Postunclipping renal blood flow in one-kidney, one-clip hypertensive rats

Removal of the arterial clip (unclipping) in one-kidney, one-clip (1K, 1C) Goldblatt hypertensive rats causes rapid return of mean arterial pressure (MAP) to normotensive levels. An extracorporeal circulation was established between the renal and jugular veins to evaluate the influence of unclipping on renal blood flow (RBF) in Inactin-anesthetized 1K, 1C rats. MAP in rats with the extracorporeal circulation was 182 +/- 5 mmHg before unclipping or sham operation. MAP decreased to 113 +/- 4 mmHg within 2 h after unclipping compared with 169 +/- 13 mmHg in sham-unclipped rats. RBF increased by 2.8 ml.min-1.g-1 from a basal level of 3.8 +/- 0.3 after unclipping and was maintained approximately 40% above the basal level for 2 h, although renal vascular resistance was 94% greater than in uninephrectomized control rats. Heart rate did not change in either unclipped or sham-operated rats. Indomethacin (7 mg/kg) did not affect unclipping-induced changes in MAP, RBF, or urine output; however heart rate decreased immediately after unclipping and remained approximately 25-35 beats/min below control levels for the 2-h observation period. In rats lacking the extracorporeal circuit, MAP decreased (P less than 0.005) and heart rate increased (P less than 0.05) in response to unclipping. Nevertheless, unclipping-induced tachycardia was significantly less than that caused by nitroprusside infusions causing similar decrements in MAP. The results suggest that the sustained increment in RBF after unclipping in chronic, established 1K, 1C hypertension may be associated with postunclipping hypotension and diuresis, that blockade of prostaglandin synthesis may unmask unclipping-induced bradycardia, and that prostaglandins are not essential for postunclipping changes in renal hemodynamics.