Do subcutaneous resistance arteries from patients with primary hypertension show altered contractility or endothelium-derived relaxing factor responses compared to normotensive controls?
Subcutaneous resistance arteries from patients with essential hypertension demonstrate enhanced contractility to vasoconstrictors and nerve stimulation without detectable medial hypertrophy or defects in endothelium-derived relaxing factor.
SUMMARY 1. We measured the reactivity of 2 mm long ring segments of human resistance arteries dissected from gluteal skin biopsies and mounted on wires in a Mulvany‐Halpern myograph for recording isometric force. Arteries were taken from eight normotensive (N) volunteers (average age 46 years, blood pressure 126/82 mmHg) and eight untreated hypertensives (H; average age 48 years, blood pressure 149/101 mmHg). 2. In small diameter arteries (internal diameter 500 μm), no response to acetylcholine was noted in either H or N arteries. The sensitivity to serotonin and angiotensin II was similar between these arteries but the EC50 to noradrenaline was less in H than in N arteries (ΔEC 50 = 0.61 ‐log mol/L). 6. Subcutaneous resistance arteries with an internal diameter less than 500 μm from hypertensive patients show enhanced contractility to noradrenaline, serotonin and nerve stimulation despite a lack of detectable medial hypertrophy. These changes may be confined to the medium small arteries acting as pharmacological amplifiers in the circulation. We could not demonstrate a significant defect in neuronal uptake nor in endothelium‐derived relaxing factor in arteries from patients with essential hypertension.
Angus et al. (Sun,) studied this question.
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