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Role of cardiac angiotensin II in isoproterenol-induced left ventricular hypertrophy.
Author(s) -
Masahiro Nagano,
Jitsuo Higaki,
Fumiaki Nakamura,
Koichi Higashimori,
N Nagano,
Hiroshi Mikami,
Toshio Ogihara
Publication year - 1992
Publication title -
hypertension
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.986
H-Index - 265
eISSN - 1524-4563
pISSN - 0194-911X
DOI - 10.1161/01.hyp.19.6.708
Subject(s) - trandolapril , medicine , endocrinology , hydralazine , angiotensin ii , muscle hypertrophy , isoprenaline , cardiac hypertrophy , blood pressure , renin–angiotensin system , left ventricular hypertrophy , angiotensin converting enzyme , ace inhibitor , stimulation
Angiotensin II (Ang II) has been shown to induce proliferation of cardiac myocytes. To examine the role of Ang II in left ventricular (LV) hypertrophy, isoproterenol was infused subcutaneously into 9-week-old male Wistar rats at 4.2 mg/kg/day for 7 days. Infusion of isoproterenol increased LV weight and Ang II concentrations in plasma and in LV tissue. In anephric rats, LV weight and tissue Ang II were increased similarly, but plasma Ang II was not changed by isoproterenol. Concomitant oral administration of trandolapril and isoproterenol prevented increases in both LV Ang II and LV weight. Treatment with hydralazine decreased blood pressure in a similar way as trandolapril but did not affect either LV weight or LV Ang II. Plasma Ang II was not decreased by either trandolapril or hydralazine when administered in combination with isoproterenol. These results suggest that cardiac tissue Ang II regulates myocyte growth in isoproterenol-induced LV hypertrophy, and the reduction of Ang II partly explains the prevention of cardiac hypertrophy by the converting enzyme inhibitor.

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