ABSTRACT
Locally produced prostaglandins (mainly prostacyclin, PGI2) stimulate renin release, apparently by a direct action on JG cells.
Intrarenal arteriolar pressure is monitored by stretch receptors (i.e., high pressure baroreceptors) in the JG body (i.e., afferent arterioles). When blood pressure falls, renin is released. In addition, a drop in GFR due to pressure and volume depletion reduces the filtered load and increases time for NaCI reabsorption in the proximal nephron. These combined events reduce delivery of NaCI to cells of the macula densa, which in turn sense the reduced NaCI concentration of the filtrate and signal adjacent JG cells to secrete renin into the circulation.
