Effect of testosterone treatment on vasoconstrictor response of left anterior descending coronary artery in male and female pigs.

Androgens may be risk factors in the pathogenesis of coronary artery disease by promoting coronary vasoconstriction. We studied the effect of testosterone treatment on coronary vascular reactivity of male and female domestic pigs treated for 2 weeks with either placebo or testosterone 10 mg/kg subcutaneous (s.c.) pellets. Vascular reactivity was studied in ring segments (4-5 mm) isolated from the left anterior descending coronary artery (LAD). No significant sex difference was noted in the response of LAD segments from placebo-treated male and female animals to KCl and prostaglandin F2 alpha (PGF2 alpha). Androgen treatment increased the maximum response (Tmax) of intact vessels to KCl from 3,647 +/- 689 mg in controls to 8,939 +/- 1,284 mg in testosterone-treated males (p < 0.01) and from 3,405 +/- 669 to 10,524 +/- 1,663 mg in testosterone-treated female pigs (p < 0.01). Testosterone similarly increased the response to PGF2 alpha 10(-6) M from a mean of 2,149 +/- 1,036 to 3,163 +/- 867 mg in males (p < 0.05) and from 2,076 +/- 810 to 3,565 +/- 578 mg in female segments (p < 0.05). Endothelial denudation significantly decreased the potentiating effect of testosterone treatment in males to both KCl and PGF2 alpha (p < 0.05), but not in segments from females. Our data show that testosterone treatment potentiates contractility of porcine LAD segments to both receptor- and nonreceptor-mediated agonists. In male pigs, this effect may be mediated by an effect on endothelium.