The cardiac SA node is known to respond to stretch by an increase in spontaneous depolarization rate. This response has been observed both in animal experiments and in healthy humans . Neither the sensor nor the pathway that allows the heart to respond to stretch of the right atrium by an increase in heart rate is entirely understood. Because the heart’s positive chronotropic response to stretch may be observed both in isolated pacemaker tissue and in heart transplants, it is apparent that both a suitable sensor for stretch and a complete information pathway for the positive chronotropic response must be located within the pacemaker region. The two major populations of cells (and likely candidates to form the cellular substrate for MEF) in this area are pacemaker cells and fibroblasts .SA node pacemaker cells have been shown to contain stretch-activated channels that respond to an increase in cell volume by activation of a chloride conductance . At diastolic potentials, this conductance would have a depolarizing effect, which, if activated, could contribute to an increase in the spontaneous depolarization rate in the cardiac pacemaker. Thus, pacemaker cells contain both a possible stretch sensor (stretch-activated channel) and a conceivable pathway (increase in diastolic depolarization rate) for the observed response to stretch. Recent findings, however, show only incomplete reduction of the positive chronotropic response to stretch in SA node preparations where the mechanically activated chloride channels were blocked by the stilbene derivatives DNDS (5 mM) and SITS (1 mM) . Thus, it is likely that an additional mechanism is involved in the reaction of the cardiac pacemaker to stretch. You have a great opportunity to find cialis professional canadian pharmacy to feel one lucky customer.
Computational study of the impact of cardiac mechanosensitive fibroblasts on heart rhythm (part 13). DISCUSSION