Differential structural responses of small resistance vessels to antihypertensive therapy

• Published in: Circulation (New York, N.Y.) Vol. 75; no. 3; pp. 618 - 626
• Main Authors: SANO, T, TARAZI, R. C
• Format: Journal Article
• Language: English
• Published: Hagerstown, MD Lippincott Williams & Wilkins 01.03.1987
• Subjects: Animals; Antihypertensive agents; Antihypertensive Agents - therapeutic use; Biological and medical sciences; Blood Vessels - drug effects; Captopril - therapeutic use; Cardiovascular system; Hindlimb - blood supply; Hydralazine - therapeutic use; Hydrochlorothiazide - therapeutic use; Hypertension - drug therapy; Male; Medical sciences; Pharmacology. Drug treatments; Rats; Rats, Inbred SHR; Vascular Resistance - drug effects; Hypertension; Rat; Rodentia; Cardiovascular disease; Hereditary; Left ventricle; Resistance; Vertebrata; Chemotherapy; Mammalia; Animal; Blood vessel; Antihypertensive agent; Mechanism of action; Hypertrophy
• ISSN: 0009-7322; 1524-4539
• DOI: 10.1161/01.CIR.75.3.618

Regression of left ventricular hypertrophy after control of blood pressure has been documented with some antihypertensive agents but not with others. To determine whether similar differences in regression of wall thickening also occur in resistance vessels during treatment, matched groups of spontaneously hypertensive rats (SHR) were treated for 12 weeks with either hydralazine (H) or captopril and hydrochlorothiazide (C-D) and they were compared with untreated SHR and Wistar-Kyoto rats (WKY). Perfusion pressure was then determined in the hindlimbs of pithed rats under conditions of constant blood flow (4.0 ml/min) and maximal vasodilation (hemodilution to 22% hematocrit combined with continuous nitroprusside and papaverine infusion). This perfusion pressure, which has been validated as an index of thickening (hypertrophy) of resistance vessels walls, averaged 26.8 +/- 0.4(SE) mm Hg in untreated WKY (n = 12) and 37.6 +/- 0.4 mm Hg in untreated SHR (n = 11) (p less than .01). Treatment with H or C-D controlled blood pressure equally in SHR, but the two drugs had significantly different effects on both left ventricular hypertrophy and resistance vessels. Perfusion pressure was reduced from 37.6 +/- 0.4 mm Hg to 34.0 +/- 0.5 mm Hg (p less than .01) with C-D but only to 36.5 +/- 0.5 mm Hg with H (NS). Left ventricular weight was significantly reduced by C-D (2.02 +/- 0.02 vs 2.63 +/- 0.05 mg/g, p less than .01) but only to 2.44 +/- 0.05 mg/g by H.