Shear stress and aortic histamine synthesis

DeForrest, Jack M.; Hollis, Theodore M.

doi:10.1152/ajpheart.1978.234.6.h701

Cited by 28 publications

(19 citation statements)

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“…The absence of an effect of mepyramine on the flow dependence suggests, however, that the changes probably did not result from histamine release by the wall (DeForrest & Hollis, 1978).…”

Section: Discussionmentioning

confidence: 85%

The effect of luminal flow in rabbit carotid artery on transmural fluid transport

Lever¹,

Tarbell²,

Caro³

1992

Experimental Physiology

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SUMMARYThe steady-state flow of fluid across the wall of the isolated rabbit common carotid artery has been measured in the presence and absence of flow within the lumen of the vessel. The perfusate solution contained either 10 or 40 mg ml-' albumin and transmural flux was measured by monitoring the rate of movement of fluid into a chamber enclosing the artery. Vasomotion was minimized by the inclusion of the vasodilator sodium nitrite in both the perfusate and the outer bathing solution. A relatively slow luminal flow caused a reversible increase in the transmural flux by 20 30 % relative to the value in the absence of flow. The mechanism responsible for the increasc is not clear, but since it was not affccted by the H1 antagonist, mepyramine, it would not appear to have been mediated by histamine release.

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“…The absence of an effect of mepyramine on the flow dependence suggests, however, that the changes probably did not result from histamine release by the wall (DeForrest & Hollis, 1978).…”

Section: Discussionmentioning

confidence: 85%

The effect of luminal flow in rabbit carotid artery on transmural fluid transport

Lever¹,

Tarbell²,

Caro³

1992

Experimental Physiology

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“…4 -7 In vitro studies have demonstrated that flowrelated shear stress alters several aspects of endothelial cell structure and function, including cytoskeletal organization, 8 histamine 9 and tissue plasminogen activator synthesis, 10 endocytosis, 11 and the status of K + channels. 12 Some alterations in vasomotor tone are mediated by the effects of shear stress on the endothelium through the release of agents such as endothelium-derived relaxing factor, 13 prostaglandins, 14 and possibly endothelin.…”

mentioning

confidence: 99%

Dynamics of shear-induced redistribution of F-actin in endothelial cells in vivo.

Langille

Graham

Kim

et al. 1991

Arterioscler Thromb

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The steady-state responses of endothelial cell F-actin distribution to changes in in vivo shear stress have been well documented. The purpose of the current work was to define the dynamics of redistribution of F-actin in the period immediately after experimental changes in shear. We used abdominal aortic coarctation in rabbits to experimentally increase shear stress downstream from the coarctation by approximately twofold. In situ staining was employed to track subsequent F-actin redistribution. Within 12-15 hours, the number of stress fibers in the central regions of the cells decreased, and some separation of junctional actin in adjacent cells occurred. Long, central stress fibers of variable thickness were evident at 24 hours, but the band of actin normally seen at the periphery of the cells could no longer be distinguished. The redistribution of F-actin was completed over the next 24 hours by an increase in thickness of central stress fibers. Restoration of normal F-actin distribution after coarctations were removed proceeded more slowly. The long, thick stress fibers that were induced by high shear were replaced by thinner or shorter microfilament bundles 48 hours after the coarctations were removed. At 72 hours, central stress fibers were primarily long, thin structures. Peripheral F-actin was not fully restored at this time. Peripheral F-actin was restored at 1 week after removal of the coarctation, but there were still more and longer stress fibers at this time than were observed in control aortas. If current hypotheses linking central stress fibers to cell-substrate adhesion and peripheral actin to permeability regulation are correct, then our data indicate that induction of high hemodynamic shear stress may transiently compromise substrate adhesion. Subsequent alterations may enhance substrate adhesion, although intercellular permeability may be altered due to reductions in peripheral actin. (Arteriosclerosis and Thrombosis 1991;ll:1814-1820)

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“…4 In vivo studies have shown that the shape and orientation of endothelial cells is determined primarily by the blood flow. 6 -8 In vitro studies have demonstrated that flow-related shear stress alters various aspects of endothelial cell structure and function, including cytoskeletal organization, 9 histamine synthesis, 10 pinocytosis, 11 prostacyclin synthesis, 12 ' 13 and K + channels. 14 Moreover, some alterations in vasomotor tone are mediated by the effects of shear stress on endothelium through the release of agents such as endothelial-derived relaxing factor 15 and, possibly, endothelin.…”

mentioning

confidence: 99%

In vivo modulation of endothelial F-actin microfilaments by experimental alterations in shear stress.

1989

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Shear stress and aortic histamine synthesis

Cited by 28 publications

References 0 publications

The effect of luminal flow in rabbit carotid artery on transmural fluid transport

The effect of luminal flow in rabbit carotid artery on transmural fluid transport

Dynamics of shear-induced redistribution of F-actin in endothelial cells in vivo.

In vivo modulation of endothelial F-actin microfilaments by experimental alterations in shear stress.

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