title: Antihypertensive drugs and reversing of endothelial dysfunction in hypertension.
abstract: Essential hypertension is associated with impaired endothelium-dependent vasodilation and is caused mainly by production of oxygen free radicals that can destroy nitric oxide (NO), impairing its beneficial and protective effects on the vessel wall. Antihypertensive drugs can improve or restore endothelium-dependent vasodilation depending on their ability to counteract the mechanisms that impair endothelial function. Although treatment with atenolol gives negative results in peripheral subcutaneous and muscle microcirculation, acute nebivolol exerts a modest vasodilating effect in the forearm circulation. Whether this compound can activate NO production in essential hypertensive patients is controversial. Calcium entry blockers, particularly the dihydropyridine-like drugs, can reverse impaired endothelium-dependent vasodilation in different vascular districts, including the subcutaneous, epicardial, and peripheral arteries and forearm circulation. In the forearm circulation, nifedipine and lacidipine can improve endothelial dysfunction by restoring NO availability. Angiotensin-converting enzyme (ACE) inhibitors, however, seem to improve endothelial function in subcutaneous, epicardial, and renal circulation, but are ineffective in potentiating the blunted response to acetylcholine in the forearm of patients with essential hypertension. Finally, recent evidence suggests angiotensin II receptor antagonists can restore endothelium-dependent vasodilation to acetylcholine in subcutaneous, but not in the forearm muscle, microcirculation. However, treatment with an angiotensin II receptor antagonist can improve basal NO release and decrease the vasoconstrictor effect of endogenous endothelin-1.
authors.affiliation: Department of Internal Medicine, University of Pisa, Italy, Via Roma, 67, 56100 Pisa, Italy.
authors.forename: S
authors.initials: S
authors.lastname: Taddei
authors.forename: A
authors.initials: A
authors.lastname: Virdis
authors.forename: L
authors.initials: L
authors.lastname: Ghiadoni
authors.forename: I
authors.initials: I
authors.lastname: Sudano
authors.forename: A
authors.initials: A
authors.lastname: Salvetti
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000959:Antihypertensive Agents / Q000494:pharmacology* / Q000627:therapeutic use*; D002121:Calcium Channel Blockers / Q000627:therapeutic use; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000503:physiopathology; D005609:Free Radicals / Q000009:adverse effects; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000503:physiopathology; D009569:Nitric Oxide / Q000378:metabolism
chemical_list: D000319:Adrenergic beta-Antagonists; D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D000959:Antihypertensive Agents; D002121:Calcium Channel Blockers; D005609:Free Radicals; D009569:Nitric Oxide