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Arterial hydration during vasoconstriction Holtby, Mark Ernest


The relationship between vasoconstriction and the hydration of the artery wall was examined using the tail artery of the rat. Freeze substitution was used to prepare histological sections of arteries fixed in a known state of constriction. Measurements of wall dimensions showed that the more constricted arteries had smaller wall and media cross-sectional areas than the less constricted arteries. The constant length of the constricting artery meant that the wall volume decreased by 14%. Considering the vascular smooth muscle cell as a double cone enabled formulation of relationships between the cell radius, length, surface area, and volume. Radius and length measurements of the smooth muscle cells of the freeze-substituted arteries demonstrated that the cell radius doubled and the length decreased by half during vasoconstriction. These measurements revealed that the surface area of the double cone model of the cell remained constant, while the volume increased during vasoconstriction. This suggested that water entered the contracting vascular smooth muscle cells. Water and ion content determination of paired control and constricted in vitro arteries indicated that the artery wall lost 16% of its water. This represented a 13% decrease in the wall volume. The associated decreases in the Na and CI contents and in the inulin space, as well as the constant K content implied that the water was expelled from the extracellular space of the constricting artery. While this was true for arteries constricted with both norepinephrine and high K solutions, it seemed that water lost from arteries constricted with PLV-2, a synthetic vasopressin, may have come from inulin-inaccessible phases of the wall. The size of the water loss depended upon the duration of vasoconstriction: the losses were largest 30 seconds after the start of constriction. Perfused rat tail arteries exhibited pressure-flow characteristics during vasoconstriction which suggested that the permeability of the wall had increased. It was discovered that the changes in permeability induced by vasoconstriction were drastically affected by changes in the intravascular pressure. In a third perfusion experiment, the dilution of Evans blue dye passing through the lumen of a constricting artery also indicated a permeability increase during vasoconstriction. Arteries were incubated in one of five isosmotic solutions of different ionic composition. Comparison of arterial contents and perfusion pressures showed that the absence of monovalent ions in the bathing media resulted in a decrease in arterial water, an increase in divalent ion content, and higher perfusion pressures. These observations can be explained by changes in the tension of the vascular smooth muscle cells and possibly by an ion exchange process in the paracellular matrix which caused conformational changes in the matrix, in turn causing an altered wall hydration. Arteries, cooled overnight at 2°C, were rewarmed in one of three solutions of different Na concentration. The arteries were transferred from a solution at 2°C to one at a temperature between 2° and 37°C for 15 minutes. Comparison of the arterial contents showed that a small amount of K was gained while large amounts of water and Na were lost from the artery wall during these short rewarming periods. Postulation of a 1:1 exchange of K for Na for the cell metabolic Na-K pump means that a fast Na component was extruded, independent of K, from the rewarming artery wall. The extrusion of the wall water may have been related to the extrusion of this extra Na component, because they both had the same temperature and external Na concentration dependencies. The monitoring of the intravascular pressure of perfused rewarmed arteries revealed pressure changes with the same temperature and external Na concentration dependencies as the above water content changes. Calculations indicated that changes in wall volume caused by changes in water content could partially explain the intravascular pressure changes during rewarming. The wall water loss, the permeability changes, and the cell water increase associated with vasoconstriction, are discussed in terms of an osmotic and hydrostatic pressure balance between the artery wall and its surroundings which is upset by vasoconstriction.

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