The direct action of 17β-estradiol in isolated omental artery from nonpregnant and pregnant women is related to calcium antagonism

OBJECTIVE: Our purpose was to study the mechanism by which 17β- estradiol modulates contractile activity in isolated rings of omental artery from nonpregnant and pregnant patients. STUDY DESIGN: Rings of omental artery with intact endothelium from nonpregnant and pregnant women were mounted in organ chambers for isometric tension recording. The concentration-relaxation relationship to 17β-estradiol (10^-7 mol/L to 3 x 10^-5 mol/L) was studied in rings contracted with 60 mmol/L potassium chloride (in both the absence and the presence of tamoxifen, 10^-6 mol/L). The effect of 17β-estradiol (10^-5 mol/L) on the contraction induced by 60 mmol/L potassium chloride and on the concentration-contraction relationships to both norepinephrine (10^{- 9} mol/L to 10^-5 mol/L) and calcium ion (0.05 mmol/L to 2.5 mmol/L in calcium-free depolarizing solution) were studied in the presence and absence of tamoxifen (10^-6 mol/L). The maximal contraction, negative logarithm of the concentration producing 50% relaxation or 50% contraction to the reference 60 mmol/L potassium chloride contraction, and the area under the curve were calculated. Data analysis was by one-way analysis of variance, Newman-Keuls test, and two-sample tests as appropriate. Probability values less than 0.05 in a two-tailed test were considered statistically significant. RESULTS: 17β-Estradiol relaxed omental arteries contracted with 60 mmol/L potassium chloride, and this effect was potentiated by tamoxifen in both groups. Incubation of the omental arteries with 17β-estradiol inhibited contractions induced by 60 mmol/L potassium chloride in rings from both groups of patients, and tamoxifen did not antagonize this effect in either group. Rings of omental artery from the nonpregnant patients (expressed as percentage of the reference potassium chloride contraction) showed greater contraction than rings from the pregnant women when exposed to norepinephrine, a statistically significant difference. 17β-Estradiol decreased the norepinephrine-induced contraction in omental arteries from nonpregnant but not pregnant women in a statistically significant way. Tamoxifen did not influence the effect of norepinephrine for either group. 17β-Estradiol inhibited calcium ion-induced contraction similarly in rings of omental artery from both nonpregnant and pregnant patients. Tamoxifen potentiated estradiol-induced inhibition in arteries from pregnant patients. CONCLUSIONS: 17β-Estradiol inhibits norepinephrine-induced contractions in omental arteries from nonpregnant but not pregnant patients. The inhibition of the tension developed after exposure to potassium chloride, norepinephrine, and calcium ion is caused by a calcium channel blocking action.