Abstract
Summary
The effect of adrenergic interruption on the renal vascular resistance (RVR) increase associated with the prosta-glandin (PG) synthetase inhibitor, indometh-acin, was studied in anesthetized, surgically stressed dogs, α-Adrenergic blockade was produced with phenoxybenzamine. In response to indomethacin, neither the increase in RVR nor the decrease in renal blood flow (RBF) differed between the α-blocked (n = 11) and the control dogs (n = 9). In a separate series of experiments, the effect of renal de-nervation on the renal vascular response to indomethacin was examined in the same kidney before and 5-6 days after that kidney was surgically denervated (n = 7). The indo-methacin-associated increase in RVR and decrease in RBF did not differ in the intact and denervated kidneys. Under conditions of anesthesia and surgical stress in normovolemic dogs, neither α-adrenergic blockade nor renal denervation changed the renal hemodynamic response to indomethacin. We, therefore, conclude that under these conditions the in-domethacin-induced increase in RVR is not mediated by elimination of PG modulation of renal sympathetic vasoconstrictor activity.
We wish to thank Millie Reeves, Loise Dunn, Nevin Breedlove, and Charles Peach for technical assistance and Trent Tadsen and Chandler McDavid for art work.
We thank Mr. Earl A. Kimes of Smith, Kline, and French for phenoxybenzamine and Dr. Horace O. Brown of Merck, Sharp, and Dohme for indomethacin.
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