Adaptation of canine saphenous veins to grafting. Correlation of contractility and contractile protein content.

Seidel, Charles L.; Lewis, R. M.; Bowers, R. L.; Bukoski, Richard D.; Kim, H S; Allen, Julius C.; Hartley, Craig J.

doi:10.1161/01.res.55.1.102

Cited by 35 publications

(9 citation statements)

References 22 publications

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“…24 However, the possibility cannot be excluded that it may be the increase in pulsatile pressure loading rather than the increased blood pressure level that gives rise to the change in vascular structure. After all, in those experiments, the vessel grafts were subjected to the largest possible relative change in pulsatile pressure: from almost zero in the veins to arterial PP.…”

Section: Discussionmentioning

confidence: 99%

Reducing pulse pressure in hypertension may normalize small artery structure.

Christensen

1991

Hypertension

126

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To investigate the relation between the small artery structure and different blood pressure parameters, spontaneously hypertensive rats were treated from 4 to 24 weeks of age (20 weeks in total) with five different antihypertensive therapies: two angiotensin converting enzyme inhibitors (perindopril and captopril), a calcium antagonist (isradipine), a beta-blocker (metoprolol), and a vasodilator (hydralazine). At 24 weeks of age, 24-hour blood pressure was measured, and two mesenteric resistance vessels were taken from each animal. Blood pressure was 227/135 mm Hg (systolic/diastolic) and 161/106 mm Hg in untreated hypertensive and normotensive control rats, respectively. Heart rates were 376 min-1 and 295 min-1 for the two strains. All treatments reduced all blood pressure parameters except for metoprolol, which did not reduce pulse pressure. In the small arteries, the media cross-sectional area was unaffected by the treatments. When a simple correlation analysis was made, pulse pressure was found to correlate more closely (r = 0.64, p less than 0.001) to the resistance vessel media/lumen ratio than any of the other pressure parameters studied: systolic (r = 0.51, p = 0.011), mean (r = 0.41, p = 0.05), or diastolic (r = 0.28, p = 0.19). When an analysis of covariance was performed that included pulse pressure, mean blood pressure, and heart rate, which also correlated significantly to the media/lumen ratio, 81% of the variation in the media/lumen ratio could be accounted for by the variation in the three covariates (p less than 10(-5)), pulse pressure being the major factor.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussionmentioning

confidence: 99%

Reducing pulse pressure in hypertension may normalize small artery structure.

Christensen

1991

Hypertension

126

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“…This is similar to findings in hypertrophied dog saphenous vein. 8 By calculating the number of myosin filaments per cell cross-sectional area on electron photomicrographs, Bemer et a17 found a decreased number of thick filaments in hypertrophied rabbit portal vein. These results agree with the decreased force per crosssectional area reported for other hypertrophic smooth muscle preparations.14 In the hypertrophied portal vein, total active force and the vessel cross-sectional area increases with time.11 After 5 days of pressure increase, active force per area was decreased,10 and after 7 days, the time used in the present study, active force per area was similar to the controls.11 The actin and myosin contents in the hypertrophied portal vein were not significantly different from the values in the controls suggesting that after 7 days, the growing cells have doubled the amount of contractile proteins in the vessel wall.…”

Section: Discussionmentioning

confidence: 99%

Isoform distribution and tissue contents of contractile and cytoskeletal proteins in hypertrophied smooth muscle from rat portal vein.

Malmqvist

Arner

1990

Circulation Research

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Growth of the smooth muscle in the rat portal vein was initiated by an increased transmural pressure. After 7 days, the cross-sectional area of the vessel wall and the maximal active force of the longitudinal muscle layer had increased twofold. Electron microscopy showed that the cell cross-sectional area was increased, suggesting cellular hypertrophy. Increased amounts of intermediate (10 nm) filaments were observed in the hypertrophied cells. The hypertrophied vessels had decreased DNA content per unit wet weight compared with the control vessels (hypertrophied, 1.5 +/- 0.1; control, 1.9 +/- 0.1 micrograms/mg; p less than 0.01). Protein composition was studied with electrophoretic methods. Compared with control preparations the hypertrophied veins had similar myosin and actin contents per unit wet weight (myosin: hypertrophied, 4.4 +/- 0.8; control, 5.9 +/- 0.9; actin: hypertrophied 12.2 +/- 0.6; control, 11.8 +/- 1.0 mg/g). Two different forms of the myosin heavy chain were detected with 5% sodium dodecyl sulfate-polyacrylamide gels. The proportion of the lower molecular weight heavy chain relative to total heavy chain content was about 30% and similar in both preparations. The relation filamin/myosin was increased in the hypertrophied vessels. Pyrophosphate gel electrophoresis revealed two protein bands, with an increase in the slower migrating band in the hypertrophied vessels possibly reflecting an increase in filamin content in the extracts. In the control portal vein alpha-actin is the dominating isoform constituting about 55% of total actin. In hypertrophied vessels, alpha-actin decreased (by 15%) and gamma-actin increased (by 20%). The portal vein contained desmin and vimentin in a ratio of about 6:1. The hypertrophied vessels showed a marked increase in the amount of these proteins (desmin/actin: hypertrophied, 0.32; control, 0.14). In conclusion, during pressure-induced growth of the portal vein, contractile protein contents increase in proportion to the increase in weight. A change in isoforms of actin occurs but no evidence for a change in myosin isoforms was found. The structural proteins increase relative to tissue weight, possibly associated with the increased number of intermediate filaments demonstrated with electron microscopy.

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“…Decreased pressure has been shown to decrease the amount of smooth muscle in the rat aorta . In the hypertrophy associated with vessel coarctation (Olivetti et al 1980), venousto-arterial autologous grafts (Seidel et al 1984), pulmonary hypertension in calves (Mecham et a.l. 1987) and in the model used in the present study, increased pressure load is present.…”

Section: Discussionmentioning

confidence: 99%

Contractile properties during development of hypertrophy of the smooth muscle in the rat portal vein

Malmqvist

Arner²

1988

Acta Physiologica Scandinavica

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Structural and mechanical alterations during hypertrophy of the rat portal vein were investigated. Growth of the vessel was induced by a partial ligature of the vessel causing an increased transmural pressure. Vessel segments from animals kept with ligature for 1, 3, 5 and 7 days, were compared with vessels from sham-operated animals. Maximal active force and vessel cross-sectional area increased with time in the ligated group. On day 7, force and cross-sectional area at the optimal length, were markedly increased in the ligated group (21.1 +/- 1.0 mN, 0.55 +/- 0.04 mm2, n = 9) compared with the control vessels (11.7 +/- 1.0 mN, 0.30 +/- 0.02 mm2, n = 7). Light and electron microscopy of preparations fixed at optimal length showed that the amount of smooth muscle and the cross-sectional area of cell profiles were almost doubled in the ligated group on day 7, consistent with hypertrophy of the smooth muscle. The force per smooth muscle cell area was similar in the two groups (ligated: 132 +/- 15; control: 145 +/- 16 mN mm-2, n = 4-5). The maximal shortening velocity was significantly lower in the hypertrophied group (ligated: 0.28 +/- 0.02; control: 0.41 +/- 0.01 optimal length s-1, n = 6). In chemically skinned preparations, activated by maximal thiophosphorylation of the myosin light chains, force was higher in the ligated group compared to the controls but no difference in maximal shortening velocity was observed. In conclusion, the increased transmural pressure is associated with a rapid increase in the amount of smooth muscle in the portal vein. The mechanical data show that after 7 days the force generating ability of the contractile system has increased in proportion to the smooth muscle cell mass. The unaltered maximal shortening velocity in the skinned hypertrophied preparations suggests that the kinetic properties of the maximally activated contractile system are unaltered. The decreased maximal shortening velocity in the intact hypertrophied preparations may reflect alterations in the excitation-contraction coupling.

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Adaptation of canine saphenous veins to grafting. Correlation of contractility and contractile protein content.

Cited by 35 publications

References 22 publications

Reducing pulse pressure in hypertension may normalize small artery structure.

Reducing pulse pressure in hypertension may normalize small artery structure.

Isoform distribution and tissue contents of contractile and cytoskeletal proteins in hypertrophied smooth muscle from rat portal vein.

Contractile properties during development of hypertrophy of the smooth muscle in the rat portal vein

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