Potentiation of Baroreceptor Reflex Response by Heat Shock Protein 70 in Nucleus Tractus Solitarii Confers Cardiovascular Protection During Heatstroke

Li, Pei-Lun; Chao, Yung-Mei; Chan, Samuel H.H.; Chan, Julie Y.H.

doi:10.1161/01.cir.103.16.2114

Cited by 80 publications

(92 citation statements)

References 24 publications

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“…Hyperthermic HS was induced by maintaining the core temperature of animals at 42Ϯ0.5°C for 15 minutes, 3,15 as monitored by a thermistor probe placed in the colon. Animals were thereafter allowed to recover at room temperature for the time interval stipulated for each experiment.…”

Section: Hs Inductionmentioning

confidence: 99%

“…3,15,16 Primary antisera used included mouse monoclonal antiserum against the inducible form of HSP70 (1:500; SPA-810, StressGen) or rat monoclonal antiserum against HSF1 (1:500, MAB88078; Chemicon) or HSF2 (1:500, MAB88079; Chemicon).…”

Section: Protein Extraction and Western Blot Analysismentioning

confidence: 99%

“…Microinjection bilaterally into the NTS of test agents was carried out 3,15 immediately after HS. The coordinates were Ϫ0.5 to ϩ0.5 mm from obex, 0.3 to 0.8 mm lateral to midline, and 0.5 to 1.0 mm below dorsal surface of the medulla oblongata.…”

Section: Microinjection Of Test Agents Into the Ntsmentioning

confidence: 99%

“…1,2 In terms of central cardiovascular regulation, we reported recently 3 that a brief hyperthermic HS increases the expression of HSP70, the major inducible form of HSPs, 1 in the nucleus tractus solitarii (NTS), the terminal site of baroreceptor afferent fibers in the medulla oblongata. 4 This HS-induced HSP70 expression in turn confers cardiovascular protection against heatstroke by potentiating the baroreceptor reflex (BRR) response.…”

mentioning

confidence: 99%

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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

et al. 2003

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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 (42Ϯ0.5°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

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Section: Hs Inductionmentioning

confidence: 99%

Section: Protein Extraction and Western Blot Analysismentioning

confidence: 99%

Section: Microinjection Of Test Agents Into the Ntsmentioning

confidence: 99%

mentioning

confidence: 99%

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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

et al. 2003

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“…27,28 This was followed by incubation with horseradish peroxidase-conjugated goat anti-rabbit IgG (Jackson). Specific antibody-antigen complex was detected with the use of an enhanced chemiluminescence Western blot detection system (NEN Life Science Products).…”

Section: Protein Extraction and Western Blot Analysismentioning

confidence: 99%

Downregulation of Angiotensin Subtype 1 Receptor in Rostral Ventrolateral Medulla During Endotoxemia

Chan

Ling-lin

et al. 2003

Hypertension

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Abstract-We reported recently that an upregulation of the inducible nitric oxide synthase (iNOS) in the rostral ventrolateral medulla (RVLM), where sympathetic premotor neurons are located, is a crucial determinant for the elicitation of cardiovascular depression during experimental endotoxemia. The current study evaluated the hypothesis that a downregulation of the molecular synthesis and functional expression of angiotensin subtype 1 receptor (AT1R) in the RVLM is consequential to this upregulated iNOS. In adult Sprague-Dawley rats maintained under propofol anesthesia, intravenous administration of Escherichia coli lipopolysaccharide (15 mg/kg) elicited a reduction, followed by an augmentation and a secondary decrease in sympathetic vasomotor outflow, together with progressive hypotension and bradycardia. There was also a progressive increase in iNOS mRNA and protein level in the ventrolateral medulla. This was followed by a significant downregulation of both mRNA and protein levels of AT1R in the ventrolateral medulla, alongside reduced efficacy of angiotensin II (50 pmol) to induce an increase in systemic arterial pressure, heart rate, or sympathetic vasomotor outflow on unilateral microinjection into the RVLM. Pretreatment with microinjection of a selective iNOS inhibitor, S-methylisothiourea (250 pmol) bilaterally into the RVLM significantly reversed the reduction in both synthesis and activity of AT1R. We conclude that a downregulation of molecular synthesis and functional expression of AT1R in the ventrolateral medulla is consequential to the overproduction of NO through upregulation of iNOS in the RVLM and may underlie the cardiovascular depression that takes place during experimental endotoxemia. Key Words: receptors, angiotensin Ⅲ nitric oxide synthase Ⅲ central nervous system Ⅲ hypotension Ⅲ bradycardia Ⅲ nervous system, sympathetic S epsis is associated with profound cardiovascular abnormalities characterized by hypotension, decreased systemic resistance, altered vascular reactivity to contractile agents, and a high mortality rate. 1 One well-known mediator of sepsis-induced circulatory failure is nitric oxide (NO) produced through activation of the inducible NO synthase (iNOS) in macrophages at the peripheral vasculature. 2,3 In addition, we reported recently 4 that overproduction of NO by iNOS in the rostral ventrolateral medulla (RVLM) is also a crucial determinant for the reduction in sympathetic vasomotor outflow and fatal cardiovascular depression during experimental endotoxemia. Whereas we proposed that the underlying mechanisms include formation of the cytotoxic substance peroxynitrite 5 and activation of GABAergic neurotransmission, 6 the possibility exists for the engagement of other mediators in the RVLM.As the medullary site of the sympathetic premotor neurons, 7 the RVLM maintains arterial pressure by providing a tonic excitation to preganglionic sympathetic neurons in the spinal cord. 7,8 It is also a target site where the brain renin-angiotensin system acts to regulate sympathetic out...

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Synergistic Impact of Air Pollution and Heat on Health and Economy in India

Sekar,

Sharma,

Mahajan

2024

The Climate-Health-Sustainability Nexus

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Potentiation of Baroreceptor Reflex Response by Heat Shock Protein 70 in Nucleus Tractus Solitarii Confers Cardiovascular Protection During Heatstroke

Abstract: These results suggest that HS-induced expression of HSP70 in the NTS may alleviate severe hypotension and bradycardia exhibited during the onset of heatstroke by potentiating both the sensitivity and capacity of BRR response.

Cited by 80 publications

References 24 publications

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

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

Downregulation of Angiotensin Subtype 1 Receptor in Rostral Ventrolateral Medulla During Endotoxemia

Synergistic Impact of Air Pollution and Heat on Health and Economy in India

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