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Endothelium-dependent and cyclooxygenase-dependent cutaneous vasodilatation is blunted in young men with hypertensive
1Institute of Cardiovascular Science, College of Medical & Dental Sciences, University of Birmingham, Birmingham, UK.
Insights
Young adults with a family history of hypertension show impaired blood vessel function due to reduced cyclooxygenase (COX) products. This endothelial dysfunction may indicate an increased risk for developing high blood pressure.
Area of Science:
- Cardiovascular Physiology
- Endothelial Function
- Vascular Biology
Background:
- Offspring of hypertensive parents (OH) have a higher risk of developing hypertension compared to offspring of normotensive parents (ON).
- Previous research in normotensive OH individuals indicated sympathetic hyperactivity and reduced nitric oxide availability.
- The specific role of vasodilator cyclooxygenase (COX) products in this population remained unclear.
Purpose of the Study:
- To investigate the role of cyclooxygenase (COX) products in the cutaneous microcirculation of young, normotensive offspring of hypertensive (OH) versus normotensive (ON) parents.
- To determine if ethnic background influences these vascular responses.
- To assess potential early markers of endothelial dysfunction in OH individuals.
Main Methods:
- Studied 12 normotensive OH and 12 normotensive ON men (19-24 years old), including White Europeans and South Asians.
- Measured forearm skin reactive hyperemia and acetylcholine (ACh)-induced vasodilation using laser Doppler fluximetry.
- Assessed the impact of cyclooxygenase (COX) inhibition on these vascular responses.
Main Results:
- Peak reactive hyperemia and ACh-evoked vasodilation were significantly lower in OH men compared to ON men.
- COX inhibition attenuated reactive hyperemia and ACh-evoked vasodilation in ON men but not in OH men.
- While ACh-evoked dilation differed between European and Asian participants, the impaired COX contribution was observed in OH men across both ethnicities.
Conclusions:
- Young, normotensive OH men exhibit blunted cutaneous vascular responses (reactive hyperemia and ACh-evoked dilation) compared to ON men, irrespective of ethnicity.
- These impairments are linked to a reduced contribution of COX vasodilator products in OH individuals.
- These findings suggest early endothelial dysfunction in OH, potentially serving as a marker for future hypertensive risk.
Background:
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.
Methods:
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.
Results:
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.
Conclusion:
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.
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