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The intrarenal distribution of blood flow in the baboon was measured using the 133xenon clearance technique, and dose-response curves for the various components of renal blood flow were determined during intra-arterial infusions of noradrenaline; the α-adrenergic blocking agent, phenoxybenzamine; the β-adrenergic blocking agent, propranolol; and tyramine which causes the release of endogenous NA. High doses of noradrenaline reduced flow in the outer cortex; this effect was attenuated by phenoxybenzamine, but not by propranolol. Tyramine had no effect. These results suggest that there are α-adrenergic receptors in the resistance vessels of the kidney but are inconsistent with an important role for NA-mediated autonomic control of renal blood flow. [ABSTRACT FROM PUBLISHER]

In rabbits, injection of angiotensin II into the lateral cerebral ventricle caused a rise of blood pressure, bradycardia, and tachypnoea. Vertebral artery infusions of angiotensin caused tachycardia and a larger increase in blood pressure than the same dose infused intravenously. Angiotensin produces cardiovascular effects by activation of the central nervous system and one site of action is within the area of distribution of the vertebral artery. [ABSTRACT FROM PUBLISHER]

Alterations in renal perfusion have been shown in a variety of liver diseases. We have examined the possibility that the syndrome is due to a renal vascular hypersensitivity to noradrenalin (NA). Isolated perfused kidneys and segments of rabbit femoral artery were used. Potentiation of the pressor effects of injected NA occurred in all (five artery and five kidney) preparations when jaundiced baboon plasma was perfused. These changes were significant (P less than 0.05) in nine out of the ten experiments. Controls to which normal baboon plasma was administered showed no such change. No correlation was found between the degree of NA potentiation and the plasma concentrations of bilirubin (total and conjugated), serum glutamic oxaloacetic transaminase, blood urea nitrogen, serum glutamic pyruvic transaminase, alkaline phosphatase, Na+ ions or K+ ions in the jaundiced plasma. Plasma renin levels were not significantly changed. When arteris were perfused with Krebtentiation of NA was found. Perfusion of sodium taurocholate or sodium deoxycholate (400 mug/ml) yielded no potentiation. Thus, the altered renal perfusion associated with jaundice may be attributed to a potentiated pressor response to NA which may be caused by an increased level of cholesterol carried on the beta-lipoprotein.

1. Local blood flow has been measured in the hypothalamus and other areas of the brain in the conscious rabbit, by measuring the rate of clearance of small volumes (2.5-10 mul.) of a saline solution of the inert tracer (133)Xe injected locally.2. Increasing the arterial P(CO2) caused a mean rise in the hypothalamic blood flow of 34%.3. The hypothalamic blood flow remained relatively constant over a mean arterial blood pressure range of 41-140 mm Hg.4. Hypothalamic blood flow was relatively unaffected by anaesthesia with intravenous pentobarbitone; by contrast, blood flow in the cerebral cortex was greatly reduced.5. It is concluded that the technique is a valid and useful one, since CO(2) responsiveness and autoregulation is maintained. Different areas of grey matter have different flow rates, and vary in their responsiveness to barbiturate anaesthesia.