We have provided evidence that the renal PG's intimately participate in the release of renin. Prostaglandins are the sole mediators of renin release secondary to the stimulation of the renal baroreceptors and the macula densa. In addition, stimulation of α-adrenergic receptors result in PG-mediated renin release via the activation of the macula densa. The β-adrenergic mechanism of renin release is independent of the PG system. Of the PG's produced by the renal cortex, only PGI2 and PGE2 are active in releasing renin both in vitro and in vivo. Although PGI2 is a more attractive candidate than PGE2 as a mediator of the release of renin, because it is produced by the vascular endothelium, which is in direct proximity to the juxtaglomerular apparatus, the present evidence cannot incriminate one PG over the other as the mediator. The knowledge that PG's participate in the release of renin has enhanced our understanding of clinical entities like Bartter's syndrome and hypertension.
CITATION STYLE
Gerber, J. G., Olson, R. D., & Nies, A. S. (1981). Interrelationship between prostaglandins and renin release. Kidney International, 19(6), 816–821. https://doi.org/10.1038/ki.1981.85
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