Interaction between perfusion pressure and sympathetic nerves in renin release by carotid baroreflex in conscious dogs.

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Abstract
The effect of bilateral carotid occlusion on carotid sinus pressure, systemic blood pressure, heart rate, renal blood flow, renal-venous and arterial plasma renin activity was studied in 12 trained conscious foxhounds on a normal Na diet (4.7 mmol/kg per day). When renal perfusion pressure was allowed to rise with systemic pressure by 51.0 .+-. 6.3 mmHg during carotid occlusion, renin release decreased by 72.3 .+-. 22.2 ng/min (78% of control; P < 0.05) while renal blood flow remained at its resting level of 232.7 .+-. 20.1 ml/min (n = 8 dogs). When renal perfusion pressure was maintained constant at 93.0 .+-. 3.6 mmHg during carotid occlusion (suprarenal aortic cuff), renin release increased by 154.6 .+-. 60.4 ng/min (73% of control; P < 0.05), again there was no significant change of renal blood flow (n = 7 dogs). After .beta.-adrenergic blockade [propranolol] carotid occlusion increased systemic blood pressure by 47.7 .+-. 7.8 mmHg, decreased renin release by 34.6 .+-. 9.9 ng/min (67% of control; P < 0.05) and had no effect on renal blood flow (n = 4 dogs). When renal perfusion pressure was controlled at its resting level, no significant change of renin release and renal blood flow was observed during carotid occlusion in the surgically denervated kidney (n = 3 dogs) or in the intact kidney after .beta.-adrenergic blockade (n = 4 dogs). A reduction of carotid sinus pressure in the conscious dog apparently increases renin release by a direct .beta.-adrenergic stimulation without exerting vasomotor effects provided renal perfusion pressure is maintained at control level. The vascular receptor mechanism can effectively counteract the stimulating influence of the renal sympathetic nerves when perfusion pressure is allowed to rise.