title: Differential effects of antihypertensive drug therapy on arterial compliance.
abstract: Although vascular compliance, deltaV/deltaP, is abnormal in essential hypertension and can be improved by antihypertensive drug therapy, it is not clear whether drug-induced changes in compliance are attributable solely to lower achieved blood pressure (BP), and thus equally likely with different drugs possessing similar antihypertensive efficacy. Therefore, we used computerized arterial pulse waveform analysis (CAPWA) to measure capacitive (C1) and oscillatory (C2) components of arterial compliance in essential hypertensive subjects (n = 39) before, and 1 and 3 months after achieving normotensive BP values with administration of either dihydropyridine calcium channel antagonists (CaBl, n = 11), converting enzyme inhibitors (CEI, n = 9), angiotensin receptor blockers (ARB, n = 9), or beta-blockers (BBl, n = 10). Despite equivalent effects on BP (CABL: -19 +/- 4/-15 +/- 2 mm Hg; CEI: -12 +/- 3/-13 +/- 2 mm Hg; ARB: -10 +/- 3/-12 +/- 2 mm Hg; and BBl: -14 +/- 3/-12 +/- 2 mm Hg; P <.005 for each drug v pretreatment), CaBl, CEI, and ARB significantly increased arterial compliance (CaBl: %deltaC1 = 30.0 +/- 5.8, %Delta C2 = 43.7 +/- 23.3; CEI: %deltaC1 = 32.7 +/- 5.4, %deltaC2 = 26.7 +/- 7.1; ARB: %deltaC1 = 36.3 +/- 11.8, %deltaC2 = 43.6 +/- 23.1; P <.01 for CaBl, CEI, and ARB v pretreatment), but BBl did not (%deltaC1 = -3.9 +/- 7.6, %deltaC2 = -7.0 +/- 11.5, P = not significant v pretreatment, sig = 0.01 v other drugs). We conclude that for an equivalent effect on BP, arterial compliance improves after therapy with some, but not all antihypertensive drugs. We hypothesize that a greater clinical benefit may result from the preferential use of drugs that concomitantly improve arterial compliance.
authors.affiliation: Hypertension Center, New York Presbyterian Hospital-Cornell University Medical Center, New York, New York 10021, USA. lmresnick@aol.com
authors.forename: Lawrence M
authors.initials: LM
authors.lastname: Resnick
authors.forename: Melvin H
authors.initials: MH
authors.lastname: Lester
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000494:pharmacology / Q000627:therapeutic use; D017311:Amlodipine / Q000494:pharmacology / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D000959:Antihypertensive Agents / Q000494:pharmacology* / Q000627:therapeutic use; D001262:Atenolol / Q000494:pharmacology / Q000627:therapeutic use; D001794:Blood Pressure / Q000187:drug effects*; D002121:Calcium Channel Blockers / Q000494:pharmacology / Q000627:therapeutic use; D004656:Enalapril / Q000494:pharmacology / Q000627:therapeutic use; D005260:Female; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000503:physiopathology; D019808:Losartan / Q000494:pharmacology / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D016896:Treatment Outcome; D014655:Vascular Resistance / Q000187:drug effects*
chemical_list: D000319:Adrenergic beta-Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D000959:Antihypertensive Agents; D002121:Calcium Channel Blockers; D017311:Amlodipine; D001262:Atenolol; D004656:Enalapril; D019808:Losartan