Abstract
After cervical sympathetic nerve stimulation, the rat submandibular gland releases a significant amount of kallikrein into the circulation. To determine whether this glandular kallikrein has kininogenase activity (kinin-generating capabilities) in the peripheral circulation and whether it plays a role in blood pressure regulation, we studied the effect of captopril on blood pressure in 48 hour-nephrectomized rats with and without prior sympathetic stimulation of the submandibular gland. Administration of captopril 10 minutes after gland stimulation resulted in a mean blood pressure decrease (A BP) of 43 ± 8.3 mm Hg (P 0.05). To confirm that the effect of captopril was due to a blockage of kinin destruction generated by glandular kallikrein and not to the inhibition of angiotensin II formation, we determined the effect of captopril after gland stimulation in rats pretreated with either IgG from nonimmunized rabbits (normal-IgG), or IgG from rabbits immunized against kinins (antikinin-IgG) or kallikrein (antikallikrein-IgG). Normal-IgG did not significantly alter the hypotensive effect of captopril (A BP —30 ± 7.7; P < 0.01), while pretreatment with antikinin or antikallikrein almost completely blocked its hypotensive effect (A BP —5.8 ± 1.9 and —6.4 ± 0.4, respectively). In the latter two groups, the decrease in BP was significantly smaller (P < 0.001) than in the groups that were not pretreated or in the group pretreated with normal-IgG. These data suggest that, upon adrenergic stimulation of the submandibular gland, glandular kallikrein released into the vascular compartment has kininogenase activity in the peripheral circulation. The kinins released by glandular kallikrein induced hypotension when their breakdown was prevented by the kininase II inhibitor, captopril. These results suggest that kinins may be responsible in part for the antihypertensive effect of captopril in situations in which glandular kallikrein in blood is increased. (C/rc Res 51: 385-390, 1982)
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