The action of noradrenaline on single smooth muscle cells freshly dispersed from the guinea‐pig pulmonary artery

Byrne, N.G.; Large, William

doi:10.1111/j.1476-5381.1987.tb08986.x

Cited by 13 publications

(5 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It has been postulated that the noradrenalineinduced depolarization in whole tissue preparations is mediated by the suppression of a potassium conductance in guinea-pig mesenteric vein (Suzuki, 1981) and pulmonary artery (Suzuki, 1986). In contrast, only an increase in membrane conductance to a-adrenoceptor activation has been observed in isolated cells of rabbit portal vein (present work), guinea-pig pulmonary artery (Byrne & Large, 1987a) and rat anococcygeus muscle (Byrne & Large, 1987b). Previously (Byrne & Large, 1987a) it was argued that this discrepancy might represent difficulties in studying agonist-induced membrane mechanisms in whole tissue syncytial preparations as discussed above.…”

Section: Discussioncontrasting

confidence: 50%

“…In contrast, only an increase in membrane conductance to a-adrenoceptor activation has been observed in isolated cells of rabbit portal vein (present work), guinea-pig pulmonary artery (Byrne & Large, 1987a) and rat anococcygeus muscle (Byrne & Large, 1987b). Previously (Byrne & Large, 1987a) it was argued that this discrepancy might represent difficulties in studying agonist-induced membrane mechanisms in whole tissue syncytial preparations as discussed above. Another explanation was that different mechanisms might be activated depending on whether noradrenaline is bath applied (e.g.…”

Section: Discussioncontrasting

confidence: 50%

“…There are a number of similarities between the depolarizations to ao-adrenoceptor activation seen in isolated cells of rabbit portal vein and the depolarizations observed to x-adrenoceptor stimulation in dispersed cells of the guinea-pig pulmonary artery (Byrne & Large, 1987a) and the rat anococcygeus muscle (Byrne & Large, 1987b, c). Firstly, there is a characteristic latency of 0.5-1.Os between the ionophoretic application of noradrenaline and the onset of response.…”

Section: Discussionmentioning

confidence: 93%

See 2 more Smart Citations

Mechanism of action of α‐adrenoceptor activation in single cells freshly dissociated from the rabbit portal vein

Byrne

Large

1988

British J Pharmacology

Self Cite

View full text Add to dashboard Cite

1 The action of noradrenaline was studied in freshly dispersed cells of the rabbit portal vein using microelectrode techniques. 2 In normal physiological salt solution, the ionophoretic application of noradrenaline evoked an a-adrenoceptor-mediated depolarization and sometimes a P-adrenoceptor-mediated hyperpolarization. Experiments were carried out in the presence of propranolol to study the membrane mechanism associated with a-adrenoceptor activation. 3 In the current clamp mode of recording, the equilibrium potential of the noradrenaline-evoked depolarization was -1.9 mV. The depolarization was brought about by an increase in membrane conductance. 4 Under voltage clamp conditions, noradrenaline produced an inward current with a reversal potential of -7 + 3 mV (mean + s.e. mean). 5 The relationship between the noradrenaline-induced inward current and clamp potential was non-linear. Depolarization enhanced the conductance elicited by noradrenaline. 6 Evidence is presented which suggests that an additional conductance mechanism (probably an increase in potassium conductance) is also evoked by a-adrenoceptor stimulation in dispersed cells of rabbit portal vein.

show abstract

Section: Discussioncontrasting

confidence: 50%

Section: Discussioncontrasting

confidence: 50%

Section: Discussionmentioning

confidence: 93%

See 1 more Smart Citation

Mechanism of action of α‐adrenoceptor activation in single cells freshly dissociated from the rabbit portal vein

Byrne

Large

1988

British J Pharmacology

Self Cite

View full text Add to dashboard Cite

show abstract

“…In the dispersed cells from the guinea-pig pulmonary artery, ionophoretic application of noradrenaline depolarized the membrane at 20-23 °C [17]. However, the depolarization was not always observed and the degree of depolarization usually declined on repeated application of noradrenaline.…”

Section: Catecholaminementioning

confidence: 99%

Ionic channels in smooth muscle studied with patch-clamp methods.

Tomita

1988

Jpn.J.Physiol

View full text Add to dashboard Cite

“…There are several studies concerning the action of catecholamines on membrane currents in dispersed single cells from blood vessels (guinea-pig pulmonary artery: Byrne & Large, 1987;rabbit portal vein: Byrne & Large, 1988;rat portal vein;Pecaud et al, 1987; rabbit ear artery; Benham & Tsien, 1988;Droogmans et al, 1987). However, no consistent results have been obtained.…”

Section: Introductionmentioning

confidence: 99%

Increase in calcium channel current by β‐adrenoceptor agonists in single smooth muscle cells isolated from porcine coronary artery

Fukumitsu

Hayashi

Tokuno

et al. 1990

British J Pharmacology

View full text Add to dashboard Cite

1 The action of catecholamines (isoprenaline and noradrenaline) and forskolin on membrane currents was studied in single cells freshly dispersed from the pig coronary artery by use of the whole-cell clamp method, usually with electrodes containing CsCl. 2 In normal Krebs solution, with and without 30mM tetraethylammonium (TEA) and 0.5 mm 4-aminopyridine, isoprenaline (1-5 uM) clearly increased the inward currents elicited by membrane depolarization, without affecting the holding current at -80 mV. The same effect was observed when the external Cl-was replaced with isethionate. The outward current recorded with K+-containing electrodes was not significantly affected by isoprenaline. 3 In the presence of 67 mm Ba2+ and 30 mm TEA, the maximum inward current recorded with CsCl containing electrodes was 119 + 7 pA (the mean + s.e.mean, n = 90) in cells where the current was larger than 30 pA. The L-type Ca2+ channel was considered to be responsible for these currents, based on the threshold voltage, the slow time course of decay, the large depolarization necessary to produce inactivation, and the high susceptibility to the Ca2 + channel antagonist, nicardipine.4 Isoprenaline and noradrenaline increased the amplitude of inward currents evoked by depolarizing pulses. The maximum inward current was potentiated by 43 + 7% (n = 12) by isoprenaline and 39 + 10% by noradrenaline (n = 6) at a concentration of 1 IM. These effects were strongly inhibited by propranolol, but not phentolamine. Forskolin (1OpM) also potentiated the currents to a similar degree.5 It is suggested that stimulation of f3-adrenoceptors increases the amplitude of inward currents through L-type Ca2 + channels in the pig coronary artery and that intracellular cyclic adenosine monophosphate is likely to be inolved in this action.

show abstract

The action of noradrenaline on single smooth muscle cells freshly dispersed from the guinea‐pig pulmonary artery

Cited by 13 publications

References 21 publications

Mechanism of action of α‐adrenoceptor activation in single cells freshly dissociated from the rabbit portal vein

Mechanism of action of α‐adrenoceptor activation in single cells freshly dissociated from the rabbit portal vein

Ionic channels in smooth muscle studied with patch-clamp methods.

Increase in calcium channel current by β‐adrenoceptor agonists in single smooth muscle cells isolated from porcine coronary artery

Contact Info

Product

Resources

About