Media Hypertrophy in Hypertensive Coronary Resistance Vessels

Coronary reserve is reduced in human hypertensive hypertrophy and in the model of spontaneously hypertensive rats (SHRs). In isolated coronary resistance vessels, the role of structural and functional changes was evaluated. Furthermore, the effect of long-term antihypertensive therapy was also studied. At the age of 20 weeks, SHR and Wistar-Kyoto (WKY) rats were examined. Distal segments of the left anterior descending coronary artery were dissected and mounted on a myograph developed by Mulvany and Halpern. After recording of radius-wall tension curves, the vessels were set up to a wall tension equal to two-thirds of the systolic blood pressure. In SHRs, the vessel diameters were reduced. After equilibration with Ringerʼs solution, vessel dilatation was decreased in calcium-free solution (10 ± 3 vs. 34 ± 7%, p < 0.05), but contraction increased after 123 mM of potassium stimulation (78 ± 19 vs. 33 ± 9%). There was no difference in calcium sensitivity during methoxamine or potassium activation. In the coronary resistance vessels of SHRs, electron microscopy revealed media hypertrophy (15.6 ± 2.9 vs. 9.5 ± 2.1 μm, p < 0.05) and media hyperplasia (4.5 ± 3 vs. 3.7 ± 6 muscle layers, p < 0.05). Media hypertrophy and a decrease in the vasodilatating capacity of resistance vessels contribute to the reduction of coronary reserve in hypertensive hypertrophy. The minimal coronary vascular resistance, a parameter of the vasodilatating capacity, was significantly increased in SHRs. Antihypertensive therapy with metoprolol and hydralazine or nifedipine resulted in an improvement of coronary reserve.