Central ANG II receptor involved in carotid sinus reflex resetting in chronically stressed rats.
The performance of carotid sinus baroreceptor reflex (CSR) was characterized in chronically stressed rats by changing intracarotid sinus pressure (ISP) and constructing ISP-MAP (mean arterial pressure) relationship curve. The role of central angiotensin II (ANG II) receptors in the changes of CSR performance induced by chronic stress was determined. Rats were subjected to foot-shock stress for two weeks. The carotid sinus was isolated from the systemic circulation and the ISP changed in a stepwise manner. The results showed that in chronically stressed rats, ISP-MAP relationship curve shifted upward, the set point was significantly higher than that obtained from the unstressed group, and the reflex gain and the MAP range were significantly smaller than those in unstressed rats. After intracerebroventricular injection of saralasin (20 ng), MAP range was augmented and the set point decreased significantly. Injection of vehicle did not lead any significant differences between the parameters of the reflex measured before or after injection in either the stressed or the unstressed rats. Furthermore, administration of ANG II (10 microg) induced a significant increase in the set point and decrease in the reflex gain in the unstressed rats. The responses of CSR to ANG II were completely blocked by pretreatment of saralasin. These findings suggest that chronic stress could induce the decreased CSR function in the normotensives and central ANG II receptors involved in the resetting of CSR in the chronically stressed rats.
Qian
Z M
ZM
Department of Applied Biology and Chemical Technology, The Hong Kong Polytechnic University, Hung Hom, Kowloon.
Xiao
D S
DS
Huang
W Q
WQ
Tang
P L
PL
Xu
B
B
D000804:Angiotensin II / Q000008:administration & dosage / Q000378:metabolism* / Q000494:pharmacology; D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000008:administration & dosage / Q000494:pharmacology; D000818:Animals; D017704:Baroreflex / Q000502:physiology*; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D001923:Brain Chemistry / Q000502:physiology*; D002346:Carotid Sinus / Q000503:physiopathology*; D002908:Chronic Disease; D007276:Injections, Intraventricular; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D011945:Receptors, Angiotensin / Q000378:metabolism*; D012504:Saralasin / Q000008:administration & dosage / Q000494:pharmacology; D013315:Stress, Psychological / Q000378:metabolism* / Q000503:physiopathology*; D014662:Vasoconstrictor Agents / Q000494:pharmacology
D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D011945:Receptors, Angiotensin; D014662:Vasoconstrictor Agents; D000804:Angiotensin II; D012504:Saralasin