Mechanism of the decreased renal blood flow in the potassium-depleted conscious rat

Mechanism of the decreased renal blood flow in the potassium-depleted conscious rat. Although chronic potassium deficiency is a common clinical problem, the hemodynamic consequences of chronic sustained potassium depletion have not been clearly delineated. In this study, the hemodynamic consequences of chronic potassium depletion were evaluated in the conscious rat. Potassium-depleted rats had a decrease in mean arterial pressure which was caused by a decrease in systemic vascular resistance. In association with these changes in systemic hemodynamics, renal blood flow (RBF) was also decreased. The decreased renal blood flow was caused by an increased renal vascular resistance (RVR). Because plasma renin activity was increased the role of angiotensin II as a renal vasoconstrictor was evaluated by utilizing two angiotensin antagonists. Although the administration of saralasin to potassium-depleted rats did not alter systemic hemodynamics, RVR was decreased and RBF was increased. Similar results were obtained with the converting enzyme inhibitor teprotide. Because products of endoperoxide metabolism may cause renal vasoconstriction, the role of prostaglandins and thromboxanes as renal vasoconstrictors were evaluated by utilizing cyclo-oxygenase and thromboxane synthetase inhibitors. None of these agents altered systemic hemodynamics. Following the administration of indomethacin, RVR was decreased and RBF was increased in potassium-depleted rats. Similar results were obtained with another cyclo-oxygenase inhibitor, meclofenamate, and with imidazole, an inhibitor of thromboxane synthetase. Because neither angiotensin II nor products of endoperoxide metabolism could alone account for the increased renal vascular resistance of potassium depletion, studies were performed in potassium-depleted rats treated with indomethacin plus either saralasin or teprotide. In these potassium-depleted animals, renal blood flow was restored to normal. In conclusion, the decrease in renal blood flow and the increase in renal vascular resistance in potassium depletion is mediated by angiotensin II and a product of prostaglandin endoperoxide metabolism, most likely, thromboxane. Mecanismes de la diminution du debit sanguin renal chez le rat eveille deplete en potassium. Bien que la depletion chronique en potassium sois un probleme clinique commun, les consequences hemodynamiques de la depletion potassique chronique n'ont pas ete clairement definies. Dans cette etude, nous avons evalue les consequences hemodynamiques de la depletion potassique chronique chez le rat eveille. Les rats depletes en potassium avaient une diminution de la pression arterielle moyenne due a une diminution des resistances vasculaires peripheriques. En plus de ces modifications hemodynamiques peripheriques, le debit sanguin renal (RBF) etait diminue chez les animaux depletes en potassium. Cette diminution du debit sanguin renal etait due a l'augmentation des resistances vasculaires renales (RVR). L'activite renine plasmatique etant augmentee chez les animaux depletes en potassium, nous avons recherche un role vasoconstricteur renal de l'angiotensine II en utilisant deux antagonistes de l'angiotensine. Bien que l'administration de saralasine aux rats depletes en potassium n'ait pas altere l'hemodynamique peripherique, les RVR etaient diminuees. Nous avons obtenu des resultats identiques avec le teprotide, un inhibiteur de l'enzyme de conversion. Les produits du metabolisme des endoperoxides pouvant entrainer une vasoconstriction renale, nous avons recherche une vasoconstriction renale due aux prostaglandines et au thromboxane en employant des inhibiteurs du thromboxane, de la cyclo-oxygenase et de la synthetase. Aucun de ces agents n'a modifie l'hemodynamique peripherique. Apres administration d'indomethacine, les RVR etaient diminuees et le RBF etait augmente chez les rats depletes en potassium. Des resultats identiques ont ete obtenus avec un autre inhibiteur de la cyclo-oxygenase, le meclofenamate, et avec l'imidazole, un inhibiteur de la thromboxane synthetase. Puisque ni l'angiotensine II ni les produits du metabolisme des endoperoxides ne pouvaient a eux seuls rendre compte de l'augmentation des resistances vasculaires renales au cours de la depletion potassique, nous avons fait des etudes chez des rats depletes en potassium, traites par l'indomethacine plus de la Saralasine ou du Teprotide. Chez les animaux depletes en potassium, le debit sanguin renal est revenu a la normal. En conclusion, la diminution du debit sanguin renal, et l'augmentation des resistances vasculaires renales au cours de la depletion potassique sont mediees par l'angiotensine II et par un produit du metabolisme des endoperoxides, tres probablement le thromboxane.