Role of nitric oxide in adaptation to hypoxia and adaptive defense

Title:

Role of nitric oxide in adaptation to hypoxia and adaptive defense

Creator:

Manukhina, E. B., Mashina, S. Yu., Smirin, B. V., Lyamina, N. P., Senchikhin, V. N., Vanin, A. F., and Malyshev, I. Yu.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:b276ed6d-15ef-494f-aabb-27a037c229a6
uuid:b276ed6d-15ef-494f-aabb-27a037c229a6
issn:0862-8408

Subject:

Fyziologie člověka a srovnávací fyziologie, oxid dusnatý, hypoxie, adaptace (biologie), infarkt myokardu, nitric oxide, hypoxia, adaptation (biology), myocardial infarction, spontaneously hypertensive rats, 14, and 612

Type:

article, články, model:article, and TEXT

Format:

print, bez média, and svazek

Description:

Adaptation to hypoxia is beneficial in cardiovascular pathology related to NO shortage or overproduction. However, the question about the influence of adaptation to hypoxia on NO metabolism has remained open. The present work was aimed at the relationship between processes of NO production and storage during adaptation to hypoxia and the possible protective significance of these processes. Rats were adapted to intermittent hypobaric hypoxia in an altitude chamber. NO production was determined by plasma nitrite/nitrate level. Vascular NO stores were evaluated by relaxation of the isolated aorta to diethyldithiocarbamate. Experimental myocardial infarction was used as a model of NO overproduction; stroke-prone spontaneously hypertensive rats (SHR-SP) were used as a model of NO shortage. During adaptation to hypoxia, the plasma nitrite/nitrate level progressively increased and was correlated with the increase in NO stores. Adaptation to hypoxia prevented the excessive endothelium-dependent relaxation and hypotension characteristic for myocardial infarction. At the same time, the adaptation attenuated the increase in blood pressure and prevented the impairment of endothelium-dependent relaxation in SHR-SP. The data suggest that NO stores induced by adaptation to hypoxia can either bind excessive NO to protect the organism against NO overproduction or provide a NO reserve to be used in NO deficiency., E. B. Manukhina, S. Yu. Mashina, B. V. Smirin, N. P. Lyamina, V. N. Senchikhin, A. F. Vanin, I. Yu. Malyshev., 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