We studied whether stimulation of kallikrein release into the vascular compartment by sympathetic nerve stimulation of the submandibular gland resulted in an increase in the concentration of kinins in the venous effluent from the gland. Electric stimulation of a cervical sympathetic nerve was performed at 8 V, 10 Hz, 2 msec duration. At 1 minute after sympathetic stimulation, the blood flow to the gland increased from 66.1 ± 10.3 to 367.0 ± 66.0 /xl/min (p < 0.01), and the kinin output in the

more »

... nous effluent from the gland increased from 0.019 ± 0.013 to 14.4 ± 8.8 ng/min (p < 0.001), but kinin concentration in the arterial blood did not change (0.177 ± 0.037 before and 0.303 ± 0.137 ng/ml after stimulation; p > 0.05). We also studied whether arterial blood kinins were increased in 48-hour nephrectomized rats during the hypotension that results when captopril is administered after the gland has been sympathetically stimulated. Arterial blood kinins concentration were 0.19 ± 0.042 ng/ml in sham control rats (without sympathetic stimulation and captopril administration) and increased to 3.0 ± 0.8 ng/ml after sympathetic stimulation plus captopril administration (p < 0.05). Arterial blood kinin concentration in rats with sympathetic stimulation alone or captopril administration alone was similar to that of the sham control rats. Blood pressure in the rats that received sympathetic stimulation and captopril administration decreased from 99.8 ± 5.3 to 57.8 ± 5.8 mm Hg (p < 0.001). Blood kinins and blood pressure were inversely correlated (r = -0.84; p < 0.01). Blood pressure did not change in the sham control group, in the group that received sympathetic stimulation alone, or in the group that received captopril alone. Pretreatment with meclofenamate, a cyclooxygenase inhibitor, did not affect the hypotensive response to captopril administration after sympathetic stimulation. We conclude that stimulating the release of kallikrein from the submandibular gland results in a significant increase in kinin concentration in venous blood from the gland but does not significantly change kinin levels in arterial blood. In nephrectomized rats, inhibition of kininases with captopril after sympathetic stimulation of the submandibular gland significantly increased arterial blood kinins and decreased blood pressure. Prostaglandins are not involved in this hypotensive response. (Hypertension 5 (supp