Hypertrophy-induced increase of intermediate filaments in vascular smooth muscle.

Abstract

The distribution of filaments was studied in hypertrophied rabbit vascular smooth muscle . Hypertrophy was induced by partial ligation of the portal-anterior mesenteric vein . 14 d after ligation, there was an approximately threefold increase in the number of intermediate filaments per cross-sectional area, as compared to control values . The actin :intermediate:myosin filament ratio was 15 :1 .1 :1 in control and 15 :3 .5 :0 .5 in hypertrophied portal-anterior mesentric vein vascular smooth muscle . Comparison of the filament ratios with the increase in volume density of the hypertrophied cells suggests that the number of myosin filaments per cell profile remained approximately the same as in controls, whereas the number of actin filaments increased in proportion to the increase in cell volume .Intermediate (10 nm diameter) filaments are ubiquitous components ofmost, if not all, eukaryotic cells (see reference 39 for review) . In nonneural tissue, they were first described by Ishikawa et al. (35) in cultured cells and distinguished from actin filaments through the difference in size and the failure of the 10-nm filaments to bind the heavy meromyosin subfragment of myosin. Recent studies have shown that the major component ofthe intermediate filaments in muscle is a protein of 50,000-55,000 mol wt (15). In nonmuscle cells, other than nerve, a related protein of slightly higher mass (55,000-58,000 daltons) forms the 10-nm filaments, although the two proteins may also coexist in the same cell (5,20,24). A marked increase in the number of intermediate filaments, frequently in the form ofcables, can be induced in muscle and in other cells by drugs such as cytochalasin B and Colcemid (CIBA Pharmaceutical Co., Summit, N. J.) (4,29,33,34,38,55,56) .In normal adult mammalian smooth muscle, intermediate filaments generally surround dense bodies on which actin filaments insert (2) . Intermediate filaments are very numerous in cultured vascular (45-47) and other smooth muscles (11)(12)(13)60). In previous studies of normal adult vascular smooth muscle, occasional cells were found containing massive quantities ofintermediate filaments that appeared to displace the normal actin and myosin filament lattice (50, 52) . Although it was recognized that such proliferation of intermediate filaments in adult smooth muscle represented some form of cellular pathology, its specific cause was not known . We now show that a large increase in the number of intermediate filaments in vascular smooth muscle occurs during hypertrophy induced by increasing vascular distending pressure. In addition, we also 96 describe changes found in the number and distribution ofactin and myosin filaments of hypertrophied vascular smooth muscle . These studies are being pursued to enable us to eventually distinguish the secondary effects of increased pressure on vascular smooth muscle from possible primary pathology of cell organelles that may cause hypertension. MATERIALS AND METHODSNew Zealand white male rabbits (1 .8-2 .7 kg) were anesthetized w...

The dimensional characteristics of smooth muscle in rat blood vessels. A computer-assisted analysis.

“…These latter cells were irregular in outline with the nuclei often eccentrically located, as we found with vascular smooth muscle cells. The lengths of cells dissociated from the rabbit portal mesenteric vein, 258 ^im (Berner et al, 1981), were greater than we found in the rat. This tissue (Komuro et al, 1982).…”

Cellular hypertrophy in mesenteric resistance vessels from renal hypertensive rats.

“…In an ultrastructural study of hypertrophic vascular smooth muscle cells in a partially ligated rabbit portal-anterior mesenteric vein, Berner et al 34 found that there was no net change in the number of myosin filaments per cell profile and that the increased volume of the cell was occupied by actin and intermediate filaments. This finding was in agreement with similar findings in the hypertrophic cells of the stenotic guinea pig intestine.…”

Structural and functional changes in cerebral arteries from spontaneously hypertensive rats.

“…A lesser force-generating ability of vascular smooth muscle from hypertensive animals has long been recognized"- 21 22 and may be due in part to a decreased smooth muscle cell volume 23 or a decreased smooth muscle cell myosin content. 24 Conversely, Mulvany et al 25 and Whall et al 26 have reported that small mesenteric arteries from SHR generate more force than these arteries from normotensive animals. However, recent preliminary findings show that cerebral but not the mesenteric vessels from SHR had significantly lower myosin levels compared to the corresponding vessels from WKY.…”