Elevated conversion of angiotensin I to II after hemorrhagic hypotension in the cat

One hour of hemorrhagic hypotension followed by reinfusion of shed blood was tested in cats for effects on pulmonary conversion of angiotensin I to II, inactivation of bradykin, and blood pressure responsiveness to the peptides. During the control period before bleeding, 60% of the angiotensin I injected into the pulmonary circulation was found to have been converted to angiotensin II, according to the systemic blood pressure response technique. During the 'experimental' period after the reinfusion of the shed blood, this value was enhanced to 96%. By contrast, bradykinin was inactivated by about 90% both before and after the experimental procedures. At the same time, the ability of angiotensin II(amide) to cause a systemic pressor response was reduced by about 80% after reinfusion, whereas the depressor response to bradykinin was variably affected. Aspects of prolonged hypovolemia which might affect pulmonary conversion of angiotensin I to II and responsiveness to angiotensin II, e.g., acidosis, are discussed. Although refractoriness to the pressor property of angiotensin II may offset the effect of enhanced angiotensin I conversion on systemic hemodynamics, this does not preclude the possible contribution of converted angiotensin II to pulmonary vascular resistance and blood flow changes during hypovolemia.