Compartmentalization of prostaglandins and prostacyclin within the kidney: implications for renal function.
When renal function is compromised, the circulation to the kidney is sustained by a major prostaglandin component, withdrawal of which results in significant hemodynamic effects, particularly reduction in blood flow to the inner cortex and medulla. Prostaglandins modulate the effects of vasoactive hormones by attenuating the renal actions of the renin-angiotensin system and contributing to and, perhaps, mediating some of those of the kallikreinkinin system. In addition, a prostaglandin mechanism, presumably located in the renal arterioles, participates in the regulation of renin release. Although cyclooxygenase is present in several renal tissues, the major products of arachidonic acid metabolism may be tissue specific and, consequently, their effects may be primarily restricted to one compartment, e.g., the proposed interaction of prostacyclin and renin within the vascular pole of the glomerulus; and PGE2/PGF2a with the kallikrein-kinin system within the urinary compartment. The former is related to the regulation of renin release and renal vascular resistance and the latter to the excretion of water and perhaps salt.
D000818:Animals; D004231:Diuresis; D004285:Dogs; D011464:Epoprostenol / Q000502:physiology*; D007668:Kidney / Q000098:blood supply / Q000502:physiology*; D007679:Kidney Medulla / Q000378:metabolism; D007684:Kidney Tubules / Q000378:metabolism; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism; D011453:Prostaglandins / Q000502:physiology*; D012039:Regional Blood Flow; D012077:Renal Artery / Q000378:metabolism; D013931:Thromboxanes / Q000502:physiology; D014882:Water-Electrolyte Balance
D011453:Prostaglandins; D013931:Thromboxanes; D011464:Epoprostenol; D011451:Prostaglandin-Endoperoxide Synthases