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Acidosis or inorganic phosphate enhances the length dependence of tension in rat skinned cardiac muscle

Norio Fukuda, Jin O-Uchi, Daisuke Sasaki *, Hidetoshi Kajiwara, Shin'ichi Ishiwata *†‡ and Satoshi Kurihara

1. We investigated the effect of acidosis on the sarcomere length (SL) dependence of tension generation, in comparison with the effect of inorganic phosphate (P_i), in rat skinned ventricular trabeculae. The shift of the mid-point of the pCa-tension relationship associated with an increase in SL from 1.9 to 2.3 µm (pCa₅₀) was studied.
2. Decreasing pH from 7.0 to 6.2 lowered maximal and submaximal Ca²⁺-activated tension and increased pCa₅₀ in a pH-dependent manner (from 0.21 ± 0.01 to 0.30 ± 0.01 pCa units). The addition of P_i (20 mM) decreased maximal tension and enhanced the SL dependence, both to a similar degree as observed when decreasing pH to 6.2 (pCa₅₀ increased from 0.20 ± 0.01 to 0.29 ± 0.01 pCa units).
3. Further experiments were performed using 6 % (w/v) Dextran T-500 (molecular weight ~500 000) to osmotically reduce interfilament lattice spacing (SL, 1.9 µm). Compared with that at pH 7.0, in the absence of P_i the increase in the Ca²⁺ sensitivity of tension induced by osmotic compression was enhanced at pH 6.2 (0.18 ± 0.01 vs. 0.25 ± 0.01 pCa units) or in the presence of 20 mM P_i (0.17 ± 0.01 vs. 0.24 ± 0.01 pCa units).
4. H⁺, as well as P_i, has been reported to decrease the number of strongly binding cross-bridges, which reduces the co-operative activation of the thin filament and increases the pool of detached cross-bridges available for interaction with actin. It is therefore considered that during acidosis, the degree of increase in the number of force-generating cross-bridges upon reduction of interfilament lattice spacing is enhanced, resulting in greater SL dependence of tension generation.
5. Our results suggest that the Frank-Starling mechanism may be enhanced when tension development is suppressed due to increased H⁺ and/or P_i under conditions of myocardial ischaemia or hypoxia.

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