ENHANCED CONTRACTION TO NORADRENALINE, SEROTONIN AND NERVE-STIMULATION BUT NORMAL ENDOTHELIUM-DERIVED RELAXING FACTOR RESPONSE IN SKIN SMALL ARTERIES IN HUMAN PRIMARY HYPERTENSION

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-mu=m), the cumulative concentration-response curves to noradrenaline, serotonin and angiotensin II had a greater maximum by 72, 300 and 69%, respectively, in vessels from hypertensive patients than in those from normal volunteers. Nerve stimulation also caused a greater maximum contraction in hypertensive vessels (by 352%). 3. Arteries from H and N patients contracted submaximally by the thromboxane mimetic U46619 were similarly sensitive to the endothelium-dependent relaxing factor (EDRF) acetylcholine, indicating no difference in EDRF release or sensitivity. 4. Morphological measurements of the ratio of wall thickness to lumen radius of the wire-mounted vessels showed no significant difference between H and N vessels. 5. In larger arteries (internal diameter > 500-mu-m), no response to acetylcholine was noted in either H or N arteries. The sensitivity to serotonin and angiotensin 11 was similar between these arteries but the EC50 to noradrenaline was less in H than in N arteries (DELTA-EC50 = 0.61 - log mol/ L). 6. Subcutaneous resistance arteries with an internal diameter less than 500-mu-m 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.