Abstract

The role of prostaglandins (PGs) and baroreflex in the pressor response to norepinephrine (NE) were examined in one-kidney, one clip rabbits with renal artery stenosis for 3-day' s duration (3-day clipped rabbits) and in sham operated rabbits with one-kidney without renal artery stenosis.An exaggerated pressor response to NE, 800ng/kg/min, was observed in the 3-day clipped rabbits, and it was abolished by angiotensin II antagonist, [Sar1, Ile8] angiotensin II (AIIA). Treatment with indomethacin, 10mg/kg, induced hyperresponsiveness to NE in the sham operated rabbits and also produced a further increase in the response in the 3-day clipped rabbits : the enhanced responses with similar levels were not attenuated by AIIA in either group. A subdepressor dose of PG E2, 800ng/kg/min, abolished the hyperresponsiveness in the 3-day clipped rabbits, while a subdepressor or depressor dose of PG I2, 10 or 20 ng/kg/min did not. However, the concurrent infusion of AIIA with PG I2 attenuated the hyperresponsiveness.Baroreflex, which was calculated from the response of blood pressure and pulse interval to the injection of phenylephrine and nitroglycerin, was not different between the 3-day clipped rabbits and the sham operated rabbits.These results indicate that the PGs, particularly PG E2, may be and the baroreflex may not be involved in the enhanced pressor response to NE in the 3-day clipped rabbits, in addition to the altered renin-angiotensin system.

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