Basal nitric oxide production is impaired in offspring of patients with essential hypertension

There is considerable evidence that endothelium-dependent nitric oxide (NO) -mediated vasodilatation in response to acetylcholine is impaired in essent ial hypertension, whereas the endothelium-independent response to sodium ni troprusside is normal. More limited data have suggested that there is also reduced vasoconstriction in response to N-G-monomethyl-L-arginine (L-NMMA), a competitive inhibitor of basal NO release. As it is not known whether en dothelial dysfunction in hypertension, if indeed present, is a cause or con sequence of the condition, we have studied the normotensive offspring of pa rents with essential hypertension. Both basal and stimulated vascular respo nses were examined in 12 normotensive offspring [mean age (+/- S.E.M.) 26.1 +/- 1.4 years] of parents with essential hypertension and compared with th ose in 12 age-matched offspring (mean age 25.6 +/- 1.1 years) of normotensi ve subjects. Forearm blood flow was measured simultaneously in both arms by venous occlusion plethysmography, both at baseline and during intra-arteri al brachial infusion of increasing doses of acetylcholine, sodium nitroprus side, noradrenaline and L-NMMA. There were no significant differences betwe en the groups in the responses to acetylcholine, sodium nitroprusside or no radrenaline. In contrast, the vasoconstrictor response to L-NMMA was signif icantly blunted in the offspring of hypertensive parents compared with that in the offspring of normotensive parents (P = 0.005). Thus endothelial dys function, as demonstrated by impaired basal production of NO, is present in subjects at high risk of essential hypertension, and does not occur simply as a consequence of the condition.