Abstract

AbstractA tonic increase in tension was observed in the isolated rat portal vein in response to large increases in extracellular tonicity (1.5–3 times normal). The purpose of this study was to find out whether this tension increase was due to active contraction or passive shrinkage. The metabolic dependence of the response and its mechanical characteristics, as revealed by quick release experiments, lead to the conclusion that active contraction is the predominant mechanism. The maximal force developed in the hypertonicity contracture amounted to 31 per cent of the maximal K+ contracture obtained in isotonic medium. The hypertonicity contracture occurred independent of the level of membrane potential and in the absence of external Ca2+ (below 10‐‐9 M). It is thus elicited through mechanisms which differ in these respects from the electromechanical cbupling operating in the K+ contracture. The speed of shortening against a given afterload was found to be lower in a hypertonicity contracture than in a K' contracture of comparable isometric force. Explanations for observed differences between the two types of contracture are discussed.

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