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(Hypertension. 1995;26:1149-1153.)
© 1995 American Heart Association, Inc.

Articles

Basal and Angiotensin II–Induced Cytosolic Free Calcium in Adult Rat Cardiomyocytes and Fibroblasts After Volume Overload

Jeannette Fareh; Rhian M. Touyz; Gaetan Thibault; Ernesto L. Schiffrin

From the MRC Multidisciplinary Research Group on Hypertension, Clinical Research Institute of Montreal, University of Montreal (Canada).

Abstract This study investigates basal and angiotensin II (Ang II)–induced [Ca²⁺]_i concentrations in cells from hearts of rats that have undergone cardiac hypertrophy due to volume overload. [Ca²⁺]_i measurements assessed by digital imaging using fura 2 methodology were performed on isolated ventricular cardiomyocytes and fibroblasts from adult rat hearts with a 4-week aortocaval shunt. Long-term aortocaval shunt induced a significant increase in atrial (72%) and ventricular (41%) weights and a large elevation in plasma atrial natriuretic peptide-(1-98) concentration (160%). For adult cardiomyocytes [Ca²⁺]_i measurements are reported as diastolic (average of the lowest points) and systolic intracellular Ca²⁺ values (average of the maximum points corresponding to the diastolic points) over a 30-second time interval. Basal diastolic [Ca²⁺]_i (99±4.1 nmol/L for experimental cells versus 90±4.8 for control cells) was not altered, whereas basal systolic [Ca²⁺]_i was significantly greater in ventricular cardiomyocytes from overload hearts (155±2.3 versus 129±4.4 nmol/L for control cells, P<.05). Ang II increased intracellular Ca²⁺ spike frequency in a concentration-dependent manner in cardiomyocytes from control and overload myocardium. Basal and Ang II–induced intracellular Ca²⁺ spike frequencies were not modified in cardiomyocytes from hypertrophied hearts. Basal [Ca²⁺]_i in ventricular fibroblasts from overload myocardium was significantly increased (128±5.1 nmol/L for fibroblasts from hypertrophied hearts versus 104±3.5 for control cells, P<.05). Ang II–induced [Ca²⁺]_i was lower in fibroblasts from overload myocardium (P<.05). In conclusion, alterations of intracellular calcium homeostasis in the two predominant cardiac cell types involved in myocardial growth and fibrosis, cardiomyocytes and fibroblasts, respectively, may contribute to the physiopathology of heart failure in adult rats. Ang II signaling through the intracellular calcium transduction pathway in a cell-specific manner may play an important role in cardiac hypertrophy.

Key Words: angiotensin II • myocardium • fibroblasts • calcium • heart hypertrophy

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