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The biomechanical and functional adaptation of coronary resistance vessels in the coexistence of testosterone deficiency and hypertension has not been studied in detail. Therefore, we aimed to study the structural and functional adaptation of these resistance arteries under the influence of the two noxa (castration and hypertension). Sprague-Dawley rats were divided into 4 groups: control males, orchidectomized males, angiotensin II infused males, and orchidectomized plus angiotensin II infused males. Testosterone deficiency was achieved by surgical castration, and hypertension was achieved by angiotensin II administration via osmotic minipump (100 ng/min/kg). After 4 weeks of treatment, the biomechanical and functional properties of the coronary vessels were studied with a pressure angiometer. Blood pressure was measured using a cannula inserted into the right carotid artery on the day of the experiment. As a result of the combined effect of the two noxa, the inner diameter of the vessels decreased. The increased wall thickness to lumen ratio resulted in lower tangential wall tension in the orchidectomized plus angiotensin II infused group. Castration resulted in inward hypotrophic remodeling that was independent of the hypertensive stimulus. Spontaneous tone was significantly higher in the angiotensin II infused -, and in the angiotensin II infused + castrated groups than in the control and castrated groups. U46619-induced vasoconstriction was significantly reduced in the orchidectomized groups. Endothelium dependent dilatation was also decreased in testosterone-deficient groups. Vascular impairment caused by testosterone deficiency and by hypertensive stimulus add up during mechanical and functional adaptation. Together, the two noxa produced inward hypotrophic remodeling. As a result of castration, vascular reactivity decreased in the direction of both vasoconstriction and vasodilation. Based on our present study, it can be stated that coronary reactivity deteriorates upon andropause and the effects of these two noxa add up, and it might be one of the mechanisms of increasing cardiovascular risk in elderly men.
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