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CARDIOVASCULAR

Dexamethasone Decreases Contraction to Electrical Field Stimulation in Mesenteric Arteries from Spontaneously Hypertensive Rats through Decreases in Thromboxane A₂ Release

Departamento de Fisiología (R.A.-L., J.B.-R., M.F., G.B.) and Departamento de Farmacología y Terapéutica (M.S.), Facultad de Medicina, Universidad Autónoma de Madrid, Spain; and Departamento de Fisiologia e Farmacologia, Centro de Ciências Biológicas, Universidade Federal de Pernambuco, Recife, Brazil (F.E.X.)

Glucocorticoids play a role in the control of vascular smooth muscle tone through the alteration of vasoconstrictor and vasodilator factor production. We studied the effect of dexamethasone on vasoconstriction induced by electrical field stimulation (EFS) in rat mesenteric arteries (MAs) and the role of hypertension in this effect. Endothelium-denuded MAs were obtained from Wistar-Kyoto rats and spontaneously hypertensive rats (SHRs). EFS response was analyzed by isometric tension recordings and cyclooxygenase (COX-1 and COX-2) expression by Western blot. Noradrenaline (NA) release was evaluated in segments incubated with [³H]NA. Dexamethasone (0.1 and 1 µM; 2–8 h) reduced vasoconstriction to EFS (200 mA, 0.3 ms, 1–16 Hz), in a dose- and time-dependent manner only in SHRs. However, the EFS-induced release of [³H]NA was increased in SHR arteries preincubated with dexamethasone (1 µM; 6 h). The thromboxane A₂ (TxA₂) synthase inhibitor furegrelate (10 µM), the selective COX-2 inhibitor NS-398 (N-[2-cyclohexyloxy-4-nitrophenyl] methanesulfonamide; 10 µM), or the TxA₂ receptor antagonist SQ 29548 (1 µM), reduced EFS and NA induced vasoconstrictor responses. However, the effect of these drugs was abolished in arteries preincubated with dexamethasone. Both dexamethasone and phentolamine (1 µM) inhibited the increased thromboxane B₂ levels observed after EFS. COX-2 protein expression was reduced by dexamethasone in SHR arteries. Results suggest that dexamethasone reduces vasoconstriction to EFS in MAs from SHRs by decreasing COX-2 expression, thereby decreasing the smooth muscle TXA₂ release induced by -adrenoceptor activation. The undetectable COX-2 expression in MAs from normotensive animals explains the noneffect of dexamethasone in their arteries.

Address correspondence to: Dr. Gloria Balfagón, Departamento de Fisiología, Facultad de Medicina, Universidad Autónoma de Madrid, C/Arzobispo Morcillo, 4, 28029 Madrid, Spain. E-mail: gloria.balfagon{at}uam.es

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