Abstract

We have investigated the ability of the one-kidney, one-clip (1K,1C) hypertensive rat to develop a hyperthermic response to intracerebroventricular injection of prostaglandin (PG) E1. Accordingly, core temperature was monitored in response to PGE1 injections both preoperatively and on days 4, 8, 12, and 18 after either unilateral nephrectomy or the induction of hypertension due to nephrectomy plus renal artery clipping. Temperature responses to PGE1 were similar throughout each test day in normotensive, unilaterally nephrectomized control rats. In contrast, 1K,1C rats became hypertensive within 4 days of renal artery clipping, and at this time the hyperthermic response to PGE1 was virtually abolished. A reduced hyperthermic response was also seen at 8 and 12 days after clipping; by 18 days responses were again similar to controls. To determine whether central arginine vasopressin (AVP) was involved in the suppression of the hyperthermic response, we pretreated other hypertensive rats centrally with the V1-AVP antagonist [d(CH2)5Tyr(Me)]AVP before PGE1 injection. In 1K,1C animals thus treated, temperature responses 4-12 days after clipping were indistinguishable from those of similarly treated normotensive control rats. We suggest that the reduced hyperthermic responses to PGE1 seen in the 1K,1C rats during the initial development of hypertension may be due to activation of brain AVP pathways.

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