Structural and mechanical alterations in hypertrophic venous smooth muscle.

Portal hypertension was induced in rats by partial ligation of the hepatic branches of the portal vein. After 5 days the transluminal pressure of the portal vein was measured, and the vessel was fixed in situ for electron-microscopy, or dissected out and mounted in an apparatus recording force and shortening. Portal veins from sham-operated animals were used as controls. Portal venous pressure had increased about twofold after the partial ligation and the cross-sectional area of the longitudinal muscle layer about twofold. Number of muscle cells per mm2 cross-sectional area decreased to half of the control value, whereas extracellular space in the muscle layer and the dry weight of the preparations were unaltered. Number of cells was unchanged suggesting that no hyperplasia had occurred. Length-passive force relations were shifted towards higher force values in the hypertrophic vessels, whereas passive stress-strain characteristics were similar. The structures that carry passive tension have thus increased in proportion to the vessel as a whole. Length-active tension curves obtained by stimulation with AC current or high K+ solutions indicated that the hypertrophic vessels could not, in relation to optimal length for active force, shorten to the same extent as control vessels. Maximum active tension per vessel was unaltered whereas force per unit muscle area and force per cell had decreased. As the preparations were supramaximally stimulated and had optimal extracellular Ca2+ concentrations we suggest that the amount of functional contractile proteins has not increased in proportion to the increase in size of the muscle cells.