanisms of renin . Renin is generated from prorenin. Renin secretion is inhibited by increases in and stimulated by decreases in intracellular calcium (Ca) concentrations. Voltage-sensitive Ca channels in the plasma membrane are activated by membrane stretch, which correlates with arterial pressure and is assumed to mediate baroreceptor-sensitive renin secretion. Renin secretion is also stimulated when the concentration of sodium (Na) and chloride (Cl) at the macula densa (MD) decreases [12,14]. The mediators of this effect are less well characterized; however, some studies suggest that the effect of Na and Cl in the lumen is more potent than is the baroreceptor mechanism . Many other factors affect rates of renin release and contribute to the physiologic regulation of renin. Renal nerves, by way of |3 receptors coupled to adenylyl cyclase (AC), stimulate renin release by increasing the production of cyclic adenosine monophosphate (cAMP), which reduces Ca release. Angiotensin II (AII) receptors (AT1 receptors) inhibit renin release, as least in vitro. Prostaglandins E2 and I2 (PGE2 and PGI2, respectively) strongly stimulate renin release through mechanisms that remain unclear. Atrial natriuretic peptide (ANP) strongly inhibits renin secretion. Constitutive nitric oxide (NO) synthase is expressed by macula densa (MD) cells . NO appears to stimulate renin secretion, an effect that may counteract inhibition of the renin gene by AII [17,18].
AME or Licorice Basolateral
Cortisone I 11ß HSD I I Cortisol )—^(Cortisol GR
Distal nephron cell
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