Hydrogen sulfide improves the endothelial dysfunction in renovascular hypertensive rats

Title:

Hydrogen sulfide improves the endothelial dysfunction in renovascular hypertensive rats

Creator:

Xue, H., Zhou, S., Xiao, L., Guo, Q., Liu, S., and Wu, Y.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:04c82d02-f08c-42a8-96d7-c002a19141b0
uuid:04c82d02-f08c-42a8-96d7-c002a19141b0
issn:0862-8408

Subject:

Fyziologie člověka a srovnávací fyziologie, endoteliální dysfunkce, oxidační stres, endothelial dysfunction, oxidative stress, hydrogen sulfide, angiotensin II, 14, and 612

Type:

article, články, model:article, and TEXT

Format:

print, bez média, and svazek

Description:

As a novel gasotrans mitter, h ydrogen sulfide (H 2 S) has vasodilating and antihypertensive effects in cardiovascular system. Thus, we hypothesized that H 2 S might have beneficial effects on thoracic endothelial function in two -kidney one -clip (2K1C) rats, a model of renovascular hypertension. Sodium hydrosulfide (NaHS , 56 μmol/kg /day ) was administrated intra - peritoneally from the third day after the 2K1C operation. Along with the development of hypertension, t he systolic blood pressure (SBP) was measured before the operation and each week thereafter. The oxidative stress wa s determined by measurement of malondialdehyde (MDA) concentration, superoxide dismutase (SOD) activity and protein expression of oxidative stress -related proteins (AT 1 R, NADPH oxidase subunits). Acetylcholine (ACh) -induced vasorelaxation and angiotensin I I (Ang II) -induced vasocontraction were performed on isolated thoracic aorta. The SBP w as significantly increased from the first week after operation , and was lowered by NaHS. NaHS supplementation ameliorated endothelial dysfunction. The protein expression of oxidative stress -related proteins were downregulated, while SOD activity upregulated. In conclusion, improvement of endothelial function is involved in the antihypertensive mechanism of H 2 S. The protective effect of H 2 S is attributable to suppression o f vascular oxidative stress that involves inhibition of Ang II -AT 1 R action, downregulation of oxidases, as well as upregulation of antioxidant enzyme., H. Xue, S. Zhou, L. Xiao, Q. Guo, S. Liu, Y. Wu., and Obsahuje bibliografii

Language:

English

Rights:

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

Source:

Physiological research | 2015 Volume:64 | Number:5

Harvested from:

CDK

Metadata only:

false