[Renal adrenergic beta receptors and experimental neurogenic hypertension]

Sinoaortic denervation SAD in dog induces a permanent rise in blood pressure and heart rate leading to an experimental model of arterial hypertension. This model is associated with a marked increase in plasma catecholamine levels during the two first months. The present study investigates the changes in some renal vasoactive systems (renin activity, aldosterone and kallikrein) and cortical renal beta adrenoceptors during the development of this experimental neurogenic hypertension in dogs. SAD dogs exhibited a biphasic change in plasma renin activity and catecholamines: 1 month after SAD, plasma noradrenaline rose and renin activity decreased. These parameters return to normal values 18 months after SAD whereas blood pressure remained elevated. In contrast, plasma aldosterone levels decreased and urinary sodium increased. Urinary kallikrein was enhanced 1 month after SAD and showed a marked decrease 18 months later when compared with pre-SAD values. Cortical renal beta adrenoceptors (evaluated by 125I-cyanopindolol) exhibited a permanent decrease (Bmax) whatever the duration of arterial hypertension. These results show that SAD-induced hypertension in dog is associated with changes in renal vasoactive system involving urinary excretion of kallikrein and cortical renal beta adrenoceptors. These alterations could be involved in the maintenance of arterial hypertension in this experimental model.