The effects of prior chronic stress on cardiovascular responses to acute restraint and formalin injection.
Exposure to acute stressors activates both the hypothalamic-pituitary-adrenal (HPA) and cardiovascular systems. Prior chronic stress enhances HPA responses to novel, acute stressors, but whether it alters cardiovascular responsivity to novel, acute stress is unknown. In the present study, we examined mean arterial blood pressure (MAP) and heart rate (HR) to two distinct stimuli, restraint and formalin, following prior exposure to 7 days of intermittent cold. In two sets of control and chronically stressed animals, we measured MAP and HR for 60 min following onset of 30 min restraint and MAP, HR and behavioral responses to intraplantar injection of formalin. Chronic stress raised MAP and HR under resting conditions and elevated HR during, but not following termination of, restraint. These increases in HR during restraint were due to the differences in resting levels of HR, since both control and chronically stressed animals exhibited similar increases from resting levels in HR during restraint. Conversely, chronically stressed animals exhibited lower changes in MAP and HR from resting levels following termination of restraint. Formalin produced the characteristic biphasic pattern of cardiovascular and behavioral responses. Prior chronic stress did not alter behavior, but increased MAP and HR in Interphase and only MAP in Phase 2. The increases in MAP during Interphase and Phase 2 were a result of the elevations in resting levels of MAP, but even when differences in resting levels were taken into account, HR remained elevated in the Interphase in chronically stressed animals. Together, these data demonstrate that prior chronic intermittent cold stress modifies cardiovascular function both under resting conditions and, in very specific ways, under stimulated conditions produced by restraint and formalin. We propose that these modifications are produced by brain regions that are known to regulate cardiovascular function and which are activated by chronic stress.
Bhatnagar
S
S
Dept. of Physiology, Box 0444, University of California at San Francisco, San Francisco, CA 94143-0444, USA. seema@itsa.ucsf.edu
Dallman
M F
MF
Roderick
R E
RE
Basbaum
A I
AI
Taylor
B K
BK
D000324:Adrenocorticotropic Hormone / Q000097:blood; D000818:Animals; D001522:Behavior, Animal / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D002320:Cardiovascular Physiological Phenomena; D002908:Chronic Disease; D005557:Formaldehyde; D006339:Heart Rate / Q000502:physiology; D008297:Male; D010146:Pain / Q000503:physiopathology*; D011149:Pons / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012149:Restraint, Physical; D013312:Stress, Physiological / Q000503:physiopathology*; D013564:Sympathetic Nervous System / Q000502:physiology
D005557:Formaldehyde; D000324:Adrenocorticotropic Hormone