Endothelial cells contribute to the regulation of arterial blood pressure by regulating vascular tone through activation or inactivation of various circulating vasoactive substances, and by producing numerous agents that can act locally and/or systemically to affect vascular tone. Nitric oxide (NO) is a potent vasodilator that is produced in endothelial cells via the oxidation of L-arginine by the enzyme NO synthase. Inhibitors of NO synthase elicit a reduction in blood flow to some tissues and a concomitant rise in arterial blood pressure, suggesting that NO produced by endothelial cells exerts a tonic inhibitory influence on arteriolar tone, thereby contributing to basal blood pressure. Nitric oxide also mediates the endothelium-dependent vasodilation that is elicited by a variety of agents, including acetylcholine and bradykinin. Patients with some forms of chronic arterial hypertension exhibit an impaired endothelium-dependent vascular relaxation, further supporting the possibility that an inability of endothelial cells to produce NO can lead to dysregulation of blood pressure.
Endothelin-1 (ET-1) is a potent vasoconstrictor peptide that is produced by vascular endothelial cells. Upon release by endothelial cells, ET-1 interacts with specific receptors, designated as ETA and ETB, on adjacent smooth muscle cells to mediate contraction. Elevated plasma levels of ET-1 are associated with hypertension, while treatment with antagonists directed against ETA lowers blood pressure, suggesting that ET-1 contributes to the regulation of blood pressure. Furthermore, the vasoconstrictor responses to ET-1 are exaggerated, and there is an increased expression of ET-1 in the arteries of hypertensive patients.
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