Enhanced Contraction to Noradrenaline, Serotonin and Nerve Stimulation but Normal Endothelium‐derived Relaxing Factor Response in Skin Small Arteries in Human Primary Hypertension

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), 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 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.