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The adrenergic regulation of renin secretion was studied in renal cortical slices from control and pertussis toxin-treated rats. Pertussis toxin was used to study the role of adenylate cyclase in the control of renin release. It was observed that isoproterenol and epinephrine stimulated renin secretion and that clonidine decreased both basal and isoproterenol-stimulated renin secretion in the control group. Pertussis toxin: a) increased significantly basal renin secretion, b) displaced to the left the concentration-response curve for isoproterenol and epinephrine and magnified the response to epinephrine and c) abolished the inhibitory effect of clonidine on renin secretion. This work confirms our previous results obtained in vivo and suggests a direct effect of pertussis toxin on the cells that secrete renin.

The plasma renin concentration was measured after anesthesia in control and in pertussis toxin-treated rats. The anesthetics increased renin secretion and this effect was markedly magnified in rats treated with pertussis toxin. Propranolol partially blocked the increase in plasma renin concentration produced by anesthetics. It is concluded that the adrenergic system is involved in this effect and that pertussis toxin magnifies it by potentiating the beta-adrenergic action.

Basal plasma renin activity (PRA) was not modified by pertussis toxin administration. On the contrary, the modulation of PRA by adrenergic amines was markedly affected by the toxin. Administration of epinephrine did not modified PRA in the controls but markedly increased it in toxin-treated rats. This effect of epinephrine was reproduced in control rats when yohimbine was given before the catecholamine. Clonidine decreased PRA to a much more significant extent in control rats than in animals treated with the toxin. Isoproterenol stimulated PRA to a greater level in toxin-treated rats. Our data indicates that pertussis toxin blocks the alpha 2-adrenergic modulation of renin release and magnifies the ability of beta adrenergic activation to stimulate PRA.