Endocrine Abstracts

Testosterone therapy has been shown to benefit men with heart failure or coronary artery disease, an activity proposed to be mediated via its vasodilatory efficacy. Testosterone has been demonstrated to dilate human coronary arteries, but it is unknown whether testosterone has a similar action in human pulmonary or systemic vessels.
Male patients were recruited from cardiothoracic (n = 14, age = 68 plus/minus 9) or gastrointestinal (n = 8, age = 70 plus/minus 3) operating lists and gave full written consent. 2mm lengths of pulmonary conduit artery (PCA n = 11, diameter = 986 plus/minus 168), pulmonary conduit vein (PCV n = 10, diameter = 841 plus/minus 78), pulmonary resistance artery (PRA n = 13, diameter = 358 plus/minus 22), pulmonary resistance vein (PRV n=16, diameter = 387 plus/minus 20) and mesenteric resistance artery (MRA n=16, diameter = 393 plus/minus 31) were dissected and loaded in a wire myograph at a tension equivalent to the in vivo pressure, and maintained in physiological saline at 37 degrees Celsius and pH 7.4. Smooth muscle and endothelial viability was confirmed by contraction to noradrenaline (10 micromolar) or U46619 (1 micromolar) and subsequent dilatation to acetylcholine (1 micromolar). Vessels were then exposed to KCl (0.1 to 100 millimolar) followed by cumulative additions of ethanol vehicle. Vessels were then washed, the addition of KCl repeated, and exposed to testosterone (1 nanomolar to 100 micromolar).
Testosterone dilated all vessels at concentrations greater than 1 micromolar. Ethanol had no effect. Maximal relaxation at 100 micromolar was as follows; PCA 42.5 plus/minus 3.2 %, PCV 40.7 plus/minus 4.7 %, PRA 48.2 plus/minus 3.2 %, PRV 52.0 plus/minus 6.9 %, MRA 95.0 plus/minus 8.1 % (p<0.001 compared to PRA via Students unpaired t test).
This vasodilatory action may underlie the beneficial effect of testosterone replacement therapy in men with heart failure.