Abstract:
:The involvement of endothelium-derived hyperpolarizing factor (EDHF) in the protective effect of 17beta-estradiol was investigated on the phenylephrine-precontracted carotid artery from cholesterol fed rabbits. Animals were fed for 8 weeks as follows: control group, standard chow; (control+estradiol) group, standard chow+17beta-estradiol; standard chow+1% cholesterol, cholesterol group; or (cholesterol+estradiol) group, 1% cholesterol chow+17beta-estradiol. Relaxations to acetylcholine (ACh) (3 nM-30 microM) were performed with N(omega) nitro-L-arginine methyl ester (300 microM) and indomethacin (10 microM). Charybdotoxin (50 nM)+apamin (50 nM), glibenclamide (10 microM) or 4-aminopyridine (1 mM) were used to block, respectively, calcium-activated-K(+), adenosine triphosphate (ATP)-sensitive-K(+) and voltage-dependent K(+) channels. In the control group, ACh induced a residual concentration-dependent relaxation. This response was impaired by hypercholesterolemia and restored by 17beta-estradiol. In control and cholesterol groups, 4-aminopyridine or glibenclamide did not affect this relaxation, but in (control+estradiol) and (cholesterol+estradiol) groups, glibenclamide suppressed it. In all groups, this persisting relaxation was completely abolished by charybdotoxin alone or with apamin, by hemoglobin (10 microM), a nitric oxide scavenger, or by LY83183 (10 microM), a guanylate cyclase inhibitor. Thus, in the rabbit carotid artery, the protective effect of 17beta-estradiol against hypercholesterolemia is probably mediated by a nitric oxide/cyclic GMP pathway which activates calcium-targeted and ATP-dependent K(+) channels.
journal_name
Atherosclerosisjournal_title
Atherosclerosisauthors
Ghanam K,Ea-Kim L,Javellaud J,Oudart Ndoi
10.1016/s0021-9150(99)00450-5keywords:
subject
Has Abstractpub_date
2000-09-01 00:00:00pages
59-67issue
1eissn
0021-9150issn
1879-1484pii
S0021-9150(99)00450-5journal_volume
152pub_type
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