Sodium flux and electrical activity of arterial smooth muscle

Keatinge, W. R.

doi:10.1113/jphysiol.1968.sp008401

Cited by 62 publications

(41 citation statements)

References 12 publications

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“…did not significantly reduce the content of slowly lost 45Ca in experiments in which the calcium concentration was maintained constant throughout, amethocaine did not hinder the uptake of 45Ca due to exchange with unlabelled calcium but reduced the net uptake of calcium into a calcium-depleted aorta. The uptake of calcium into a calcium-depleted aorta probably involves not only the smooth muscle but also the connective tissue of the wall (Keatinge, 1968). It was therefore necessary to determine the effect of amethocaine on the uptake of 45Ca into connective tissue.…”

Section: Resultsmentioning

confidence: 99%

The effect of drugs on the constriction of isolated depolarized blood vessels in response to calcium or barium

Northover

1968

British J Pharmacology

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1. The rat isolated anterior mesenteric artery was perfused at a constant rate with a calcium-free depolarizing solution. Injection close to the cannula of 0.05-0.1 ml. of solutions of CaCI2 (117 mM) or BaCl2 (100 mM) caused a rise in perfusion pressure.2. The responses to injected CaClI solution could be obtained repeatedly but those to successive injections of BaCl2 solution slowly declined. When the responsiveness to barium had almost disappeared, it could be restored by the addition to the perfusing fluid of a small amount of calcium (0.05 mM).3. The contractile effects of calcium or barium were antagonized by the addition to the perfusing fluid of several anti-inflammatory substances, certain local anaesthetics and certain spasmolytic drugs. 4. Perfusion of the mesenteric artery with a depolarizing solution containing 0.2 mM-CaCl2 caused a persistent rise of the perfusion pressure. This was rapidly and completely reversed by the addition of indomethacin (4 mg/100 ml.) or cinchocaine hydrochloride (2 mgf 00 ml.) to the perfusing fluid.5. The uptake of 45Ca by rat aorta depleted of calcium was reduced by amethocaine hydrochloride (10 mg/ 100 ml.) or cinchocaine hydrochloride (2 mg/100 ml.) but not by indomethacin (10 mg/100 ml.) or desipramine hydrochloride (1 mg/100 ml.).Ringer (1883) first showed that cardiac muscle requires calcium ions for contraction. Since then it has been shown that almost all types of muscle require calcium for contraction. It is now generally agreed that calcium ions are the link between excitation of the muscle cell surface and shortening of the contractile proteins within the cell. The very extensive literature on this subject has been reviewed by Shanes

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Section: Resultsmentioning

confidence: 99%

The effect of drugs on the constriction of isolated depolarized blood vessels in response to calcium or barium

Northover

1968

British J Pharmacology

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“…In addition, a certain amount of cellular Na+ of smooth muscles is also contained in compartment C. In consequence, in whole arteries the cellular Na+ corresponds to the addition of both B and C, where a part of C is given by the Na+ contained in fibroblasts and endothelial cells, and only B is contained exclusively in smooth muscle cells. Keatinge (1968) studied the24Na efflux from sheep carotid arteries. He identified only two exponential components on the basis of a washout curve lasting 60 min.…”

Section: Discussionmentioning

confidence: 99%

Identification of different sodium compartments from smooth muscle cells, fibroblasts and endothelial cells, in arteries and tissue culture

Garay

Moura

Osborne-Pellegrin

et al. 1979

The Journal of Physiology

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SUMMARY1. The 22Na efflux curve from the rat tail artery, at 35 0C, can be analysed as the sum of three distinct components, from 0 to 90 min of washout. After an initial diffusional component the two late exponential components Be-kBt and Ce-ket have the following values: B = 3-03 + 0-15 m-mole/kg wet wt. and C = 0-56 + 0-04; kB = 0-145 + 0-005 min-and kc = 0-015 + 0-007.2. In order to identify the cellular origin of the different compartments we compared the 22Na efflux curve from the rat tail artery with the curves obtained from whole rabbit aortal strips, rabbit aortal medial or adventitial strips; and primary cultures from rabbit aorta medial smooth muscle cells, cultures of a non-fusing muscle cell line (BC3H1), libroblasts and endothelial cells. 4. The efflux from compartment B of smooth muscle cells is inhibited by ouabain and in the absence of extracellular K+. The efflux from compartment C is inhibited only by ouabain but not by the suppression of extracellular K+.5. We propose a distribution of Na+ in smooth muscle cells in two intracellular compartments: (1) Na+ freely dissolved in the sarcoplasm, exchanging with the kinetics of compartment B and (2) a second cellular compartment which could be contained in the sarcoplasmic reticulum exchanging with the kinetics of compartment C.* To whom correspondence and reprint requests should be sent. R. P. GARA Y AND OTHERS 6. On the basis of the previous model of Na+ distribution, considering our values, and without any correction, the estimated sarcoplasmic concentration of Na+ is 9-6 mm, compatible with the direct measurements obtained in skeletal and heart muscle. The Na+ concentration in the sarcoplasmic reticulum would be 4-10 times higher than in the cytoplasm. In order to increase the accuracy of our calculations it would be necessary to account for the interdiffusion and back diffusion of Na+ between compartments. It is not possible to attain this goal at the present time.

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“…This is approximately the space constant of these strips at rest (Graham & Keatinge, 1975;Mekata & Keatinge, 1975) and therefore close to the optimum for the 'node' in a double sucrose-gap (McGuigan & Tsien, 1974). The segment of artery in the centre chamber, assuming a thickness of 302 ,um (Keatinge, 1966) will, therefore, have contained 822 mm2 cell membrane (Keatinge, 1968b); this figure was used to relate currents and conductances to area of cell membrane throughout the present paper. Each sucrose section was 8 mm long.…”

Section: Arteries and Recording Methodsmentioning

confidence: 99%

Mechanism of slow discharges of sheep carotid artery.

Keatinge¹

1978

The Journal of Physiology

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5. When procaine was added, or Ca replaced by Mn or Mg, conductance was lower both at rest and on depolarization, and the increase on depolarization often underwent slow inactivation which it never did in simple Ca containing solutions.6. The results indicate that a slowly inactivated inward current dependent on Ca, Mn or Mg was largely responsible for the slow discharges, and that procaine, Mn or Mg assisted the discharges by reducing the normal rapid outward-rectifying K conductance and allowing it to inactivate on prolonged depolarization.

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Sodium flux and electrical activity of arterial smooth muscle

Cited by 62 publications

References 12 publications

The effect of drugs on the constriction of isolated depolarized blood vessels in response to calcium or barium

The effect of drugs on the constriction of isolated depolarized blood vessels in response to calcium or barium

Identification of different sodium compartments from smooth muscle cells, fibroblasts and endothelial cells, in arteries and tissue culture

Mechanism of slow discharges of sheep carotid artery.

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