Contraction of the rat portal vein in hypertonic and isotonic medium: rates of metabolism

Abstract

The contracture induced by hyperosmolality (HC) in the rat portal vein has been investigated with respect to its metabolic properties. Oxygen consumption (Jo2) and lactate production (JLA) were measured. Comparison was made with K+‐induced contractures (KC). Variation in active force was produced for both kinds of contracture by alteration of muscle length. Measurements were also made in normal isotonic solution, where the muscle is spontaneously active, and in Ca2+‐free isotonic solution. At short muscle lengths, where no active tension was produced, Jo2 was lower in HC than in KC. In contrast, JLA was greatly enhanced in HC, so that calculated ATP turnover (Jatp) was almost the same in both kinds of solution. Comparison of metabolic rates at long and short muscle length and correlation to force development allowed calculation of tension‐dependent metabolism. In normal solution (spontaneous activity) tension‐dependent metabolic rate was much greater than in either kind of contracture. No difference in tension‐dependent Jo2, Jla or JATP could be detected between HC and KC. In nominally Ca2+‐free solution, force development and metabolic rates in HC did not differ from those in Ca2+‐containing solution. Glucose removal abolished lactate formation in HC. The temporal variations of Jo2 and active force during 30 min of HC and KC were followed. In HC, force development increased with time, whereas in KC it decreased. Tension‐independent Jo2 declined with time in HC but stayed constant in KC. On the other hand, tension‐dependent Jo2 was unchanged in HC but declined in KC. The results of this study indicate that despite alterations in overall cell metabolism caused by the hypertonic solution, the energetic aspects of cross‐bridge operation may be similar in HC and KC, despite prominent differences in dynamic mechanical properties.