Effects of estradiol on release and disposition of norepinephrine from nerve endings

Abstract

Studies were performed to determine whether estradiol (E2) has a direct action on the release and disposition of norepinephrine (NE) from adrenergic nerve endings in isolated superfused canine saphenous veins. [3H]NE and is labeled metabolites were separated by column chromatography with measurement by liquid scintillation spectrometry. An increase in the spontaneous overflow of total 3H, [3H]NE, and [3H]dihydroxyphenylglycol ([3H]DOPEG) that occurred with 1 and 10 microgram/ml E2 in the superfusing medium suggested that E2 either induced NE release or interfered with intraneuronal NE storage. During electrical stimulation (ES), release of [3H]NE and [3H]DOPEG exceeded controls with 1 and 10 microgram/ml E2 in the superfusate, yet total 3H was little changed. The evoked release of [3H]DOPEG showed less of an elevation over its spontaneous efflux in E2-treated veins than in nontreated veins, suggesting that E2 may block neuronal reuptake of released NE. The efflux of O-methylated deaminated metabolites during and after ES was decreased by E2 treatment, suggesting also an inhibition of extraneuronal uptake of NE.

Associations of endogenous sex hormones with the vasculature in menopausal women

“…25 Additionally, estrogen may affect both vasodilation and vasoconstriction by increasing adrenergic activity. 26,27 The diameter enlargement observed in the current study may also signal a compensatory response to alterations in sheer stress levels resulting from adverse stimuli such as increased blood pressure or enhanced wall thickening. 28,29 CCA adventitial diameters were significantly larger among late perimenopausal and postmenopausal women and with lower estradiol levels, while CCA IMT values showed no association with menopause status or sex hormones after adjustment for chronological age.…”

Sex hormone modulation of serotonin-induced coronary vasodilation in isolated heart

“…With respect to the high level of CPP observed in the female group, it is known that estrogen may have indirect effects on the cardiovascular system, e.g., through an interaction with the adrenergic nervous system (28). Many studies have indicated a synergistic effect with sympathetic activity through inhibition of norepinephrine uptake (29), leading to an increase in vascular tonus. An increase in reactivity to norepinephrine has also been shown in oophorectomized (30) and prepuberal rats (23) treated with estrogen.…”

Sex-differences in catecholamine metabolites in human urine during development and at adulthood

“…An increase in estrogen levels would result in enhanced epinephrine excretion, because estradiol is able to increase adrenal tyrosine hydroxylase activity in adult rats (Kohier et al, 1975) and to enhance non stimulated epinephrine release from bovine adrenal medulla (Wiecbrnan and Borowitz, 1979). On the other hand, estradiol is known to inhibit neuronal and extraneuronal uptake of catecholamines (Hamlet et al, 1980) and to decrease catechol-O-methyltransferase activity in human liver (Bail et al, 1972;Cohn and Axelrod, 1971). Although unaltered or increased COMT activity has been found in some tissues after estradiol administration (Cohn and Axelrod, 1971;Scardapane and Cardinali, 1977;Wurtman et al, 1964) it seems likely that liver COMT plays the predominant rote to inactivate blood epinephrine in human.…”