Release of antirenin to human renin by anaphylactic shock or by antihypertensive agents.

In dogs that have had repeated intravascular injections of small doses of human renin, even for long periods, the development of antirenin to human renin in the blood has not been previously noted, and their pressor response (30 mmHg) to 1 U of human renin has remained unchanged for years. In such dogs, however, a profound, abrupt fall of the systemic blood pressure, due to an anaphylactic reaction to human renin, or to the infusion of depressor agents, such as Arfonad, histamine, or diazoxide, resulted in the appearance in the blood of an inhibitor specific for human renin. This inhibitor was suddenly released into the blood-stream from the tissues in which it presumably had been stored, and it persisted, in a relatively high concentration, in some animals for months. It did not occur in dogs that had not previously received many injections of human renin. This study has shown that the inhibitor has all of the properties of antirenin to human renin. It abolished the pressor response to hog, dog, and rat renin or to angiotensin and norepinephrine. It inactivated human renin, but not dog renin, duringits incubation with renin substrate to form angiotensin.