Sodium exchange and distribution in the arterial wall

Garrahan, Patricio J.; Villamil, M. F.; Zadunaisky, J. A.

doi:10.1152/ajplegacy.1965.209.5.955

Cited by 52 publications

(35 citation statements)

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“…For example an estimate of 116-6 m-mole/kg cell water for the intracellular concentration ofsodium in the rat aorta (Hagemeijer, Rorive & Schoffeniels, 1965) was based on determination of inulin space and total sodium, and would have included any bound sodium in the tissue. High estimates for intracellular sodium were also obtained by Garrahan, Villamil & Zadunaisky (1965) on canine carotid arteries, both from studies of inulin space and total sodium, and from measurement of a fraction of sodium whose rate of loss was sensitive to temperature, but they pointed out that the estimates might have included large amounts of extracellular bound sodium. The bound sodium in the arteries used in the present experiments would have led to considerable errors if the part of it exchanging with a similar time constant to intracellular sodium had been treated as intracellular.…”

Section: Resultsmentioning

confidence: 99%

Sodium flux and electrical activity of arterial smooth muscle

Keatinge¹

1968

The Journal of Physiology

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SUMMARY1. The intracellular concentration and transmembrane flux of Na in smooth muscle cells of sheep carotid arteries were measured by identifying a fraction of tissue Na whose efflux was markedly sensitive to removal of external Ca. This allowed intracellular Na to be distinguished from extracellular bound Na exchanging with a similar time constant.2. When the arteries were in solution containing Na 148 mM and Ca 2*5 mm the mean intracellular Na concentration was 7*3 m-mole/kg cell water and the mean transmembrane flux of Na was 0-18 p-mole cm-2 sec-1, both values being much lower than reported values for intestinal smooth muscle.3. During electrical activity induced by Ca deprivation the influx of Na increased to 3*2 p-mole cm-2 sec-1; a 50 % reduction in Na concentration stopped electrical activity and reduced influx by more than 50 %, and

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Section: Resultsmentioning

confidence: 99%

Sodium flux and electrical activity of arterial smooth muscle

Keatinge¹

1968

The Journal of Physiology

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“…This suggests that the potentiation of the initial speed of contracture in circular muscle is at least dependent on Na, and not on Cl. It is known that the intracellular Na rapidly decreases in the Na-free solution in smooth muscles (GARRAHAN et al, 1965;POTTER and SPARROW, 1968;HALJAMAE et al, 1970;WAHLSTROM, 1971;NAGASAWA, 1973). It is also known that a rise of intracellular Na by treatment with ouabain induced an increase of Ca influx in guinea pig ileum (BURTON and GODFRAIND, 1974), rabbit aorta and mesenteric artery (BoHR et al, 1969).…”

Section: Discussionmentioning

confidence: 99%

Differences between Ca Contractures in the Depolarized Longitudinal and Circular Muscles of Guinea Pig Stomach

Ishizawa¹,

Miyazaki²

1979

Jpn.J.Physiol

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Ca-induced contracture and the effect of Na on it were investigated in the K-depolarized longitudinal and circular muscles of guinea pig stomach. In the absence of Na, Ca produced rapid contracture in longitudinal muscle, but slow and S-shaped contracture in circular muscle. The sensitivity to Ca for the contracture was about tenfold higher in longitudinal muscle than in circular muscle. The presence of external Na (7.5-60 mM) inhibited the contracture induced by Ca (0.1 mM) in longitudinal muscle in a dose-dependent manner. In circular muscle, however, Na potentiated the initial speed of contracture induced by Ca (1 mM), and inhibited the height of contracture at 30 min showing maximum inhibition at 15 mM Na. Li instead of Na produced inhibition of Ca contractures in both muscle layers. Na-induced potentiation in circular muscle was markedly depressed by lowering the temperature, and was reduced by a high concentration (1 mM) of ouabain.These observations indicate that the Ca contracture in longitudinal and circular muscles differs and the effect of Na on this contracture may modulate Ca ion movements through the muscle membrane by inhibiting Ca influx in both muscle layers, and initially potentiating it in circular muscle in an ouabain-sensitive process.Ca entry to the smooth muscle is increased by substitution of isotonic sucrose for sodium in frog stomach (BOZLER, 1963), by reducing external Na in guinea pig taenia coli (GoODFORD and HERMANSEN, 1961) and in rabbit aorta (BRIGGS and MELVIN, 1961). These reports indicate that external Na affects Ca fluxes through the smooth muscle membrane. In K-depolarized vascular muscle, BIAMINO and JOHANSSON (1970) proposed that the presence of external Na increased both the initial speed and relaxation of Ca contracture, and they suggested that Na is more important for the removal of Ca from the contractile system than for supply to it. On the contrary, it has been reported that Na, added to the external solution, produced relaxation of sucrose-induced contraction in guinea pig ileum (JUDAH and WILLOUGHBY, 1974) and of Na-free contracture in guinea pig taenia

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“…The washout of Na into physiological saline at 37 0C can in larger arteries be split up into three phases (Garrahan, Villamil & Zadunaisky, 1965;Garay et al 1979), where phase 3 represents efflux from a very small compartment. We found, however, only two phases, probably because the method we have used is not sensitive enough to detect the third phase in the small vessels.…”

Section: Na Fluxesmentioning

confidence: 99%

Sodium metabolism in rat resistance vessels.

Aalkjær¹,

Mulvany²

1983

The Journal of Physiology

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SUMMARY1. Using 22Na we have investigated the Na metabolism in rat mesenteric resistance vessels (internal diameter about 200 tom).2. The intracellular Na content was determined by washing the vessels at 0 0C in saline with Li substituted for Na, and was related to smooth muscle volume determined from measurements of media thickness and internal diameter using light microscopy. On this basis an internal Na concentration of 13-7 mmol 1-1 cells was found.3. The efflux of Na into saline at 37 0C consists of two phases, a fast one and a slow one, where the slow phase was considered to be intracellular. It had a rate constant of 0 137 min-, which was decreased by 50 % if 1 mM-ouabain was added to or K withdrawn from the efflux medium.4. The gain of cell Na after addition of 1 mM-ouabain was much faster than would be expected from the decrease in efflux, indicating that 1 mM-ouabain increases the permeability to Na.

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Sodium exchange and distribution in the arterial wall

Cited by 52 publications

References 0 publications

Sodium flux and electrical activity of arterial smooth muscle

Sodium flux and electrical activity of arterial smooth muscle

Differences between Ca Contractures in the Depolarized Longitudinal and Circular Muscles of Guinea Pig Stomach

Sodium metabolism in rat resistance vessels.

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