Protracted Pressor Response to Angiotensin After Bilateral Nephrectomy in Rats

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Abstract
The pressor response of nephrectomized rats to an injection of renin is marked by a prolonged stable plateau. A similar, prolonged response to angiotensin has been demonstrated and the following aspects of this pressor effect were evaluated. 1. The protracted response was shown not to be due to a persistence of angiotensin in the blood of nephrectomized animals. There are several indications from unrelated studies that angiotensin is destroyed rapidly. Cross-circulation experiments indicate that during the protracted pressor phase blood levels of constrictor materials have fallen to undetectably low levels. 2. No evidence could be obtained to indicate that the neurogenic buffer system is involved in the development of the protracted response. Ganglionic blockade was ineffective in preventing its development. 3. The hemodynamic basis for the response must be a persistent increase in total peripheral resistance (TPR) since there is no increase in cardiac output (CO) in response to the angiotensin infusion. Before infusion, the CO of nephrectomized animals is higher than that of sham-operated control animals. 4. The increase in TPR must be due to an increase in geometric hindrance for no changes in hematocrit or in viscosity result from angiotensin infusion. Blood viscosity is lower in nephrectomized than in sham-operated animals, but this can account for only part of the lower pre-injection control pressure seen in this group. It appears that in animals depleted of endogenous renin, a large infusion of angiotensin increases vascular resistance by some non-neurogenic, non-humoral mechanism which may represent another type of vascular tone.

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