Cardiovascular Reactivity after Bilateral Nephrectomy in Rats

(1) Cardiovascular reactivity, 16 to 28 hours after bilateral nephrectomy was determined in rats by obtaining the dose-blood pressure-response curve in order to avoid the vertical bias.(2) Bilateral nephrectomy did not increase cardiovascular reactivity to pressor agents (angiotensin and norepinephrine) in rats anesthetized by pentobarbital or anesthetized and treated by pentolinium, a ganglion blocking agent.(3) In pithed animals without anesthesia nephrectomy augmented slightly but definitely the response to pressor agents.(4) Further elimination of the neural innervation in pithed animals by administration of bretylium, an adrenergic neurone blocking agent, atropine, and pentolinium, also resulted in an increased response to angiotensin after bilateral nephrectomy.(5) But it is inadequate to explain the marked augmentation of response to renin after nephrectomy only by the slight increase in response to angiotensin. Response to renin was markedly augmented in pithed animals as well as under usual condition.(6) Bilateral nephrectomy diminished cardiovascular reactivity to depressor agents (acetylcholine, adenosine triphosphate and histamine).(7) Angiotensinogen in the plasma increased 4 times more after bilateral nephrectomy. This is the main cause of marked augmentation in response to renin.(8) The claim that, if angiotensinogen is already in excess, a further increase in its concentration would not lead to an increased production of angiotensin was denied experimentally and theoretically.