American Journal of Hypertension · 1994 · 12 citations · 0 references
Life SciencesPharmacologyPhysiologyPharmacodynamicsSignal TransductionSteroid BiochemistryHormone SignalingNuclear ReceptorsReceptor PhysiologyReceptor RegulationSteroid Hormone SignalingSteroid PharmacologyEstradiol PhysiologyEstrogen ReceptorsSteroid Hormone ActionSteroid Hormone PharmacologyVascular Smooth Muscle PharmacologyVascular Smooth Muscle RegulationVascular Smooth Muscle RelaxationVascular Tone Modulation
In vivo studies suggest that 17 beta-estradiol (beta E) may regulate vascular tone. Results of recent studies suggest that beta E exerts rapid effects on intracellular calcium, possibly via cell surface receptors, distinct from conventional nuclear receptors for steroids. The present study was designed to determine whether beta E acutely modifies vascular smooth muscle contractile responses to phenylephrine (PE) and angiotensin II (AII). In experiments on tonic responses of aortic rings to 5 x 10(-8) mol/L PE, cumulative additions of beta E reduced tension at concentrations > 10(-6) mol/L. Contractile dose responses to PE were determined in rat aortic rings in absence of sex hormones and then after exposure to beta E (5 x 10(-6) mol/L, n = 6) or vehicle (ETOH, n = 6) for 30 min. beta E increased ED50 and reduced maximal responses. Application of 5 x 10(-6) mol/L beta E for 30 min also reduced the contractile response to 1 mmol/L AII from 69 +/- 4% (vehicle) to 47 +/- 6% (estradiol) of maximal KCl contraction (P < .025, n = 7). These data suggest that beta E acutely attenuates vasoconstrictor responses to PE as well as to AII, possibly by an effect exerted at the cell membrane level.