The Effect of IL‐6 on the Acute Hypertensive Response to Psychosocial Stress Depends on Angiotensin II

Abstract

We have shown that the acute hypertensive response to psychosocial stress is AngII-dependent, and also that it is attenuated in IL-6 KO mice. In addition, we have shown that chronic AngII infusion amplified the difference between KO and Wt mice. The goal of this study was to determine whether blocking AngII production would eliminate the difference in the acute hypertensive response. MAP and heart rate was continuously recorded via telemetry for 90 min. during cage-switch stress testing. Area under the curve (AUC) for MAP averaged 1759±62 and 1136±423 mmHg∗min in Wt (n=3) and KO (n=5) mice, respectively, confirming our previous report that the response was attenuated in KO mice. Captopril decreased AUC in the Wt mice (n=4) to an average of 1264±155 mmHg∗min, also confirming our report that the pressor response to acute stress is AngII dependent. In KO mice, AUC for the captopril treated vs. vehicle treated (n=5) mice was greater, averaging 1712±571 mmHg∗min. On the other hand, we measured an increase in the heart rate AUC response to stress in captopril treated KO mice vs. vehicle, averaging 9662±1441 vs. 6261±1063 bpm∗min, resp., which did not occur in the Wt mice. Although heart rate increased in all groups during stress, this difference in the response in KO mice treated with captopril vs. vehicle treated suggests that an interaction between AngII and IL-6 on the control of heart rate may play a role in the acute hypertensive response to psychosocial stress.