Stimulation of renin by blockade of alpha 2-adrenoceptors in man: role of the beta 1-adrenoceptor.

Previous experiments have shown that blockade of intrarenal alpha 2-adrenoceptors will cause a rise in renin secretion. Therefore, we designed the present study to explore whether this could be due to noradrenaline being released by a prejunctional mechanism and stimulating post-junctional beta 1-adrenoceptors. Two groups of patients in whom diagnostic renal angiography was indicated were studied before administration of contrast material. None of the patients had taken any antihypertensive medication in the 3 weeks preceding this investigation. In group I (n = 8) glucose was infused into the renal artery for 20 min; during the last 10 min yohimbine was also infused at a rate of 3 micrograms/kg per min. In group II (n = 8) the same protocol was carried out with the exception that, instead of glucose, we infused atenolol in a dose of 1 micrograms/kg per min. Blood samples for noradrenaline and renin were taken before infusions started, following 10 min of the glucose (or atenolol) and at the end of the yohimbine infusion. At the same time blood pressure and renal blood flow (133Xe-washout) were measured. The results show that yohimbine increased renin release by 310 +/- 60% in group I, but by only 80 +/- 45% in group II (P less than 0.01). However, noradrenaline 'release' was stimulated to the same degree in both groups (150 +/- 80 versus 138 +/- 75%; NS) During the experiments blood pressure and heart rate did not change. The data are consistent with the hypothesis that the effect of alpha 2-adrenoceptors on renin release is mediated by beta-adrenoceptors. Thus, the relevant alpha 2-receptor may be located prejunctionally.