Cross-talk between nitric oxide and HSP70 in the antihypotensive effect of adaptation to heat

Title:

Cross-talk between nitric oxide and HSP70 in the antihypotensive effect of adaptation to heat

Creator:

Malyshev, I. Yu., Bayda, L. A., Trifonov, A. I., Larionov, N. P., Kubrina, L. D., Mikoyan, V. D., Vanin, A. F., and Manukhina, E. B.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:3b0a9284-af00-442b-acfe-7e7b068808f8
uuid:3b0a9284-af00-442b-acfe-7e7b068808f8
issn:0862-8408

Subject:

Fyziologie člověka a srovnávací fyziologie, oxid dusnatý, adaptace (biologie), hypotenze, nitrous oxide, adaptation (biology), hypotension, heat shock protein, heat shock, 14, and 612

Type:

article, články, model:article, and TEXT

Format:

print, bez média, and svazek

Description:

In this work, we evaluated the effect of adaptation to heat on the fall of blood pressure (BP) induced by heat shock (HS) and the interrelation between nitric oxide (NO) and heat shock protein, HSP70. Experiments were carried out on Wistar rats. It was shown that HS resulted in a generalized and transient increase in NO production (the electron paramagnetic resonance method) and a fall of BP from 113± 3 to 88± 1 mm Hg (?<0.05). Adaptation to heat itself did not affect BP, but completely prevented the NO overproduction and hypotension induced by HS. The adaptation simultaneously increased the brain NO-synthase content and induced HSP70 synthesis (the Western blot analysis) in various organs. Both the antihypotensive effects of adaptation and HSP70 accumulation were completely prevented by L-NNA, an inhibitor of NO synthesis, or quercetin, an inhibitor of HSP70 synthesis. The data suggest that adaptation to heat stimulates NO synthesis and NO activates synthesis of HSP70. HSP70, which hampers NO overproduction, thus restricts the BP fall induced by heat shock., I. Yu. Malyshev, L.A. Bayda, A.I. Trifonov, N.P. Larionov, L.D. Kubrina, V.D. Mikoyan, A.F. Vanin, E.B. Manukhina., and Obsahuje bibliografii

Language:

English

Rights:

http://creativecommons.org/licenses/by-nc-sa/4.0/
policy:public

Source:

Physiological research | 2000 Volume:49 | Number:1

Harvested from:

CDK

Metadata only:

false