Cardiovascular Reactivity in Acute and Chronic Renal Hypertensive Dogs
Both before and after pentobarbital anesthesia, cardiovascular responsiveness to norepinephrine, epinephrine and serotonin was increased and that to angiotensin was decreased when experimental renal hypertension was first elicited. Response to tyramine was strikingly enhanced.
Several weeks later, during the chronic phase of hypertension, there was a slight and scarcely significant heightened response to norepinephrine, a clearly increased response to tyramine, and no change in that to serotonin, dimethylphenylpiperazinium iodide, and 3-hydroxy-phenyl-ethanolamine HCl.
Study of the problem of variability of responsiveness showed relatively little difference in mean response to any of five pressor drugs with or without anesthesia and after sham operation.
Hypertension produced by infusion of angiotensin into normal anesthetized dogs did not change the response to norepinephrine but more than doubled that to tyramine. When acute renal hypertension was produced in the same dogs, angiotensin infusion failed to cause further change in response to either substance. Infusion of angiotensin into dogs with chronic renal hypertension caused increased response to tyramine but not to norepinephrine.
The perfused hind legs of dogs with acute renal hypertension showed clearly reduced responses to angiotensin with no concurrent change in responses to norepinephrine. The pressor response to serotonin was increased while that to tyramine was unchanged. During chronic hypertension responses were like the normal values.
Hypertension caused by infusion of angiotensin decreased greatly the vasoconstrictor response to superimposed injections of angiotensin into the perfused leg circuit while norepinephrine responses were unchanged. Response to another peptide, vasopressin, was reduced like that to angiotensin.
These studies suggest that during acute renal hypertension increased quantities of angiotensin are present and that there is a decrease in neural tone. The finding that during the chronic phase of hypertension, the response to tyramine alone remained elevated, suggests the presence of small amounts of angiotensin, i.e., enough to increase the pressor effectiveness of endogenous norepinephrine released by tyramine. During the chronic phase of hypertension, peripheral resistance appears relatively more dependent on neural control.
- Accepted September 28, 1965.
- © 1966 American Heart Association, Inc.