Effects of Extracellular Calcium and of Calcium Antagonists on the Contractile Responses of Isolated Human Pial and Mesenteric Arteries

  title={Effects of Extracellular Calcium and of Calcium Antagonists on the Contractile Responses of Isolated Human Pial and Mesenteric Arteries},
  author={Lennart Brandt and Karl Erik Andersson and Lars Edvinsson and Bengt Ljunggren},
  journal={Journal of Cerebral Blood Flow \& Metabolism},
  pages={339 - 347}
In isolated human pial arteries (diameter 0.4–0.5 mm), contractions were produced by potassium, noradrenaline, serotonin, and prostaglandin F2α. For comparison, experiments were also performed on human mesenteric arteries. Threshold concentration for potassium-induced contraction in pial arteries was about 10 mm; in mesenteric arteries it was 3–5 mm higher. In pial arteries the calcium antagonists nifedipine and nimodipine caused an almost complete relaxation of contractions induced by… 

Cellular Calcium and the Contraction Induced by Prostaglandin F2α in Feline Cerebral Arteries

The present findings strongly support previous suggestions that a major part of the PGF2 alpha-induced contraction in calcium-free medium is mediated via the release of calcium bound to the exterior aspect of the cell membrane.

Effects of Extracellular Calcium and of the Calcium Entry Blockers Flunarizine and Nimodipine on Contractile Responses in Human Temporal Arteries

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in vitro Effects of Calcium Antagonists PN 200-110, Nifedipine, and Nimodipine on Human and Canine Cerebral Arteries

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  • Medicine, Chemistry
    Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
  • 1983
The results suggest that due to its potent calcium-blocking activity on cerebral arteries, PN 200–110 might be of value for the prevention and treatment of cerebrovascular spasms following subarachnoid hemorrhage.

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An acute reduction in potassium conductance in cerebrovascular smooth muscle produced by TEA has complex, concentration-dependent effects and reproduces only part of the spectrum of effects of cisternal injection of blood on cerebroVascular reactivity.

Comparison of the calcium entry blockers nimodipine and flunarizine on human cerebral and temporal arteries: role in cerebrovascular disorders

Both calcium entry blockers induced a parallel shift in calcium-induced contraction studied by application of calcium to vessels preincubated in calcium free medium, and flunarizine was more potent on cerebral than on temporal arteries and there was no difference between the two vessels in this action of nimodipine.



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Isometric tension was recorded in ring preparations of human peripherial arteries and veins contracted by potassium (127mM) and noradrenaline (1.8 X 10(-5)M). In the veins, nifedipine had a marked

Cerebral arterial spasm: part 9. In vitro effects of nifedipine on serotonin-, phenylephrine-, and potassium-induced contractions of canine basilar and femoral arteries.

A relatively selective effect of nifedipine on the basilar artery is demonstrated, and a mechanism to explain this selective effect is postulated.

Contractile effects of prostaglandin F2alpha on isolated human peripheral arteries and veins.

It is suggested that PGF2alpha induces contraction both by enhancing the transmembrane flow of calcium, and by facilitating release of calcium from intracellular stores.

Evidence for Greater Susceptibility of Isolated Dog Cerebral Arteries to Ca Antagonists than Peripheral Arteries

Dog cerebral arteries contracted with PGF2α, one of endogenous rasospastic substances, are more susceptible to agents which interfere with the influx of Ca++ across cell membranes than coronary and mesenteric arteries; these agents may thus be of value in the treatment and prophylaxis of cerebral vasospasm.

On the roles of calcium ion during potassium induced contracture in the smooth muscle cells of the rabbit main pulmonary artery.

It is postulated that the mechanical response of the pulmonary artery induced by excess K is mainly due to influx of Ca++ and the depolarization plays only a minor role, which means that release of stored Ca by depolarized is not an essential factor in generation of K-induced contracture in this tissue.

Effect of a calcium antagonist on experimental constriction of human brain vessels.

It is suggested that calcium antagonists might be of value in the treatment of cerebrovascular spasm following a subarachnoid hemorrhage.

Correlated Electrical and Mechanical Responses of Isolated Rabbit Pial Arteries to Some Vasoactive Drugs

A high degree of correlation between membrane electrical events and mechanical activity of these spontaneously-active myovascular cells is demonstrated to demonstrate the presence of receptors to these agents in pial arteries.

Calcium antagonistic drugs. Mechanism of action.

The results suggest that calcium antagonistic drugs act by other mechanisms than the inhibition of transmembranous Ca flux, probably on the release and binding of Ca2+ in intracellular pools.

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  • A. SomlyoA. Somlyo
  • Biology, Medicine
    The Journal of pharmacology and experimental therapeutics
  • 1968
The existence of two major electrophysiologic types of vascular smooth muscle, one gradedly responsive and the other producing repetitive action potentials, is suggested.

Electro- and pharmacomechanical coupling in the smooth muscle cells of the rabbit ear artery

A comparison of tension development and 45Ca release induced by noradrenaline in Ca-free medium suggests that Ca extrusion could be very efficient in the rabbit ear artery and that it could play a direct role in its relaxation.