The mechanisms underlying the protective role of estrogens on vascular function have not been clearly defined. Impaired signalling of the G1.2-protein can induce endothelial dysfunction and may contribute to the pathophysiology of arteriosclerosis. Therefore, experiments were conducted to determine whether female sex hormones may regulate the activity of this endothelial signal transduction pathway. Position-matched rings of isolated coronary arteries from male and female pigs were suspended for isometric tension recording in isolated organ chambers. Contractile responses to prostaglandin F2α were similar in rings from males and females. Endothelium-dependent relaxations evoked by the Gi-2-protein-dependent stimuli, serotonin or fluoride (direct activator) were increased in rings from females compared to males. Endothelial responses to Gi.2-protein-independent stimuli, ADP and A23187, were similar in rings from males and females. Endothelium-dependent relaxations were inhibited by L-NAME, a blocker of NO synthase, in rings from males and females. Western blot analysis was performed using plasma membranes of human aortic endothelial cells that had been cultured in the presence and absence of 17β-estradiol. Immunoreactive levels of the Gi.2-protein were increased by hormone treatment. Therefore, increased activity of the endothelial Gi-2 protein may contribute to the anti-arteriogenic influence of estrogens.
|Original language||English (US)|
|State||Published - 1996|
ASJC Scopus subject areas
- Molecular Biology