Pressure generation in a contracting myocyte

Abstract

The central hypothesis of this investigation is that a shortening myocyte generates a time-varying transmural pressure, or intracellular pressure. A mathematical model was formulated for a single myocyte, consisting of a fluid-filled cylindrical shell with axially arranged contractile filaments, to quantitate the fiber-fluid interaction. In this model, the intracellular pressure mediates the interaction between myofilament force, cell shortening, and the mechanical properties of the sarcolemma. Shortening of myofibrils, which are embedded in the fluid-filled myocytes, deforms the myocyte, thereby altering its transmural fluid pressure. This increase in transmural pressure counteracts fiber shortening, hence constituting an internal load to shortening. The shortening of the myocyte is accompanied by thickening, due to the incompressible nature of its contents. Consequently, the overall contractile performance of the cell is integrally linked to the generation of intracellular pressure. The model manifests a positive transmural pressure during shortening, but not without shortening. The pressure in the myocyte, therefore, is not a direct function of the force generated, but rather of shortening. Intracellular pressure was measured through a fluid-filled glass micropipette (5 mu ID) employing a servo-nulling pressure transducer in a standard micropuncture technique. Measured intracellular pressure in a contracting isolated skeletal myocyte of the giant barnacle is observed to be dynamically related to shortening, but not to tension without shortening. The relation between the force of contraction, cell shortening, and intracellular pressure was assessed during both isotonic and isometric contractions. The results support the prediction that isometric, or nondeforming, contractions will not develop intracellular pressure and identify a reason for relengthening of the myocytes during relaxation.

Examining the Role of Mechanosensitive Ion Channels in Pressure Mechanotransduction in Rat Bladder Urothelial Cells

“…In the field of continuum mechanics, cells are generally considered to be incompressible, and thus, cells are not expected to deform under hydrostatic pressure, especially at physiologically relevant levels. 15,33 These results, however, suggest that UCs may undergo deformation to cause membrane stretch when exposed to hydrostatic pressure. A more plausible explanation, however, is the off-target effects of the GdCl 3 used in these experiments.…”

“…These results provide evidence that UCs are sensitive to pure hydrostatic pressure, assuming that there was no cell deformation since cells are considered incompressible. 15,33 In contrast to this study, previous studies have typically used a modified Ussing chamber and examined UC response to mechanical stimuli by exposing either the mucosal or serosal side of urothelium tissue to a column of buffer solution with the other side unsupported. 8, 16,26,41 It should be noted that this method of pressure application also causes tissue deformation (bowing), introducing another variable, namely stretch, to the model.…”

“…PCR amplification was carried out for 35 cycles at 94°C (15 s), 60°C (30 s), and 72°C (30 s). After confirming that amplification for all genes of interest occurred within appropriate threshold cycles, [30][31][32][33][34][35] the PCR products were electroporated on a 2% agarose gel at 100 V for 1 h 15 min using a 500-bp ladder for visual confirmation of the base pair size of amplicons.…”

Plasma detection of NO by a catheter

“…Release of endothelium-derived relaxing factors in response to hydrodynamic shear stress is modulated by the pulsatile mechanics. It is greater when flow is pulsatile than steady [66,70], and is reported to be maximal at a pulse flow frequency of 4-6 Hz in a variety of different mammalian species and is inversely proportional to the amplitude of the pulse pressure in isolated vessel segments perfused at constant flow [33].…”

Why is the subendocardium more vulnerable to ischemia? A new paradigm

“…PEV was validated in our previous study (1) to stem from the combined effect of LVP-induced interstitial pressure and contraction-induced intramyocyte pressure (38) (Fig. 2D), as follows (see Eq.…”