An Autoradiographic and Pathological Study of Cellular Proliferation in Rabbit Arteries Correlated with an Increase in Arterial Pressure

Bevan, Rosemary D.

doi:10.1159/000158083

Cited by 53 publications

(65 citation statements)

References 17 publications

(26 reference statements)

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“…Manifestations of hypertrophy include evidence of mitosis and an increase in wall thickness and the number and size of smooth muscle cells in the distended segment (1,6,8,9,21,25,30,32,63) . These changes are absent on the "low-pressure" side of the coarctation .…”

mentioning

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

Berner¹,

Somlyo²,

Somlyo³

1981

The Journal of Cell Biology

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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...

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mentioning

confidence: 99%

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

Berner¹,

Somlyo²,

Somlyo³

1981

The Journal of Cell Biology

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“…have diverted attention from the media and adventitia (ADV), whereas in hypertension, attention has been focused mainly on the media. In both diseases, however, intimal and medial lesions are almost invariably accompanied by alterations in the subjacent ADV.1 ' 2 According to observations in experimental models, the development of vascular disease is in most cases accompanied by increases in vascular mass, which may be focal or generalized to the entire intima-media (IM).3 -4 DNA replication increases, and may be followed by cell division leading to increased cell number (hyperplasia) 3 or by an increase in the total content of DNA per cell (hyperploidy).6 An accompanying hypertrophy also occurs due to increases in the amount of fibrous 7 and nonfibrous protein (NFP). …”

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confidence: 99%

“…3 -4 DNA replication increases, and may be followed by cell division leading to increased cell number (hyperplasia) 3 or by an increase in the total content of DNA per cell (hyperploidy).…”

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confidence: 99%

“…3 -4 DNA replication increases, and may be followed by cell division leading to increased cell number (hyperplasia) 3 or by an increase in the total content of DNA per cell (hyperploidy). 6 An accompanying hypertrophy also occurs due to increases in the amount of fibrous 7 and nonfibrous protein (NFP).…”

mentioning

confidence: 99%

“…The purity of these arterial segments and the reproducibility of the biochemical determinations were verified by comparing groups of normotensive rats of different age and weight, and also by comparing the results wiui experiments performed by other authors with tissues from animals larger than the rat. In experiments with hypertensive animals, DNA synthesis and content were measured after in vivo incorporation of [methyl- 3 H]thymidine and the results were compared with autoradiographic studies.…”

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Increased DNA replication in the arterial adventitia after aortic ligation.

Chatelain¹,

Dardik²

1988

Hypertension

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SUMMARY After mkrosurgicaJ dissection of the thoracic aorta of normotensive rats, biochemical and morphological comparisons were performed between the intima-media and adventitia. The DNA content, wet weight, and dry defatted weight of the adventitia were half that of the intima-media. Collagen was the main component of the adventitia (collagen > nonfibrous protein > elastin) whereas elastin was the main protein in the intima-media (elastin > nonfibrous protein >collagen), and the results correlated with morphological observations. Hypertension induced by aortic ligation between the renal arteries resulted in rapid elevations in circulating humoral factors and blood pressure. A sixfold increase in DNA synthesis was observed in the adventitia (p < 0.001), resulting in a significant increase in DNA content as early as 6 days after aortic ligation (75% increase; p<0.001). Increased DNA replication was accompanied by elevations hi nonfibrous protein and elastin contents. Autoradiograms showed labeled adventitia] fibroblasts throughout the thickness of the adventitia and along the entire length of the aorta and smaller vessels. DNA synthesis and content and labeled smooth muscle cells were increased hi the intima-media. These studies indicate that the adventitia participates hi the development of vascular hypertrophy and arterial disease produced by aortic ligation. have diverted attention from the media and adventitia (ADV), whereas in hypertension, attention has been focused mainly on the media. In both diseases, however, intimal and medial lesions are almost invariably accompanied by alterations in the subjacent ADV.1 ' 2 According to observations in experimental models, the development of vascular disease is in most cases accompanied by increases in vascular mass, which may be focal or generalized to the entire intima-media (IM).3 -4 DNA replication increases, and may be followed by cell division leading to increased cell number (hyperplasia) 3 or by an increase in the total content of DNA per cell (hyperploidy).6 An accompanying hypertrophy also occurs due to increases in the amount of fibrous 7 and nonfibrous protein (NFP). 41The purpose of our experiments was to assess if the ADV is also affected by some of these processes during the initiation of vascular disease produced by aortic ligation in the rat. the thoracic aorta were characterized after microsurgical dissection. The purity of these arterial segments and the reproducibility of the biochemical determinations were verified by comparing groups of normotensive rats of different age and weight, and also by comparing the results wiui experiments performed by other authors with tissues from animals larger than the rat. In experiments with hypertensive animals, DNA synthesis and content were measured after in vivo incorporation of [methyl-3 H]thymidine and the results were compared with autoradiographic studies. Materials and MethodsNormotensive male Sprague-Dawley rats (Hsd: (SD)BR, Harlan Farm, Madison, WI, USA) were killed at 6 and 10 weeks of age. The aor...

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Structural alterations in proliferating, remodeling, and regressing tooth pulp arterioles

1979

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In the continuously growing upper incisor of 100 g rats about 25 arterioles arise from an artery outside the tooth and pass through the apical foramen to run parallel to one another in the central part of the pulp, each supplying a well-defined sector of the migrating odontoblast layer. The arterioles pass through a cycle of proliferation, growth, remodeling, regression and decay, phase displaced in relation to each other. Proliferative and degenerative processes occur in the arteriole wall throughout the cycle, but vary considerably in intensity at different phases. Proliferation takes place by mitosis in the endothelium and the innermost smooth muscle cells. The degenerative process consists of reduction in size of smooth muscle cells by partial autodigestion and by cell death. When the odontoblasts reach the incisal extremity of the tooth, they die, and the associated regressed arteriole disappears. The system of pulpal arterioles has remarkable spatio-temporal features and each of its vessels appears to be in a state of sensitive structural equilibrium.

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An Autoradiographic and Pathological Study of Cellular Proliferation in Rabbit Arteries Correlated with an Increase in Arterial Pressure

Cited by 53 publications

References 17 publications

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

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

Increased DNA replication in the arterial adventitia after aortic ligation.

Structural alterations in proliferating, remodeling, and regressing tooth pulp arterioles

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