scholarly journals Relations between nitric oxide synthase DNOS1, Hsp70 and apoptosis regulatory gene grim in Drosophila melanogaster after heat stress induction

2010 ◽  
Vol 26 (3) ◽  
pp. 194-199
Author(s):  
E. M. Khussainova ◽  
Z. A. Bulentayeva ◽  
B. O. Bekmanov ◽  
L. B. Djansugurova ◽  
R. I. Bersimbayev
Keyword(s):  
Nitric Oxide ◽  
Drosophila Melanogaster ◽  
Heat Stress ◽  
Nitric Oxide Synthase ◽  
Regulatory Gene ◽  
Stress Induction ◽  
Oxide Synthase

Heat Stress-Activated, Calcium-Dependent Nitric Oxide Synthase in Sponges

Nitric Oxide ◽  
2001 ◽  
Vol 5 (5) ◽  
pp. 427-431 ◽  
Author(s):  
Marco Giovine ◽  
Marina Pozzolini ◽  
Anna Favre ◽  
Giorgio Bavestrello ◽  
Carlo Cerrano ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heat Stress ◽  
Nitric Oxide Synthase ◽  
Calcium Dependent ◽  
Oxide Synthase

scholarly journals Heat shock protein 90 contributes to cutaneous vasodilation through activating nitric oxide synthase in young male adults exercising in the heat

2017 ◽  
Vol 123 (4) ◽  
pp. 844-850 ◽  
Author(s):  
Naoto Fujii ◽  
Sarah Y. Zhang ◽  
Brendan D. McNeely ◽  
Takeshi Nishiyasu ◽  
Glen P. Kenny
Keyword(s):  
Nitric Oxide ◽  
Heat Stress ◽  
Heat Shock ◽  
Nitric Oxide Synthase ◽  
Heat Shock Protein ◽  
Heat Shock Protein 90 ◽  
Hsp90 Inhibition ◽  
Cutaneous Vasodilation ◽  
Cutaneous Perfusion ◽  
Oxide Synthase

While the mechanisms underlying the control of cutaneous vasodilation have been extensively studied, there remains a lack of understanding of the different factors that may modulate cutaneous perfusion during an exercise-induced heat stress. We evaluated the hypothesis that heat shock protein 90 (HSP90) contributes to the heat loss response of cutaneous vasodilation via the activation of nitric oxide synthase (NOS) during exercise in the heat. In 11 young males (25 ± 5 yr), cutaneous vascular conductance (CVC) was measured at four forearm skin sites that were continuously treated with 1) lactated Ringer solution (control), 2) NOS inhibition with 10 mM NG-nitro-l-arginine methyl ester (l-NAME), 3) HSP90 inhibition with 178 μM geldanamycin, or 4) a combination of 10 mM l-NAME and 178 μM geldanamycin. Participants rested in a moderate heat stress (35°C) condition for 70 min. Thereafter, they performed a 50-min bout of moderate-intensity cycling (~52% V̇o2peak) followed by a 30-min recovery period. We showed that NOS inhibition attenuated CVC (~40–50%) relative to the control site during pre- and postexercise rest in the heat ( P ≤ 0.05); however, no effect of HSP90 inhibition was observed ( P > 0.05). During exercise, we observed an attenuation of CVC with the separate inhibition of NOS (~40–50%) and HSP90 (~15–20%) compared with control (both P ≤ 0.05). However, the effect of HSP90 inhibition was absent in the presence of the coinhibition of NOS ( P > 0.05). We show that HSP90 contributes to cutaneous vasodilation in young men exposed to the heat albeit during exercise only. We also show that the HSP90 contribution is due to NOS-dependent mechanisms. NEW & NOTEWORTHY We show that heat shock protein 90 functionally contributes to the heat loss response of cutaneous vasodilation during exercise in the heat, and this response is mediated through the activation of nitric oxide synthase. Therefore, interventions that may activate heat shock protein 90 may facilitate an increase in heat dissipation through an augmentation of cutaneous perfusion. In turn, this may attenuate or reduce the increase in core temperature and therefore the level of heat strain.

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