Effects of drugs on depolarized plain muscle

Evans, D. H. L.; Schild, H. O.; Thesleff, S.

doi:10.1113/jphysiol.1958.sp006072

Cited by 191 publications

(97 citation statements)

References 10 publications

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“…Vascular smooth muscle ceases to respond to constrictor agents in the absence of calcium (Evans, Schild & Thesleff, 1958;Briggs & Melvin, 1961;Bohr & Goulet, 1961;Briggs, 1962;Waugh, 1962;Hinke, Wilson & Burnham, 1964;Cuthbert & Sutter, 1965;Axelsson, Johansson, Jonsson & Wahlstrom, 1966;Briggs & Shibata, 1966;Shibata & Briggs, 1966;Alexander, 1967;Burks, Whitacre & Long, 1967;Northover, 1967a;Shibata & Carrier, 1967;Hudgins & Weiss, 1968). Several of these reports also mention that calcium ions cause constriction of depolarized blood vessels.…”

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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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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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“…The consequent block of the spike generation then results in the relaxation of the muscle, in the manner proposed by JENKINSON and MORTON (1967a). On the other hand, acetylcholine might increase Na-, K-and Ca-permeabilities of the depolarized membrane (EVANS, SCHILD and THESLEFF, 1958;DURBIN and JENKINSON, 1961;SCHILD, 1964;JENKIN-SON and MORTON, 1967b). If the relaxation of the tonic response is not related to the ionic permeability of the membrane, isoprenaline might either reduce the free Ca ion in the myoplasm or inactivate the contractile process by some unknown means.…”

Section: Resultsmentioning

confidence: 99%

Effects of Noradrenaline and Isoprenaline on the Electrical and Mechanical Activities of Guinea Pig Depolarized Taenia Coli

Magaribuchi

Kuriyama²

1972

Jpn.J.Physiol

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Summary The effects of noradrenaline and isoprenaline on the electrical and mechanical properties of depolarized smooth muscle of the guinea pig taenia coli were investigated by the double sucrose gap method. 1. Noradrenaline (10-7-10-5 g/ml) decreased the membrane resistance at any given concentration of excess K ion. When increased K ion concentration accelerated the spike discharges, noradrenaline blocked the spike generation as a result of the consequent reduction in membrane resistance, thus causing relaxation. When the excess K ion depolarized the muscle and no spike generation was observed due to depolarization block, noradrenaline no longer caused relaxation of the tissue. Phentolamine (10-5 g/ml) completely blocked the effect of noradrenaline. 2. Acetylcholine (10-5 g/ml) and noradrenaline (10-5 g/ml) reduced the membrane resistance and blocked the spike generation to the same extent in 59 mm K-Krebs solution. However, acetylcholine enhanced and noradrenaline reduced the contraction. 3. Isoprenaline (10-7-10-5 g/ml) reduced the tonic response of the contraction without any marked changes in the membrane resistance, membrane potential and membrane activity, at any given concentration of excess K ion. 4. Isoprenaline (10-7-10-5 g/ml) did not reduce the tonic response evoked by excess K ion in Na-free solution. It is suggested that external Na ion might be important for the reduction of the internal free Ca ion concentration. In the Cl-deficient (C6H5S0O3), excess K+ condition, isoprenaline again had no effect on the depolarized muscle. 5. When Ca ion in the excess K-Krebs solution was replaced by Sr and Ba ions, the effect of isoprenaline on the tonic response was markedly suppressed. 6. Ouabain (10-5-10-4 g/ml) reduced the membrane resistance and the tonic response evoked by excess K+ (below 59 mm) solution. In

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“…It was found that amnion tissue-incubated for 2 hr with 10-2 M Mipafox at 370 C showed an intensity of staining comparable to tissue which had been incubated in 10' M dyflos under the same conditions. DISCUSSION Evans, Schild & Thesleff (1958) and Ferguson (1940) have previously reported the effects of acetylcholine on the chick amnion and the antagonism of acetylcholine by atropine. A pA2 value of 8.8 for acetylcholine-atropine antagonism was obtained by Evans & Schild (1959) on the amnion, which agrees well with the value for other smooth-muscle tissues.…”

Section: Resultsmentioning

confidence: 99%

Actions of Some Anticholinesterases on the Smooth Muscle of the Chick Amnion

Cuthbert

1962

British Journal of Pharmacology and Chemotherapy

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The actions of both reversible and irreversible anticholinesterase drugs on the nerve-free smooth muscle of the chick amnion are described. The tertiary compound physostigmine and the irreversible inhibitor diisopropylfluorophosphonate were found to be active in causing contractions, whereas the quaternary compound neostigmine and the irreversible inhibitor Mipafox were only slightly active in this respect. Manometric studies showed that all four compounds were highly active, however, in inhibiting the cholinesterase found in the chick amnion. The effects produced by these compounds in the organ bath are thought to be due to the accumulation of endogenously produced acetylcholine within the tissue. Evidence for an intracellular action of endogenously produced acetylcholine in the smooth muscle of the chick amnion is discussed.

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Effects of drugs on depolarized plain muscle

Cited by 191 publications

References 10 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

Effects of Noradrenaline and Isoprenaline on the Electrical and Mechanical Activities of Guinea Pig Depolarized Taenia Coli

Actions of Some Anticholinesterases on the Smooth Muscle of the Chick Amnion

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