Background-Epidemiological studies demonstrate an inverse relation between dietary flavonoid intake and cardiovascular risk. Recent studies with flavonoid-containing beverages suggest that the benefits of these nutrients may relate, in part, to improved endothelial function.

Abstract-Presentation, response to therapy, and clinical outcome in hypertension differ according to race, and these observations could relate to differences in microvascular function. We examined forearm microvascular function in age-matched black (nϭ56) and white subjects (nϭ62) using intra-arterial agonist infusion and venous occlusion plethysmography. In normotensive subjects (nϭ70; 34 black and 36 white normotensives), methacholine-, sodium nitroprusside-, and verapamil-induced vasodilation was equivalent in black and white subjects. In hypertensive subjects (nϭ48; 22 black and 26 white hypertensives), the vasodilator response to methacholine was markedly lower in black subjects compared with white subjects (PϽ0.001). The vasodilator responses to sodium nitroprusside and verapamil, however, were equivalent in black and white hypertensive subjects. Acute ascorbic acid infusion improved the methacholine response equally in black and white hypertensive patients, suggesting that a difference in a rapidly reversible form of oxidative stress does not explain these findings. Thus, the present study demonstrates important racial differences in vascular function and a marked impairment in endothelial vasomotor function in black patients with hypertension. Further studies will be required to elucidate the mechanisms and determine whether these insights will lead to more appropriately tailored management of hypertension and its complications.

Abstract-Recent studies suggest that hypertension associated with low renin status and hyperaldosteronism is associated with increased risk for end-organ damage and cardiovascular events compared with other forms of hypertension.Additionally, experimental studies have demonstrated impaired nitric oxide-mediated bioactivity in these states. To investigate the relation between renin/aldosterone status and resistance vessel function, we examined plasma renin activity, serum aldosterone level, and forearm blood flow responses to the endothelium-dependent vasodilator methacholine and the endothelium-independent vasodilators sodium nitroprusside and verapamil using venous occlusion plethysmography in 130 volunteers (43 hypertensive, 87 normotensive). Key Words: aldosterone Ⅲ blood flow Ⅲ endothelium Ⅲ mineralocorticoids Ⅲ renin A pproximately one-third of patients with hypertension have "low-renin hypertension," 1 and such patients are more likely to be salt-sensitive and may respond better to diuretic therapy. [2][3][4] The spectrum of low-renin hypertension includes patients with normokalemic primary hyperaldosteronism (mostly idiopathic hyperaldosteronism), which occurs in up to 15% of hypertensive subjects 5-8 and may represent an end-stage in the evolution of neurohormonal changes in "essential" hypertension. 7,8 Despite early evidence that patients with low renin levels might have a relatively favorable prognosis, 1,9 more recent epidemiological studies suggest that patients with low-renin and/or salt-sensitive hypertension have increased risk of endorgan damage, cardiovascular events, and mortality compared with other hypertensives. 3,10 -12 These observations might seem difficult to reconcile with our current understanding of the vascular consequences of neurohormonal activation. For example, experimental and clinical studies strongly suggest that activation of the reninangiotensin-aldosterone system leads to endothelial dysfunction, 13,14 which contributes importantly to the pathogenesis of cardiovascular events in hypertension. 15,16 In this regard, treatment with angiotensin II, aldosterone, or deoxycorticosterone and salt in rats reduces the bioavailability of endothelium-derived NO, increases superoxide production, and produces other pathological changes in the vasculature. [17][18][19] In humans, patients with elevated aldosterone levels 20,21 or renovascular hypertension 20 have impaired endotheliumdependent vasodilation in forearm microvessels, and intra-arterial aldosterone infusion impairs endothelium-dependent vasodilation. 22 Finally, treatment of hypertensive patients with angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and aldosterone receptor blockers generally improves endothelial function in hypertensive patients, providing further support for a link between endothelial dysfunction and increased activity of the renin-angiotensin system in hypertension. 21,23 On the basis of this experimental and clinical work, we hypothesized that increased activity of the renin-aldo...

No abstract

No abstract