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.