Contribution of captopril thiol group to the prevention of spontaneous hypertension

Title:

Contribution of captopril thiol group to the prevention of spontaneous hypertension

Creator:

Oľga Pecháňová

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:78db1db1-bdcb-4678-bae4-19b7f83e90d8
uuid:78db1db1-bdcb-4678-bae4-19b7f83e90d8
issn:0862-8408

Subject:

Fyziologie člověka a srovnávací fyziologie, hypertenze, thioly, hypertension, thiols, spontaneous hypertension, captopril, enalapril, nitric oxide synthase, reactive oxygen species, 14, and 612

Type:

article, články, model:article, and TEXT

Format:

print, bez média, and svazek

Description:

We aimed to compare the effect of angiotensin converting enzyme (ACE) inhibitors captopril (containing thiol group) and enalapril (without thiol group) on the development of spontaneous hypertension and to analyze mechanisms of their actions, particularly effects on oxidative stress and NO production. Six-week-old SHR were divided into three groups: control, group receiving captopril (50 mg/kg/day) or enalapril (50 mg/kg/day) for 6 weeks. At the end of experiment, systolic blood pressure (SBP) increased by 41 % in controls. Both captopril and enalapril prevented blood pressure increase, however, SBP in the captopril group (121±5 mmHg) was significantly lower than that in the enalapril group (140±5 mmHg). Concentration of conjugated dienes in the aorta was significantly lower in the captopril group compared to the enalapril group. Captopril and enalapril increased NO synthase activity in the heart and aorta to the similar level. Neither captopril nor enalapril was, however, able to increase the expression of eNOS. Both ACE inhibitors increased the level of cGMP. However, cGMP level was significantly higher in the aorta of captopril group. We conclude that captopril, beside inhibition of ACE, prevented hypertension by increasing NO synthase activity and by simultaneous decrease of oxidative stress which resulted in increase of cGMP concentration., O. Pecháňová., and Obsahuje bibliografii

Language:

English

Rights:

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

Source:

Physiological research | 2007 Volume:56 | Number:Suppl 2

Harvested from:

CDK

Metadata only:

false