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Low doses (1-10 ng) of angiotensin I (AI) injected Intravenously into conscious rats produced greater pressure changes than when injected intraaortically. This finding again indicates the importance of the pulmonary circulation in the conversion of AI to angiotensin II (All). At high doses of hormone (30 ng, which produces pressure rises of 40-50 mm Hg) the Intravenous and intraarterial responses tended to be the same. However, the role of the lung for conversion is still indicated by comparing the time for onset of the pressure rise and the time to reach maximum pressure rise for the intravenous and intraarterial injection of AI. Bradykinin degradation in the pulmonary circulation, estimated by comparing intravenous and intraaortic equipressor doses, was higher in conscious rats with chronic one-kklney renal hypertension (RHR; 217 3 mm Hg) than in the normotensive control rats (NCR; 126 3 mm Hg), 99.6% and 97.5%, respectively. Vascular hyperreactivity to bradykinin was seen in RHR in response to both intraaortic bolus injection and intraaortic infusion. The intraaortic equipressor dose was 15-30 times smaller In RHR than in NCR, while the differences with Isoproterenol and nitropnisside were less pronounced. Indomethacin infusion (5 mg/kg/min) for 10 minutes had no effect on intraarterial hyperreactivity to bradykinin. The marked increase in vascular reactivity to bradykinin more than compensated for the larger pulmonary Inactivation. The equipressor doses of bradykinin injected intravenously were 200 24 ng in RHR and 1060 143 ng in NCR. Conversion AI to AH, assessed by the equipressor doses of the hormones which produce 20 mm Hg rise in pressure, was also higher in the RHR than in the NCR, 55% vs 25%, with no change in vascular reactivity to AH. Hyperreactivity to bradykinin reverted entirely to normal 20 hours after unclipping the RHR, when blood pressure had also normalized. The responsiveness to nitroprusside tended to increase rather than decrease after unclipping. While the vascular hyperreactivity to bradykinin and the increased pulmonary degradation of bradykinin seen in the RHR were markedly affected by unclipping, the increased conversion of AI to AH and reactivity to AH remained unchanged after unclipping. These results suggest that the mechanism underlying the alterations in AI conversion and bradykinin degradation in one-kidney renal hypertensive rats can be partially dissociated.(Hypertension 4: 77-83, 1982)
Salgado et al. (Fri,) studied this question.