Renal prostanoids after unclipping the denervated one-kidney, one-clip hypertensive rat

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Abstract
The contribution of the renal nerves in maintaining blood pressure and modulating renal prostanoid synthesis was examined in established (less than 8 wk in duration) one-kidney, one-clip (1K,1C) hypertension in the rat. Systolic blood pressure was measured for 7 days after renal denervation, at which time the renal artery clip was removed. Twenty-four-hour urinary excretion of PGE2 and 6-keto-PGF1.alpha. (stable degradation product of PGI2)was determined before and after denervation and unclipping. Compared with sham-denervated rats, denervation (n = 15) resulted in a small but significant fall in blood pressure (from 216 .+-. 4 to 182 .+-. 4 mmHg after 48 h) and an increase in urinary 6-keto-PGF1.alpha. (from 31 .+-. 4 to 43 .+-. 5 ng/24 h after 24 h). There was no change in PGE2 excretion. Seven days after surgery, blood pressures were similar in denervated (202 .+-. 4 mmHg) and sham-denervated (211 .+-. 5 mmHg) rats and fell to a similar extent 24 h after unclipping (142 .+-. 3 and 147 .+-. 4 mmHg, respectively). Urinary 6-keto-PGF1.alpha. increased from 25 .+-. 5 to 74 .+-. 11 in denervated and 21 .+-. 2 to 72 .+-. 9 ng/24 h in sham-denervated rats in the 24 h after unclipping. PGE2 excretion increased approximately twofold over this period. These findings indicate that the renal nerves have only a minor role in established hypertension in the 1K, 1C rat and that the reversal of hypertension and stimulation of renal prostanoid synthesis following unclipping is not dependent on neural mechanisms.