Endogenous levels of ovarian hormones modulate the activity of β-adrenoceptors in isolated rat aorta and tail arteries

Puerto de la Cruz, Tenerife (2003) J Physiol 548P, P71

Poster Communications: Endogenous levels of ovarian hormones modulate the activity of β-adrenoceptors in isolated rat aorta and tail arteries

M.V. Conde, S.M. Arribas and M.C. González

Departamento de Fisiología, Facultad de Medicina, Universidad Autónoma, c/Arzobispo Morcillo 1, 28029 Madrid, Spain

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The aim of this study was to assess whether the physiological status of ovarian hormones modifies the function of vascular β-adrenoceptors, as has been previously reported in ageing and hypertension.

We have analysed vascular function of aorta and tail arteries from 15-week-old female Wistar rats, in oestrus phase and age-matched ovariectomized prepubertal (OVXp), with isometric tension recording. Rats were killed by CO2 inhalation. To study muscular and endothelial β-adrenoceptors, concentration- response curves to isoprenaline were performed in aortic segments with endothelium. Presynaptic β-adrenoceptors were studied in tail arteries without endothelium by means of electrical field stimulation (EFS, 200 mA, 0.2 ms, 0.5-8 Hz, for 15 s, at 2 min interval) in the presence of α2-adrenoceptor blockers. In tail artery segments, endothelium removal was achieved by gentle rubbing of the intimal surface with a stainless steel wire. The presence of functional endothelium was assessed by a relaxation with acetylcholine (0.01-10 µM) in precontracted arteries greater than 70 %. The absence of relaxation confirmed that endothelium had been removed.

In aortic segments precontracted with noradrenaline (NA, 0.1 µM), isoprenaline (0.01-100 µM) elicited relaxations that were significantly decreased in OVXp rats. Isoprenaline-induced relaxations were significantly diminished by propranolol (1 µM, a β-adrenoceptor antagonist) and L-NAME (100 µM, an inhibitor of nitric oxide synthase). L-NAME blockade was significantly larger in estrus than OVXp rats. Cholera toxin (0.003-1 µg ml-1, an activator of the stimulatory G-protein, Gs) caused relaxations in aorta that were significantly decreased by deprivation of ovarian hormones.

In tail arteries, isoproterenol (0.01-100 µM) did not induce relaxation in precontracted segments either from oestrus nor from OVXp rats. NA (0.001-10 µM) induced contractions that were not modified by deprivation of ovarian hormones. In this artery, EFS induced contractile responses in the presence of yohimbine (1 µM, an α2-adrenoceptor antagonist). Isoprenaline (1 µM) enhanced these EFS-induced contractions, the increase being significantly larger in arteries from OVXp rats.

These results suggest that the physiological status of ovarian hormones: (1) improves the muscular and endothelial β-adrenoceptor mediated relaxation, through increases in both nitric oxide and the activity of arterial Gs, and (2) decreases the presynaptic release of noradrenaline by means of a β-adrenoceptor-mediated mechanism.

All of the surgical and experimental procedures used in these studies followed the directions of the European Community Guidelines (Real Decreto 223/88, March 14, Spain). Supported by Grants from DGCYT (PM 97/0011) and Ministerio de Ciencia y Tecnología (BFI 2001-0638)



Where applicable, experiments conform with Society ethical requirements.

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