Mechanisms of the increase in heart rate induced by mechanical stretch

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Ionic mechanisms underlying the enhancement of cardiac pacemaking activity by mechanical stretch was investigated in the isolated rabbit sinoatrial (SA) node. A 5s stretch of 0.2-2.0g was applied to small tissue strips (1.5*3.0mm) of the SA node by using a mechanical stimulator. Cycle length of spontaneous excitation (SPCL) was monitored by recording endocardial surface potential through modified bipolar electrodes with high-gain amplification. Influence of neurotransmitters released from nerve terminals was eliminated by atropine and propranolol. A stretch>0.2g caused a significant shortening of SPCL ; there was a positive correlation between the force and the maximum shortening of SPCL. Treament of the preparation with gadolinium (10muM) or glibenclamide (1muM) did not affect the force-response relationship. The positive chronotropic response to the mechanical stretch>0.5g was reduced significantly by treatment with DNDS (5mM) or SITS (1mM). The positive chronotropic response was also reduced in the low Ca^<2+> (0.36mM) medium, and by bath application of ryanodine (0.1muM) or thapsigargin (2muM). In the electron microscopic examination on the morphology of SA node cells, an increase of caveolae opening in the cell membrane was observed. These findings suggest thah the stretch-induced enhancement of pacemaking activity in the mammalian SA node is mediated in part by stretch-activated C1^- channels and in part by an alteration of Ca^<2+> dynamics.