Angiotensin ii and contraction of isolated myocytes from human,
guinea pig and infarcted rat hearts.
Lefroy, David C., Giorgio Vescovo, Federica Del Monte, Tom Crake,
Luciano Dalla Libera, Sian Harding, Philip A. Poole-Wilson.
DEPARTMENT OF CARDIAC MEDICINE, NATIONAL HEART, AND LUNG INSTITUTE,
DOVEHOUSE ST, LONDON SW3 6LY, UK, FIRST DEPARTMENT OF INTERNAL
MEDICINE, VENICE CITY HOSPITAL, VENICE, ITALY, DEPARTMENT OF
CARDIOLOGY, ST BARTHOLOMEW'S HOSPITAL, WEST SMITHFIELD, LONDON EC1A
7BE, UK, ISTITUTO DI PATOLOGIA GENERALE, UNIVERSIT[grave]a DI PADOVA,
35121 PADOVA, ITALY
APStracts 3:0005H, 1996.
The effects of angiotensin II on myocardial contractility were
assessed in isolated cardiac myocyte preparations using video
microscopy with a computerized edge detection system. Angiotensin II
1 nmol/l - 10 [mu]mol/l did not affect the contraction of rat (n =
10), guinea pig (n = 11), or human ventricular myocytes (n = 8), nor
of human atrial myocytes (n = 12). Isoproterenol or raised
extracellular calcium increased the contraction amplitude of the
cardiac myocytes to a maximum of between 150% and 560% above basal,
and there were corresponding increases in the velocities of
contraction and relaxation. In rat and guinea pig ventricular
myocytes angiotensin II 1 [mu]mol/l did not affect the inotropic
response to isoproterenol. Seven days after left coronary artery
ligation in 7 rats, the basal contraction amplitude was reduced in
myocytes from the infarcted region (4.0 +/- 1.9%) compared with the
non-infarcted region (5.0 +/- 2.8%, P = 0.03) and with myocytes from
6 sham-operated hearts (5.0 +/- 2.8%, P = 0.03). There was a switch
in the myosin isoform expression from the V1 to the V3 isoform in the
myocytes from both the infarcted and non-infarcted regions.
Angiotensin II 1 nmol/l - 10 [mu]mol/l had no significant effect upon
the contraction characteristics of myocytes from the infarcted rat
hearts. In conclusion, angiotensin II had no significant inotropic
effect on isolated cardiac myocyte preparations from guinea pig
ventricle, normal and infarcted rat ventricle, human ventricle, and
human atrium.
Received 9 December 1994; accepted in final form 9 November 1995.
APS Manuscript Number H1077-4.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 22 January 96