Restriction of nitric oxide rather than elevated blood pressure is responsible for alterations of vascular responses in nitric oxide-deficient hypertension

Title:

Restriction of nitric oxide rather than elevated blood pressure is responsible for alterations of vascular responses in nitric oxide-deficient hypertension

Creator:

Holécyová, A., Török, J., Bernátová, I., and Pecháňová, O.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:be837e0a-e36d-4b7a-94f5-06048c027554
uuid:be837e0a-e36d-4b7a-94f5-06048c027554

Subject:

nitric oxide, L-NAME, hypertension, pulmonary and systemic vascular reactivity, and rat

Type:

article, model:article, and TEXT

Description:

The responsiveness of isolated high-pressure (aorta, renal artery) and low-pressure vessels (pulmonary artery) was compared during systemic hypertension induced by chronic inhibition of nitric oxide synthesis by NG-nitro-L-arginine methyl ester (L-NAME) in rats. L-NAME (40 mg/kg/day) was given to animals in their drinking water. After 4 weeks of L-NAME treatment, systolic blood pressure increased by 37 % as compared with that in the control group. Chronic L-NAME treatment resulted in significant reduction of endothelium-dependent relaxation to acetylcholine (10-8 to 3xl0-6 mol/1) in both types of vessels. The reduced relaxation was not influenced by acute pretreatment with indomethacin (10"5 mol/1), however, it was further reduced by acute pretreatment with additional L-NAME (10-4 mol/1). L-arginine (10-4 mol/1) improved the reduced relaxation. Endothelium- independent relaxation to sodium nitroprusside (10-9 to 10-6 mol/1) was unaffected by L-NAME treatment. /3-adrenoceptor-mediated relaxation to isoprénaline (10“8 to 3xl0-6 mol/1) was also not influenced by chronic L-NAME treatment Similar alterations in the responsiveness of high- and low- pressure vessels indicate rather the decisive role of nitric oxide restriction than that of elevated blood pressure in their development

Language:

English

Rights:

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

Source:

Physiological research | 1996 Volume:45 | Number:4

Harvested from:

CDK

Metadata only:

false