Thermosensitivity, a possible new locus involved in genetic hypertension.

Malo, Danielle; Schlager, Gunther; Tremblay, Johanne; Hamet, Pavel

doi:10.1161/01.hyp.14.2.121

Cited by 32 publications

(16 citation statements)

References 34 publications

(30 reference statements)

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“…A unique feature of hypertension is heightened susceptibility to ambient temperature, 22,23 and hsp genes were suggested to be attractive candidates for such an altered response to environmental stress. 23 The present study expounded on this suggestion and provided novel evidence to support the notion that an altered temporal profile of HS-induced HSF1 phosphorylation, HSP70 expression or potentiation of BRR response, and engagement of both PKA and PKC pathways in the activation of HSF1 at the NTS may be associated with greater susceptibility to heatstroke during hypertension.…”

Section: Discussionmentioning

confidence: 99%

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: Discussionmentioning

confidence: 99%

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 It is noteworthy that SHR are also hypersensitive to heat and ether. 3,4,28 Genes of calcium channel subunits and Na channel subunits mapped on human Chr 7q have been proposed as candidate genes for malignant hyperthermia. 29 -31 The Hsp27 stress gene is also a good positional candidate on Chr 12, because we have shown its modulation by SHR-Y.…”

Section: Discussionmentioning

confidence: 99%

“…2 Spontaneously hypertensive rats (SHR) and mice are more reactive to stress than their normotensive counterparts. [3][4][5][6] On exposure to several psychogenic stressors, such as cage-switch, placement in an open field, or immobilization, they display higher changes in heart rate, BP, and body temperature (BT). 5,7 The increase in BT with immobilization stress may, thus, be proposed as an intermediate phenotype of the stress response.…”

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confidence: 99%

Contribution of Autosomal Loci and the Y Chromosome to the Stress Response in Rats

et al. 2000

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Abstract-Stress is a critical contributor to cardiovascular diseases through its impact on blood pressure variability and cardiac function. Familial clustering of reactivity to stress has been demonstrated in human subjects, and some rodent models of hypertension are hyperresponsive to stress. Therefore, the present study was designed to uncover the genetic determinants of the stress response. We performed a total genome linkage search to identify the loci of the body temperature response to immobilization stress in a set of recombinant inbred strains (RIS) originating from reciprocal crosses of spontaneously hypertensive rats (SHR) with a normotensive Brown Norway Lx strain. Two quantitative trait loci (QTLs) were revealed on chromosomes (Chrs) 10 and 12 (logarithm of odds scores, 2.2 and 1.3, respectively). The effects of these QTLs were enhanced by a high sodium diet (logarithm of odds scores, 4.0 and 3.3 for Chrs 10 and 12, respectively), which is suggestive of a salt-sensitive component for the phenotype. Congenics for Chr 10 confirmed both the QTL and the salt effect in RIS. Negatively associated loci were also identified on Chrs 8 and 11. Interaction between the loci of Chrs 10 and 12 was demonstrated, with the rat strains bearing SHR alleles at both loci having the highest thermal response to stress. Furthermore, the Y Chr of SHR origin enhanced the response to immobilization stress, as demonstrated in 2 independent models, RIS and Y Chr consomics. However, its full effect requires autosomes of the SHR strain. These findings provide the first evidence for the genetic determination of reactivity to stress with interactions between autosomal loci and between the Y and autosomal Chrs that contribute to the explanation of the 46% of variance in the stress response. T he response to environmental stress is a predictor of cardiovascular diseases, including future high blood pressure (BP), in prehypertensive patients with a positive family history 1 and the development of left ventricular hypertrophy. 2 Spontaneously hypertensive rats (SHR) and mice are more reactive to stress than their normotensive counterparts. 3-6 On exposure to several psychogenic stressors, such as cage-switch, placement in an open field, or immobilization, they display higher changes in heart rate, BP, and body temperature (BT). 5,7 The increase in BT with immobilization stress may, thus, be proposed as an intermediate phenotype of the stress response. To identify the genetic determinants of the BT response to immobilization stress, we performed a full genome scan in a set of rat recombinant inbred strains (RIS) originating from reciprocal crosses of SHR and normotensive Brown Norway (BN) Lx strains. This is the only set of rat RIS available to study the genetics of hypertension and its related traits. 8 Any quantitative phenotype that can be measured accurately and that displays a significant gradient across strains can be mapped in the RIS panel, irrespective of the differences between progenitor strains, 9 in this permanent replica of...

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“…Raised BP has direct effects on the vasculature, 24,25 and vessels subjected to greater mechanical and shear stress express heat shock proteins and are more prone to the development of atherosclerosis. 20,22,25,26 In addition, Hsp70 mRNA levels are enhanced in hypertensive animals, 27,28 and there is a greater accumulation of heat stress-induced Hsp70 mRNA in peripheral blood lymphocytes from hypertensive humans compared with that in NT control subjects. 29 Although these findings demonstrate a stress response to hypertension, a definitive causative link between heat shock protein expression/release and the development of vascular disease has yet to be established.…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular disease

2011

Oxford Handbook of Anaesthesia

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Abstract-The phylogenetically conserved nature of heat shock proteins (Hsp) has led to the proposition that they may provide a link between infection and the inflammatory component to vascular disease. Hypertension is associated with atherosclerosis. Here, we measured circulating heat shock protein and heat shock protein antibody levels in association with borderline hypertension. Seventy-two men with borderline hypertension patients and 75 normotensive control subjects (diastolic blood pressure 85 to 94 and Ͻ80 mm Hg, respectively) were selected from a population-screening program. The levels of Hsp60; Hsp70; and anti-human Hsp60, anti-human Hsp70, and anti-mycobacterial Hsp65 antibodies were determined with enzyme immunoassay. The presence of carotid atherosclerosis and the intima-media thickness values were determined with ultrasonography. A major novel observation in this report was the detection of circulating Hsp60, which was present at a significantly enhanced level in patients with borderline hypertension. Furthermore, serum Hsp60 was associated with intima-media thicknesses (PϽ0.01). Anti-Hsp65 antibody levels were higher in borderline hypertension (PϽ0.001), whereas Hsp70 and anti-Hsp70 antibody levels did not differ. In contrast to anti-Hsp65 antibody, anti-Hsp60 antibody levels were lower in borderline hypertension (PϽ0.03), although the difference was quantitatively small. None of the parameters evaluated were associated with atherosclerosis, metabolic factors, or smoking. We identified elevated Hsp60 levels in patients with borderline hypertension and an association between early atherosclerosis and Hsp60 levels. The physiological role of Hsp60 release has yet to be defined, but given the proinflammatory properties, these proteins could be involved in the induction/progression of both hypertension and atherosclerosis, as well as being markers for early cardiovascular disease. (Hypertension. 2000;36:303-307.)

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Thermosensitivity, a possible new locus involved in genetic hypertension.

Cited by 32 publications

References 34 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

Contribution of Autosomal Loci and the Y Chromosome to the Stress Response in Rats

Cardiovascular disease

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