The vascular endothelium is an essential organ that exerts important roles in the cardiovascular system. Not only does it control underlying smooth muscle tone, but it also modulates other functions such as activation of leucocytes and platelets, the coagulation cascade, vascular permeability, and proliferation of vascular smooth muscle cells. Vascular smooth muscle tone is continuously regulated by a delicate balance of vasodilating (that is, nitric oxide (NO), prostacyclin, and endothelium derived hyperpolarising factor) and contracting (that is, endothelin-1, thromboxane A2, prostaglandin H2, and superoxide anion) substances.

Dysfunction of the endothelium is generally expressed by either a decreased release of these vasodilators, or increased production of endothelium derived vasoconstrictors, or both.

Human essential hypertension has been associated with alterations in endothelial function. Indeed, most studies have shown blunted forearm and coronary blood flow responses to muscarinic agonists, along with a preserved response to sodium nitroprusside. Furthermore, inhibition of NO synthase has suggested that basal NO mediated vasodilatation is abnormal in patients with essential hypertension. In addition, measurement of a specific biochemical marker of the L-arginine-NO pathway—conversion of L-[¹⁵N]₂-arginine to [¹⁵N] nitrate—has shown that the basal production of NO is decreased in essential hypertension. Flow mediated vasodilatation is a useful index of endothelial function.1 It measures the change in the calibre of conductance arteries (that is, brachial, radial or femoral artery) during reactive hyperaemia, a manoeuvre that increases …