Racial Differences in Maximal Vasodilatory Capacity of Forearm Resistance Vessels in Normotensive Young Adults

Abstract

This study was performed to determine whether alterations in vascular structure exist in a biracial population of young (age 22.3 +/- 0.6 yrs [mean + SE]) normotensive men. We examined maximal vasodilatory capacity in 21 blacks and 20 whites (average blood pressure = 122/75 and 118/72 mm Hg, respectively). Forearm blood flow was determined at rest and after 10 min of ischemic handgrip exercise using venous occlusion plethysmography. Forearm vascular resistance was computed from blood flow and mean arterial blood pressure determined by auscultation. Minimum forearm vascular resistance was 23% higher in blacks (2.60 +/- 0.60) than in whites (2.11 +/- 0.41) (P = .005), and was unrelated to parental history of hypertension. The regression equation for minimum forearm vascular resistance (Y) and casual blood pressure (X) for blacks was Y = -1.782 + 0.0487X (r = 0.522); for whites it was Y = -1.165 + 0.0367X (r = 0.418). When the data were covaried on resting mean arterial blood pressure, blacks still had a higher minimum forearm vascular resistance (P = .014). The results suggest a racial difference in the vascular structure of the forearm resistance vessels.

Effects of Black Race on Forearm Resistance Vessel Function

“…For example, exerciseinduced, 5 ischemia-induced, 20 and mental stress-induced 7 forearm vasodilation were reported to be lower in healthy black subjects compared with healthy white subjects. Lang and colleagues observed lower forearm blood flow responses to intra-arterial isoproterenol infusion in healthy black men compared with white men.…”

“…Several previous studies have demonstrated impaired vascular function in forearm resistance vessels of healthy young black subjects compared with whites. [5][6][7][8] These differences are likely to be clinically important because endothelium-derived nitric oxide plays a major role in vascular homeostasis via its effects as a vasodilator and as an inhibitor of platelet activity, monocyte adhesion, and smooth muscle proliferation. 9 Furthermore, recent studies have demonstrated that impaired endothelial function in the microvasculature is predictive of future cardiovascular disease events.…”

Anestesia na população negra

“…O fenótipo vascular favorecendo a HAS mais grave no negro pode ser melhor compreendido através da avaliação farmacológica de substâncias vasoativas na microcirculação. O efeito vasodilatador atenuado do isoproterenol (agonista β 2 ), sobretudo no negro hipertenso, inclusive com facilitação da vasoconstrição noradrenérgica, fala a favor de polimorfismo racial no receptor adrenérgico β que pode contribuir na fisiopatologia da insuficiência cardíaca [39][40][41][42][43] .Além de mecanismos não adrenérgicos (renina reduzida, hipernatremia, vasopressina etc. ), o aumento da reatividade simpática no negro americano contribui para o desenvolvimento da HAS.…”

“…O hipertenso com insuficiência cardíaca de diferentes raças responde favoravelmente à administração do bloqueador α e β como o carvedilol, podendo ser associado ou não a antagonistas de canais lentos de cálcio ou a uma terapêutica diuréti-ca 3, 54,55 . O alelo polimorfo T do gen C825T do unidade β 3 da proteína G facilita a excreção renal de Na + /H + em resposta à manoterapia com diurético benzotiazídico em negros hipertensos com baixo nível de renina 38,39 . O manejo farmacológi-co adequado da HAS deve levar em conta as diferenças raciais em sua fisiopatologia.…”

“…Os benzotiazídicos natriuréticos e antagonistas de canais de cálcio são exemplo de uma boa associação no tratamento de HAS na população negra. Enquanto os diuréticos e os antagonistas de cálcio constituem a primeira linha terapêutica, os bloqueadores β e os IECA são menos efetivos em reduzir os níveis tencionais nos paciente negros com baixo nível de renina 38,39 .…”