The role of protein–polysaccharides in hydration of the arterial wall

Palatý, Vladimír; Gustafson, Brigid; Friedman, Sydney M.

doi:10.1139/y70-009

Cited by 13 publications

(5 citation statements)

References 13 publications

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“…Elevations in Na (corrected for 60 CoEDTA space) and total tissue Ca are consistent with the findings of others for DOCA treatment (10,17). Although some of this material may be bound to mucopolysaccharides (18,19), such sites offer only limited capacity (6,11). Significant alterations in smooth muscle behavior would result if part of the ionic shift (in excess of binding) were intracellular.…”

Section: Discussionsupporting

confidence: 86%

Altered ion transport in aortic smooth muscle during deoxycorticosterone acetate hypertension in the rat.

Jones¹,

Hart²

1975

Circulation Research

165

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Change in aortic water and electrolyte distribution and in ion turnover were studied during the development of deoxycorticosterone acetate (DOCA) hypertension in the rat. Treatment with DOCA plus saline during the prehypertensive phase was associated with increases in 42K turnover (0.0142 +/- 0.0005 vs. 0.0102 +/- 0.0003 min-1), cell water (0.89 +/- 0.03 vs 0.76 +/- 0.02 kg/kg dry weight), and the ratio of weight to length. These parameters were further increased during the development of hypertension. Significant increases were also observed in total K, Ca, and Mg contents and in Na and C1 contents corrected for the extracellular space. The turnover of 36Cl was increased (0.230 +/- 0.006 vs. 0.136 +/- 0.004 min-1) in DOCA hypertensive rats as was the content of slowly exchanging Cl. Removal of extracellular Ca greatly increased the steady-state turnover of 42K. For control rats, a Ca concentration of 0.1 mM reduced the rate of 42K turnover to less than 50% of the Ca-free value (0.063 +/- 0.004 min-1), whereas DOCA hypertensive rats exhibited only a 10% reduction. At the highest Ca concentration, 5 mM, the 42K turnover was greater in DOCA-treated rats with the hypertensives operating at 67% of maximum efflux or about twice the efflux in controls. It is concluded that significant alterations in ion transport by vascular smooth muscle occur before and during the development of hypertension induced by treatment with DOCA plus saline. Such changes may result from a reduced ability of Ca to stabilize the membrane. It is proposed that such alterations contribute to the changes in vascular reactivity and the hypertrophy associated with hypertension.

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Section: Discussionsupporting

confidence: 86%

Altered ion transport in aortic smooth muscle during deoxycorticosterone acetate hypertension in the rat.

Jones¹,

Hart²

1975

Circulation Research

165

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“…At the end of the experimental incubation, the artery was blotted gently on filter paper, weighed in a stoppered glass weighing bottle, dried to a constant weight, and extracted for 7 days with 0.75M HNO 3 . Na, K, and Li were determined in the extract by an atomic absorption spectrophotometer with the usual precautions (11). Results are expressed as means ± SE in terms of mmoles/ kg dry weight unless noted otherwise.…”

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confidence: 99%

Lithium Substitution and the Distribution of Sodium in the Rat Tail Artery

Friedman

1974

Circulation Research

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The exchange of lithium (Li) with sodium (Na) was explored in an effort to quantify cellular Na in the rat tail artery. Two phases of cellular Na were demonstrated by the kinetics of exchange at 37°C. Cellular Na, was rapidly lost following cell disruption and increased in proportion to potassium (K) loss during conventional Na enrichment in a Kfree medium. Cooling to 2°C almost abolished the transmembrane movement of Li; therefore, a simple 30-minute incubation in cold Li medium removed extracellular but not cellular Na. To prove that the residual Na after such a wash in cold Li was cellular, we demonstrated that Na exchanges readily with Li even at 2°C after cells are disrupted, increases slowly in proportion to K loss during prolonged cooling, and increases rapidly in a precise one-to-one ratio with K loss when active Na transport is stopped by incubation in a K-free medium. Cellular Na in the normal artery was about 20-25 mmoles/kg dry weight when cellular K was about 225 mmolesAg dry weight. In arteries from rats with deoxycorticosterone acetate-induced hypertension of 8 weeks duration, a 13% fall in cellular K was balanced one to one by an increase in cellular Na.

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“…This difference may be due to the protein anabolic effect of DOCA. 27 This interpretation is supported by our observation that there was a negligible increase in DOCA hypertensive rats fed a low protein diet.…”

Section: Discussionmentioning

confidence: 54%

Vascular changes in DOCA hypertension. Influence of a low protein diet.

Moreland

Webb²,

Bohr

1982

Hypertension

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SUMMARY The goal of this study was to characterize the influence of a low protein d iet on vascular changes induced by deoxycorticosterone acetate (DOCA) hypertension. DOCA hypertensive and control normotensive rats were placed on a low protein (5%) diet for 4 weeks. This intervention blocked the further increase in systolic blood pressure of rats treated with DOCA; systolic blood pressures of control rats were not influenced by the low protein diet. The sensitivity of isolated mesenteric arteries to norepinephrine was increased in DOCA hypertensive rats compared to that in arteries from control rats; arterial strips from rats maintained on the low protein diet were less sensitive to the catecholamine than arteries from their respective control diet group. Vascular sensitivity to calcium was identical in both normotensive and DOCA hypertensive rats, and the low protein diet had no effect on this measure of calcium activation. Calcium-induced relaxation was depressed in arteries from DOCA hypertensive rats, suggesting a decreased stabilizing influence of the cation on the excitable membrane. Arteries from rats maintained on the low protein diet showed enhanced relaxation to calcium compared to those from their respective control diet group. Membrane stores of calcium available for activation by norepinephrine were increased in arteries from DOCA hypertensive rats; the low protein diet decreased the storage capacity of these membrane sites. The total protein content of the aorta was increased in DOCA hypertensive rats and depressed to control level in DOCA rats maintained on low protein diet. No change was observed in actomyosin content nor in the aclinto-myosin ratio during the DOCA hypertension or the addition of a low protein diet. Since one action of DOCA is to increase cellular protein synthesis, the attenuation of these vascular changes in DOCA rats maintained on a protein-deficient diet is probably due to a decrease in available substrate. T HE importance of the vascular system in the pathogenesis and maintenance of hypertension has been well documented. ' 3 Both functional and structural alterations in the vasculature contribute to the development and maintenance of the increased arterial pressure. Since these vascular alterations occur in all forms of hypertension, regardless of the initiating factor, they may be considered to be the final common pathway in the pathogenesis of hypertension. 'The structural alterations are of two types. One type is a thickening of the vessel wall, due to hypertrophy of

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The role of protein–polysaccharides in hydration of the arterial wall

Cited by 13 publications

References 13 publications

Altered ion transport in aortic smooth muscle during deoxycorticosterone acetate hypertension in the rat.

Altered ion transport in aortic smooth muscle during deoxycorticosterone acetate hypertension in the rat.

Lithium Substitution and the Distribution of Sodium in the Rat Tail Artery

Vascular changes in DOCA hypertension. Influence of a low protein diet.

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