Atrial fibroblasts are considered to modulate the contractile activity of the heart in response to mechanical stretch. In this study we examined whether atrial fibroblasts are possibly involved in bradyarrhythmia, which is a severe complication after myocardial infarction. For this purpose, transmembrane electrical potentials were recorded in cardiac fibroblasts near the sinoatrial node from sham-operated rats and from rats with myocardial infarction. Twenty days after infarction due to coronary artery ligation, the right atrial tissue weights and the sensitivity of the fibroblast membrane potential to mechanical stretch correlated positively with the infarct size. Cardiac growth was enhanced, but the stretch sensitivity and the resting membrane potential of the atrial fibroblasts declined between 8 and 30 days after infarction. The frequency of spontaneous atrial contractions was significantly reduced 8 days after myocardial infarction and recovered in parallel with the membrane potential of the fibroblasts. These findings suggest that changes in the susceptibility of atrial fibroblasts to mechanical stretch may contribute to bradyarrhythmia during postinfarct remodeling of the heart.

Electrically non-excitable but mechanosensitive right-atrial fibroblasts are thought to be involved in the chronotropic response of the heart to stretch. After myocardial infarction, altered chronotropic response may be due to the remodeling process which also involves the right atrium. Remodeling is associated with the development of hypertrophy of cardiomyocytes and proliferation of fibroblasts. Electrical properties of atrial mechanosensitive fibroblasts from chronic infarcted hearts and their possible role for altered chronotropic response has not, to our knowledge, been studied until now. Thus, resting membrane potential as well as mechanically induced potential of fibroblasts, action potential (AP) of cardiomyocytes, spontaneous frequency and mechanical activity of preparations from the sinus node region were studied 10 weeks after myocardial infarction induced by ligation of the left coronary artery in rats. The prolongation of AP repolarization (increases in APD50and APD90) correlated closely to the infarct size (IS) and the degree of hypertrophy, respectively. Along with increasing IS, membrane potentials of fibroblasts were shifted to more negative values, with a peak of frequency distribution at −15 mV (control and very small IS), at −35 mV (intermediate IS), and −55 mV (large IS), and spontaneous electrical activity was decreased. Membrane resistance of fibroblasts also correlated to IS and was eight-fold greater at large IS than in control. We hypothesize that, in the infarcted heart, increased membrane potential and membrane resistance of fibroblasts may alter electrical activity of neighbouring myocytes in the sinus–venosus region via intercellular electrical coupling.