Estrogen induced inhibition of3H‐noradrenaline release in the uterus and portal vein of the rat

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Abstract
The influence of estrogen treatment on3H‐noradrenaline release, induced by potassium or calcium, was studied in isolated preparations of the uterus and the portal vein of the rat. Uterine strips of oophorectomized rats responded with contraction followed by transient relaxation when immersed in a medium containing 127 mM potassium. The transient relaxation was accompanied by an increased rate of3H‐nor‐adrenaline efflux. When the uterine strips were bathed in calcium‐free potassium solution, addition of calcium (3 mM) evoked an increased outflow of3H‐noradrenaline coinciding with a relaxation phase of the contractile response to calcium. After estrogen treatment of the rats the pattern of response was altered. The uterus then responded to potassium and calcium with sustained contractures and with a relatively small (potassium) or with no (calcium) increase of3H‐noradrenaline efflux. Normetanephrine (5 × 10‐‐5M) did not influence the uptake or release of3H‐noradrenaline in either non‐estrogenized or estrogen treated rats uterus. Calculations, based on the amounts of3H‐noradrenaline released by potassium and on the inhibitory effects of desipramine (10‐‐5M) on neuronal uptake of noradrenaline, suggested that similar amounts of tracer were accumulated in the adrenergic nerves of both non‐estrogenized and estrogen treated preparations. Tyramine (10‐‐4M) had a weaker stirnulatory effect on3H‐noradrenaline release than potassium, and the tyramine induced release was not inhibited by estrogen treatment. Strips of the rat portal vein responded to potassium with an increased rate of3H‐noradrenaline efflux. As in the uterus, estrogen treatment reduced the release of3H‐noradrenaline in response to potassium. The adrenolytic effect of estrogen is possibly due to reduced entry of calcium ions into the nerve terminal.