Potentiation of baroreceptor reflex response by heat shock protein 70 in nucleus tractus solitarii confers cardiovascular protection during heatstroke

Background-Whereas hypotension and bradycardia seen during the onset of hea tstroke may be protected by prior induction of heat shock protein 70 (HSP70 ) in the brain, the underlying mechanism is not fully understood. We evalua ted the hypothesis that HSP70 may confer cardiovascular protection during h eatstroke by potentiating the baroreceptor reflex (BRR) control of peripher al hemodynamic performance. Methods and Results-Adult male Sprague-Dawley rats subjected to a brief hyp erthermic heat shock (HS; 42 degreesC for 15 minutes) induced discernible e xpression of HSP70 in the bilateral nucleus tractus solitarii (NTS), the te rminal site in the brain stem for primary baroreceptor afferents. This HSP7 0 expression was detected fit 8 hours! peaked at 24 hours, and returned to baseline by 45 hours after HS. Brief hyperthermia also significantly potent iated the ERR response in a temporal profile that correlated positively wit h changes in HSP70 expression at the NTS. Prior HS also appreciably allevia ted hyperthermia, severe hypotension, and bradycardia manifested during the onset of heatstroke (45 degreesC for 60 minutes) elicited 24 hours later. Microinjection bilaterally of anti-HSP70 antiserum (1:20) into the NTS or d enervation of the sinoaortic baroreceptor afferents significantly reversed the enhancement of ERR response and cardiovascular protection during heatst roke induced by prior HS. Conclusions-These results suggest that MS-induced expression of HSP70 in th e NTS may alleviate severe hypotension and bradycardia exhibited during the onset of heatstroke by potentiating both the sensitivity and capacity of E RR response.