Abstract
We attempted to clarify the contribution of the altered neural mechanism associated with increased angiotensin II to two-kidney, one clip (2K IC) hypertension on the 3rd and 35th days after renal artery stenosis. 2K1C hypertension was produced in 20 rabbits, and a sham operation was performed in 11 rabbits. Sarl, 11e8 angiotensin II (AIIA) infusion tests and baroreflex sensitivity determinations by bolus injection of phenylephrine were performed on the 3rd and 35th days after renal artery stenosis. The blood pressure was 12 mmHg higher in the hypertensive rabbits than in the sham operated rabbits on the 3rd day after clipping. The blood pressure returned to the control level during the infusion of AIIA. On the 35th day after clipping, AIIA-sensitive or AIIA-resistant hypertension developed. The blood pressure was higher in the AIIA-sensitive rabbits than in the AIIA-resistant rabbits (131.±5 vs 116.±4 mmHg, p <0.05). The baroreflex sensitivity was lower in the AIIA-sensitive rabbits than in the AIIA-resistant rabbits (1.8.±0.3 vs 2.8.±0.3 msec/mmHg, p <0.05). There was no difference in plasma norepinephrine between the two groups on either the 3rd or 35th day. Thus, impaired baroreflex sensitivity was found in the accelerated hypertension seen in the chronic phase of 2K1C hypertension. Neural mechanisms mediated by the peripheral sympathetic nervous system did not appear to contribute to the development of 2K1C hypertension.
