Glomerular prostaglandins, angiotensin II, and nonsteroidal anti-inflammatory drugs.
The glomerulus can, in part, regulate its own flow and filtration characteristics, both of which are determinants of the glomerular filtration rate. This occurs in part as the result of interactions between vasoconstrictors, e.g., angiotensin II (AII), and the vasodilatory prostaglandins E2 or I2. It is well accepted that these prostaglandins modulate the constrictor effects of AII on systemic and renal vasculature. Experimental data accumulated from micropuncture studies, analyses of isolated glomeruli in vitro, and glomerular mesangial cell cultures also support the hypothesis that AII-stimulated production of vasodilatory prostaglandins attenuates AII-induced constriction at the glomerular level as well. These studies help to explain the deleterious actions of nonsteroidal anti-inflammatory drugs on glomerular filtration in clinical conditions associated with a decreased effective blood volume and, therefore, activation of AII and other neurohormonal constrictors. These results have also furthered our understanding of the role of prostaglandins in maintaining renal function in human and experimental renal diseases that may be associated with enhanced hormonal constrictor activity.
D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000378:metabolism; D001127:Arginine Vasopressin / Q000494:pharmacology; D006801:Humans; D007674:Kidney Diseases / Q000378:metabolism; D007678:Kidney Glomerulus / Q000187:drug effects / Q000378:metabolism*; D011453:Prostaglandins / Q000096:biosynthesis* / Q000502:physiology
D000893:Anti-Inflammatory Agents; D001095:Arachidonic Acids; D011453:Prostaglandins; D000804:Angiotensin II; D001127:Arginine Vasopressin; D016718:Arachidonic Acid