| Abstrakt: |
The effect of Captopril on blood pressure and hind‐limb vascular resistance was studied in normotensive (N) and genetically hypertensive (GH) rats of the New Zealand strain who were anaesthetized with chloralose (75 mg/kg, intravenously). The hind limbs were perfused at a constant rate of 1 mL/min with the rat's own blood, and a five‐minute delay coil was incorporated into the circuit. Captopril (10 μg/kg to 1000 μg/kg), given either intravenously (in the jugular vein) or intra‐arterially (into the femoral artery of the perfused limb), lowered the blood pressure and the limb vascular resistance in a dose‐dependent manner. When Captopril was given intravenously, the delay in the pump circuit allowed the responses of the systemic blood pressure and the responses of the hind‐limb perfusion pressure to be separated by about five minutes. A fall in perfusion pressure occurred only when Captopril entered the limb; it was not abolished by surgical denervation of the limb and had no reflex neurogenic component. When Captopril was given intra‐arterially (200 μg/kg) into the limb there was an immediate drop in resistance followed five minutes later by a second fall in resistance when the circulating drug reentered the limb. This locally mediated response was not diminished by prior nephrectomy or concurrent infusion of saralasin, although both of these procedures abolished the blood pressure response. The local limb response is possibly due to potentiation of bradykinin‐induced vasodilatation. Responses of GH and N rats were similar, and there was no evidence that a captopril‐sensitive mechanism involving either the renin‐angiotensin or the kallikrein‐ bradykinin systems plays any part in maintaining genetic hypertension. |
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