Published Online
on December 30, 2002

A more recent version of this article appeared on January 21, 2003

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Submitted on August 13, 2002
Revised on September 18, 2002
Accepted on September 18, 2002

Altered Temporal Profile of Heat Shock Factor 1 Phosphorylation and Heat Shock Protein 70 Expression Induced by Heat Shock in Nucleus Tractus Solitarii of Spontaneously Hypertensive Rats

Samuel H.H. Chan PhD, Ling-Lin Wang MS, Kuei-Feng Chang BS, Chen-Chun Ou MS, and Julie Y.H. Chan PhD^*

From the Center for Neuroscience (S.H.H.C.), National Sun Yat-sen University, and Department of Medical Education and Research (L.L.W., K.F.C., C.C.O., J.Y.H.C.), Kaohsiung Veterans General Hospital, Taiwan, Republic of China.

^* To whom correspondence should be addressed. E-mail: yhwa{at}isca.vghks.gov.tw.

Background—We demonstrated recently that heat shock (HS)-induced heat shock protein 70 (HSP70) expression in bilateral nucleus tractus solitarii (NTS), the terminal site in the brain stem for primary baroreceptor afferents, confers cardiovascular protection against heatstroke by potentiating baroreceptor reflex (BRR) response. This study evaluated the hypothesis that altered regulation of HSP70 expression may be associated with the heightened susceptibility to heatstroke during hypertension.

Methods and Results—Spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats anesthetized with propofol were used. Compared with WKY rats, significant induction in HSP70 or phosphorylation of heat shock factor 1 (HSF1), but not HSF2, in the NTS and potentiation of BRR response in SHR occurred earlier (4 versus 8 hours), reaching peak magnitude sooner (16 versus 24 hours), and declined more rapidly after a brief hyperthermic HS (42±0.5°C for 15 minutes). The protection conferred by HS against hypotension and bradycardia during the onset of heatstroke (45°C for 60 minutes), although effective, was less effective in SHR. Microinjection bilaterally into the NTS of the selective protein kinase A (PKA) inhibitor H-89 (100 pmol) or the selective PKC inhibitor calphostin C (100 pmol) significantly attenuated all of the above events induced in SHR by HS. However, only H-89 was effective in WKY rats.

Conclusions—An altered temporal profile of HS-induced HSP70 expression or potentiation of BRR response by concurrent activation via both PKA and PKC pathways of phosphorylation of HSF1 in the NTS may be associated with greater susceptibility to heatstroke during hypertension.

Key words: blood pressure • heart rate • nervous system • stroke

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