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901–39 Testosterone-induced Coronary Conductance and Resistance Vessel Relaxation In Vivo: Potential Mechanisms of Action

1995; Elsevier BV; Volume: 25; Issue: 2 Linguagem: Inglês

10.1016/0735-1097(95)91516-z

1558-3597

Tony M. Chou, Krishnankutty Sudhir, Thomas M. Amidon, Peter Collins, Paul G. Yock, Kanu Chatterjee,

Cardiovascular Disease and Adiposity

Although testostone causes relaxation of the coronary vascular bed, its mechanisms of action has not been defined. We examined the effect of in-tracoronary testosterone (10-6to 10-5M) on epicardial and resistance coronary arteries in vivoin 10 dogs (5 male, 5 female). Changes in coronary average peak velocity (APV) were assessed using a 0.014" Doppler guidewire (Cardiometrics), and epicardial cross-sectional area (CSA) was measured using a 4.3F, 30 MHz ultrasound imaging catheter (CVIS). After establishing a baseline response, the contribution of nitric oxide (NO), prostaglandins and ATP-sensitive K+channels was assessed. Testosterone induced a significant increase in both CSA and APV at the 10-6and 10-5M concentrations (CSA: 12.6 ± 5.0 and 13.7 ± 8.8%, APV: 53.5 ± 21.9% and 37.8 ± 12.2% at 10-6and 10-5M respectively (p < 0.01 in all cases)). Pre-treatment with ωNitro-L-arginine methylester (L-NAME, 100 μM intracoronary) to block NO synthesis decreased testosterone-induced increase in CSA (13.4 vs. 8.0%, p = 0.06) and APV (89.4% vs. 39.8%, p = 0.06). Pre-treatment with gliben-clamide (10-5M) to assess role of ATP-sensitive K+channels did not attenuate testosterone-induced dilation in epicardial arteries though it did in the microcirculation (74.8vs. 32.8%, p = 0.03). Pre-treatment with indomethacin (5 mg/kg IV) did not alter changes. We conclude that acute testosterone-induced conductance coronary vasorelaxation is mediated in part by endothelium-derived NO. In contrast, ATP-sensitive K+channels appear to modulate testosterone effects on resistance arteries. The prostanoid system is not involved in either conductance or resistance coronary vascular relaxation.