M Preik1, M Kelm, S Schäfer, B E Strauer. 1. Medizinische Klinik B, Abteilung für Kardiologie, Heinrich-Heine-Universität Düsseldorf.
Abstract
BACKGROUND: Adenosine is a potent mediator of arteriolar tone in particular during ischemia, hypoxia, and exercise. Functional disturbance of this dilatory pathway may be highly significant for the pathophysiology and pathogenesis of arterial hypertension. PATIENTS AND METHODS: Forearm blood flow (FBF) was quantified by venous occlusion plethysmography following intra-arterial infusion of adenosine at increasing doses in 13 patients with arterial hypertension (HT) and 12 age-matched normotensive controls (NT). Hyperemic peak flow was measured following 3 minutes of non-flow ischemia. RESULTS: FBF at rest was comparable in both groups and was dose-dependently increased by adenosine in both groups. In patients with HT adenosine-induced vasodilation was significantly impaired over the entire dose-response curve compared with NT (6.0 mumol/min: 14.5 +/- 1.0 versus 8.6 +/- 0.9 ml.min-1.100 ml-1 of tissue, p < 0.01). Maximum forearm blood flow during reactive hyperemia was also profoundly impaired in the hypertensive patients (-38%, p < 0.01). In the overall group of normotensive and hypertensive subjects, flow responses to adenosine were i) significantly correlated with peak flow (adenosine 2.0 mumol/min: r = 0.79, p < 0.001), and total flow during reactive hyperemia and ii) inversely related to the magnitude of arterial blood pressure. CONCLUSIONS: The study reported presents first evidence that adenosine-dependent dilation of forearm resistance arteries is impaired in patients with arterial hypertension. This vascular dysfunction is associated with the impairment of ischemia-induced reactive hyperemia which in turn may contribute to progressive end-organ damage in arterial hypertension.
BACKGROUND:Adenosine is a potent mediator of arteriolar tone in particular during ischemia, hypoxia, and exercise. Functional disturbance of this dilatory pathway may be highly significant for the pathophysiology and pathogenesis of arterial hypertension. PATIENTS AND METHODS: Forearm blood flow (FBF) was quantified by venous occlusion plethysmography following intra-arterial infusion of adenosine at increasing doses in 13 patients with arterial hypertension (HT) and 12 age-matched normotensive controls (NT). Hyperemic peak flow was measured following 3 minutes of non-flow ischemia. RESULTS: FBF at rest was comparable in both groups and was dose-dependently increased by adenosine in both groups. In patients with HTadenosine-induced vasodilation was significantly impaired over the entire dose-response curve compared with NT (6.0 mumol/min: 14.5 +/- 1.0 versus 8.6 +/- 0.9 ml.min-1.100 ml-1 of tissue, p < 0.01). Maximum forearm blood flow during reactive hyperemia was also profoundly impaired in the hypertensivepatients (-38%, p < 0.01). In the overall group of normotensive and hypertensive subjects, flow responses to adenosine were i) significantly correlated with peak flow (adenosine 2.0 mumol/min: r = 0.79, p < 0.001), and total flow during reactive hyperemia and ii) inversely related to the magnitude of arterial blood pressure. CONCLUSIONS: The study reported presents first evidence that adenosine-dependent dilation of forearm resistance arteries is impaired in patients with arterial hypertension. This vascular dysfunction is associated with the impairment of ischemia-induced reactive hyperemia which in turn may contribute to progressive end-organ damage in arterial hypertension.