Inducible NO synthase activity in blood vessels and heart: new insight into cell origin and consequences

Title:

Inducible NO synthase activity in blood vessels and heart: new insight into cell origin and consequences

Creator:

Muller, B., Kleschyov, A. L., Gyorgy, K., and Stoclet, J.-C.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:9ea36ba4-6b06-4560-9bc6-b4cbeb9ac16f
uuid:9ea36ba4-6b06-4560-9bc6-b4cbeb9ac16f
issn:0862-8408

Subject:

Fyziologie člověka a srovnávací fyziologie, krevní cévy, blood-vessels, cardioprotection, dinitrosyl-iron complexes, inducible NO synthase, nitric oxide stores, 14, and 612

Type:

article, články, model:article, and TEXT

Format:

print, bez média, and svazek

Description:

Induction of the inducible form of nitric oxide synthase (iNOS) in the vascular and cardiac tissue by several inflammatory stimuli may result in the production of large amounts of nitric oxide (NO) for a sustained period. Recent data obtained in the rat aorta in which iNOS was induced by lipopolysaccharide (LPS) have demonstrated that adventitial cells represent the main site of NO production. Adventitial-derived NO can exert an immediate down-regulatory effect on smooth muscle contraction (via activation of the cyclic GMP pathway) but may also initiate longer lasting effects through the formation of NO stores within the medial layer. One candidate for such NO stores are dinitrosyl non-heme iron complexes. Low molecular weight thiols interact with preformed NO stores and promote vasorelaxation by a cyclic GMP-independent mechanism involving the activation of potassium channels. In the heart, the induction of iNOS is involved in delayed protection against ischemia-reperfusion-induced functional damages. Recent data obtained with monophosphoryl lipid A, a non-toxin derivative of LPS, strongly suggest that iNOS-derived NO in the rat heart does not act as an immediate mediator of the cardioprotection but rather as a trigger of long-term protective mechanisms. Thus, the present data reveal the important role of adventitial cells as a site of iNOS expression and activity in intact blood vessels. The induction of adaptive mechanisms in the heart and the formation of releasable NO stores in blood vessels are examples of long-term consequences of iNOS induction. These new information are relevant for a better understanding of the circumstances in which NO overproduction by iNOS may play either a beneficial or deleterious role in these tissues., B. Muller, A. L. Kleschyov, K. Gyorgy, J.-C. Stoclet., 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