Phenylephrine induced aortic vasoconstriction is attenuated in hyperthyroid rats

Background. Abnormal vascular responsiveness to vasoconstrictors may play a n important role in peripheral vascular resistance in hyperthyroidism. The aim of the present study was to evaluate whether the vascular response to p otassium chloride and phenylephrine is abnormal in a rat model of thyroxine -induced cardiac hypertrophy. Methods. Left ventricular hypertrophy was induced in Wistar rats by subcuta neous administration of L-thyroxine for two weeks ("THYR"), n=17. Animals t reated with normal saline served as controls, ("NORM"), n=20. The thoracic aorta was dissected and cut into rings that were suspended in an isolated o rgan bath with Krebs-Henseleit buffer. Maximal tension, Tmax, in g was meas ured in response to KCI and PE at the highest concentration in rings with e ndothelium (+E) and without endothelium (-E) in both groups. Relaxation res ponse (Relax %) to acetylcholine administration was expressed as % of the m aximal tension induced by phenylephrine. Results. Left ventricular weight was 0.9 (SEM, 0.04) g for THYR group vs 0. 7 (0.02) g for the NORM group, p <0.05. With KCl, Tmax was not different be tween the THYR and NORM groups with and without endothelium. With PE, there was a difference in Tmax between THYR+E and NORM+E, 1.2 (0.05) g vs 1.5 (0 .09) g, p <0.05. Tmax was also different between THYR-E and NORM-E, 1.5 (0. 08) g vs 1.7 (0.07) g, p <0.05. Relax % was not significantly different bet ween THYR+E and NORM+E (45.9% vs 42.8%, p >0.05). Conclusions. We conclude that: a) Vascular tension of the thoracic aorta in response to PE is lower in thyroxine-treated rats as compared to controls, probably due to enhanced PE-induced vasorelaxation at high concentration. b) Relaxation response of the thoracic aorta to acetylcholine is not differ ent between THYR and NORM groups.