Mechanisms involved in the renal responses to intravenous and renal artery infusions of noradrenaline in conscious dogs.

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Abstract
The renal hemodynamic and glomerular filtration rate (GFR) responses to i.v. and intrarenal infusions of noradrenaline [norepinephrine, NE] were studied in conscious dogs, either with or without prior blockade of angiotensin [A] II formation with teprotide. NE infusion by either route resulted in dose-related rises in plasma renin activity. Pretreatment with teprotide reduced the rise in mean arterial pressure and abolished the rise in GFR seen during i.v. infusions of NE (0.1, 0.2 and 0.4 .mu.g/kg.cntdot.min). NE also reduced filtration fraction more after teprotide pretreatment. Renal blood flow rose and renal vascular resistance fell in response to i.v. NE infusions. This renal vasodilatation was unaffected by pretreatment of the dogs with teprotide, indomethacin or DL-propranolol. After pentolinium pretreatment, i.v. NE infusion caused a dose-related renal vasoconstriction. NE infusion into the renal artery (0.02, 0.05 and 0.1 .mu.g/kg.cntdot.min) resulted in rises in mean arterial pressure and GFR which were abolished by teprotide pretreatment. Filtration fraction rose when NE was administered alone but fell when it was infused after teprotide treatment. AII formed as the result of increased renin release acted to maintain GFR and filtration fraction during NE infusion. In addition, i.v. NE infusions in conscious dogs caused reflex vasodilatation of the renal vasculature.