The Effect of Adrenergic Drugs on Spontaneously Active Vascular Smooth Muscle Studied by Long-Term Intracellular Recording of Membrane-Potential

Loh, D. v.

doi:10.1159/000157889

Cited by 9 publications

(3 citation statements)

References 6 publications

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“…Our present findings must be reconciled with reports of others indicating that in some tissues isoprenaline can decrease the rate of calcium influx (Meisheri & Van Breemen, 1982), increase the rate ofcalcium uptake into microsomes (Baudouin-Legros & Meyer, 1973;Webb & Bhalla, 1976), or hyperpolarize the cell membrane and decrease electrical spike activity (Somlyo et al 1970;von Loh, 1971;Yamaguchi et al 1982;Prehn & Bevan 1983). All of these effects would be expected to cause a decrease in cytoplasmic [Ca2+].…”

Section: Discussionsupporting

confidence: 79%

“…Considerable controversy surrounds the mechanism of action of the vasodilators, J. P. MORGAN AND K. G. MORGAN especially with respect to the agents reported to cause changes in cytoplasmic cyclic AMP levels. Several laboratories have reported that isoprenaline causes a hyperpolarization of the vascular smooth muscle cell membrane (Somlyo, Haeusler & Somlyo, 1970;von Loh, 1971; Yamaguchi, Honeyman & Fay, 1982;Prehn & Bevan, 1983). However, tissues depolarized by very high [K+] can still be relaxed by isoprenaline (Meisheri & Van Breemen, 1982) even though there is no change in membrane potential (Somlyo et al 1970) and relaxation can be obtained at concentrations of isoprenaline which cause no change in membrane potential (Ito, Kitamura & Kuriyama, 1980).…”

Section: Introductionmentioning

confidence: 99%

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Alteration of cytoplasmic ionized calcium levels in smooth muscle by vasodilators in the ferret.

Morgan¹,

Morgan²

1984

The Journal of Physiology

154

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SUMMARY1. Aequorin was used as an indicator of cytoplasmic Ca2+ levels during the action of vasodilators in potassium-depolarized strips of ferret portal vein.2. Moderate concentrations of isoprenaline produced either no change or an increase in cytoplasmic Ca2+ levels during smooth muscle relaxation. Only in the presence of very high concentrations of isoprenaline (greater than 10-4 M) was a decrease in intracellular Ca2+ levels detectable.3. Both papaverine and forskolin also caused relaxations of the muscle while cytoplasmic Ca2+ levels were observed either not to change or to increase.4. When the muscles were relaxed either by decreasing the calcium concentration in the bathing medium or by the addition of sodium nitroprusside, light and force fell together.5. The ratio of force to light was greater when the muscle was relaxed with calcium depletion than with the addition of sodium nitroprusside, indicating that sodium nitroprusside was relaxing the muscle by more than just decreasing cytoplasmic Ca2+ levels.6. These results indicate that not all vasodilators cause a lowering of cytoplasmic Ca2+ levels and indicate that, in intact cells, agents associated with increases in cytoplasmic cyclic AMP levels can cause an uncoupling of calcium-force relations.

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Section: Discussionsupporting

confidence: 79%

Section: Introductionmentioning

confidence: 99%

Alteration of cytoplasmic ionized calcium levels in smooth muscle by vasodilators in the ferret.

Morgan¹,

Morgan²

1984

The Journal of Physiology

154

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“…In the guinea-pig portal vein, exogenously applied noradrenaline depolarized the membrane and increased the frequency of spike discharges (von Loh, 1971). Figure 2 shows effects of amosulalol (10-8 10-6M) on electrical responses produced by exogenously applied noradrenaline (10-7M) in the guinea-pig portal vein.…”

Section: Introductionmentioning

confidence: 99%

Effects of amosulalol on the electrical responses of guinea‐pig vascular smooth muscle to adrenoceptor activation

Fujioka

Suzuki

1985

British J Pharmacology

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1The effects of amosulalol, a newly synthesized sulphonamide-substituted phenylethylamine derivative, on electrical responses of smooth muscle cells of the guinea-pig vascular tissues to noradrenaline, isoprenaline and perivascular nerve stimulation were investigated. 2 Amosulalol (10--10-M) did not alter the resting membrane potential of smooth muscle cells of the mesenteric artery, the mesenteric vein, the main pulmonary artery and the portal vein. 3 In the mesenteric artery, main pulmonary artery and portal vein, but not in the mesenteric vein, membrane depolarizations produced by noradrenaline were antagonized by amosulalol. 4 In the portal vein, membrane hyperpolarizations produced by isoprenaline were antagonized by amosulalol. 5 In the mesenteric artery, amosulalol (over 10-6M) enhanced the amplitude of excitatory junction potentials (ej.ps) produced by perivascular nerve stimulation. 6 Amosulalol antagonized the noradrenaline-induced decrease in the ej.p. amplitude; this effect was much weaker than that of phentolamine. Amosulalol also antagonized the isoprenaline-induced enhancement of the ej.p. amplitude. 7 In the mesenteric vein, the slow depolarizations produced by perivascular nerve stimulation were depressed by amosulalol (over 10-6M), but the effect was much weaker than that of prazosin, yohimbine or phentolamine. 8 Actions of amosulalol on electrical properties of vascular tissues can be summarized as follows:amosulalol blocks a,-and P-adrenoceptors. It also blocks a2-adrenoceptors, though weakly.

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Seasonal variation in responses of the toad renal vasculature to adrenaline

Morris

1982

Naunyn-Schmiedeberg's Arch. Pharmacol.

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Adrenaline and noradrenaline produced both constriction and dilatation of the toad renal vasculature: constrictor effects were mediated by alpha-adrenoceptors; dilator effects were mediated by beta-adrenoceptors. Vasoconstriction was the predominant response to these amines. Dilatation was only revealed after blockade of alpha-adrenoceptors and constriction of the vasculature. There was a marked seasonal variation in the constrictor responses to adrenaline, but not to noradrenaline. The maximal increase in renal vascular resistance produced by adrenaline in summer was greater, by a factor of three, than the maximum constrictor response in winter. The response to adrenaline in summer was also significantly greater than the responses to noradrenaline in both summer and winter. However, after treatment with propranolol there was no difference between the maximum vasoconstrictions to these two amines, in summer or in winter. Determination of dissociation constants for phentolamine indicated that adrenaline and noradrenaline acted on the same population of alpha-adrenoceptors in both summer and winter. The enhanced vasoconstriction to adrenaline in summer appears to be due to a reduced potency of adrenaline on renal vascular beta-adrenoceptors. The reduction in potency may be caused by a subtle configurational change in the beta-adrenoceptors, perhaps induced by hormonal changes associated with the onset of breeding.

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The Effect of Adrenergic Drugs on Spontaneously Active Vascular Smooth Muscle Studied by Long-Term Intracellular Recording of Membrane-Potential

Cited by 9 publications

References 6 publications

Alteration of cytoplasmic ionized calcium levels in smooth muscle by vasodilators in the ferret.

Alteration of cytoplasmic ionized calcium levels in smooth muscle by vasodilators in the ferret.

Effects of amosulalol on the electrical responses of guinea‐pig vascular smooth muscle to adrenoceptor activation

Seasonal variation in responses of the toad renal vasculature to adrenaline

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