Selective cyclo-oxygenase-2 inhibition with parecoxib acutely impairs endothelium-dependent vasodilatation in patients with essential hypertension

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Abstract
Cyclo-oxygenase (COX)-2 isoform appears to be a major source of the vasodilator, prostacyclin. Both prostacyclin and nitric oxide may contribute to the regulation of vascular tone and endothelial-mediated homeostasis. To evaluate the effects of acute COX-2 inhibition on endothelial function in the forearm circulation of patients with essential hypertension. Forty patients with essential hypertension as the only risk factor were studied. Forearm blood flow was measured by venous occlusion phlethysmography. Vascular responses were measured after intra-arterial infusion of the endothelium-dependent agonist acetylcholine (15, 30, or 40 μg/min) and the endothelium-independent agonist nitroprusside (1.6, 3.2, or 4.0 μg/min). Patients were allocated randomly to groups to receive the non-selective COX-inhibitor, acetylsalicylate-lysin (500 mg intravenously), or the selective COX-2 inhibitor, parecoxib, an injectable prodrug of valdecoxib (20 mg intravenously). The infusion procedure was repeated 30 min later. Acetylcholine increased concentration-dependent forearm blood flow. This increase was significantly augmented by acetylsalicylate-lysin, but significantly diminished by parecoxib. Neither acetylsalicylate-lysin nor parecoxib modified the vasodilator responses to nitroprusside. COX-2 inhibition with the prodrug, parecoxib, diminishes the acetylcholine-induced vasodilatation in the forearm circulation of patients with essential hypertension. It is speculated that the production of vasodilator prostaglandins may be important in pathological states with endothelial dysfunction, at least in patients with essential hypertension.

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