Sympatholytic effect of captopril in regression of cardiovascular remodeling in spontaneously hypertensive rats.
Fifty-eight spontaneously hypertensive rats (SHR) at 12 wk of age were divided into 3 groups: A) captopril (Cap) 20 mg.kg-1.d-1; B) clonidine (Clo) 30 micrograms.kg-1.d-1; C) Clo 30 micrograms.kg-1.d-1 + Cap 20 mg.kg-1.d-1 orally for 24 wk. Concomitant administration of Cap and Clo did not result in more lowering of the systolic blood pressure (SBP) than that by Cap alone. Regression of left ventricular hypertrophy (LVH) were remarkable in Groups A and C, but not to the extent in that of WKY. No significant difference between these two groups was found. Cap alone resulted in a greater decrease of myocardial norepinephrine (NE) than that of Groups B and C. The wall/lumen ratio and the number of smooth muscle cell (SMC) layers of renal artery decreased in Groups A and C, but little difference was found between them. It seemed that combined blockade of renin-angiotensin-aldosterone (RAA) system and sympathetic nervous system (SNS) did not produce more significant BP reduction and reversal of cardiovascular remodeling than Cap alone did. The sympathetic inhibitory effect of angiotensin converting enzyme inhibitor (ACEI) was not enhanced by sympatholytic treatment.
Xie
L D
LD
Hypertension Division, First Affiliated Hospital, Fujian Medical College, Fuzhou, China.
Chen
D G
DG
Zhang
S
S
Wang
H J
HJ
Chen
H J
HJ
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002216:Captopril / Q000494:pharmacology*; D003000:Clonidine / Q000494:pharmacology; D006973:Hypertension / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000188:drug therapy / Q000473:pathology; D009206:Myocardium / Q000378:metabolism; D009638:Norepinephrine / Q000378:metabolism; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D012084:Renin-Angiotensin System / Q000502:physiology; D013564:Sympathetic Nervous System / Q000502:physiology
D002216:Captopril; D003000:Clonidine; D009638:Norepinephrine