Experiments were carried out to examine whether angiotensin II (AII) is involved in the regulation of release of norepinephrine (NE) elicited by renal nerve stimulation in anesthetized dogs. It was assessed in terms of alterations in the NE secretion rate (NE-SR) elicited by continuous renal nerve stimulation (RNS, 0.5-1 Hz, 10-15 V, 1 ms) under two different experimental conditions associated with opposite directional changes in the plasma AII level. In dogs previously treated with captopril (1 mg kg-1, i.v.), RNS increased NE-SR without any significant reduction in renal blood flow (RBF). During intrarenal arterial infusion of AII (1 ng kg-1 min-1), the RNS-induced increase in NE-SR was enhanced by 46% and there was a slight potentiation of the RBF reduction in response to RNS. In the other group of dogs, i.v. infusion of angiotensin I (AI, 15 ng kg-1 min-1) increased the mean arterial blood pressure (ABP) and renal vascular resistance (RVR). During AI infusion, the RNS-induced increase in NE-SR was decreased by 47-48% after administration of captopril (1 mg kg-1, i.v.). Also, the increases in ABP and RVR during AI infusion were decreased and restored almost to their respective control levels after dosing with captopril. These results indicate that an elevation or lowering of the blood AII level is associated with an increase or decrease of NE release, respectively, induced by renal nerve stimulation in anesthetized dogs.
|Number of pages||9|
|Journal||Asia Pacific Journal of Pharmacology|
|Publication status||Published - 1991 Jan 1|
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