Endothelium-dependent and cyclooxygenase-dependent cutaneous vasodilatation is blunted in young men with hypertensive parents

Abstract

Across ethnicities, offspring of hypertensive parents (OH) have higher risk of hypertension than offspring of normotensive parents (ON). Sympathetic hyperactivity and reduced nitric oxide availability have been reported in normotensive OH; but the role of vasodilator cyclooxygenase (COX) products is unclear. In 12 OH and 12 ON men (19-24 years old), each group comprising six white Europeans and six South Asians with resting ABP less than 129/89 mmHg, reactive hyperaemia and responses evoked by iontophoresis pulses of acetylcholine (ACh) were recorded in forearm skin by laser Doppler fluximetry before and after COX inhibition. Peak reactive hyperaemia was larger in ON than OH (71.0 ± 7.8 vs. 43.4 ± 8.3 perfusion units (perf.units); P < 0.05). It was attenuated by COX inhibition in ON (24.8 ± 5.2 perf.units, P < 0.01), not OH (54.2 ± 7.5 perf.units). Similarly, increases in perfusion evoked by ACh were greater in ON than OH (169.1 ± 20.4 vs. 142.1 ± 19.9 perf.units; P < 0.05) and attenuated by COX inhibition in ON (94.5 ± 13.7; P < 0.05), not OH (132.6 ± 16.1 perf.units). Considering ethnicities, ACh-evoked dilation, though not reactive hyperaemia was greater in Europeans than Asians (176.8 ± 21.7 vs. 130.4 ± 15.0; P < 0.01; 61.0 ± 8.7 vs. 51.7 ± 9.2 perf.units). However, within both Europeans and Asians, COX inhibition attenuated reactive hyperaemia and ACh-induced dilatation in ON only. Reactive hyperaemia and ACh-evoked dilatation in cutaneous circulation are blunted in young, normotensive OH relative to ON men irrespective of white European, or South Asian ethnicity and are attributable to impaired contribution of COX vasodilator products in OH. These features may provide early markers of endothelial dysfunction that contribute to hypertensive risk in OH men.