Evidence for suppression of potassium conductance by noradrenaline in smooth muscle of guinea-pig vas deferens.

Wakui, Makoto; Fukushi, Yasuo

doi:10.1620/tjem.150.365

Cited by 3 publications

(2 citation statements)

References 13 publications

(15 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We had shown that NA-induced depolarization was mostly due to the reduction of K+ conductance (Wakui and Inomata 1985;Wakui and Fukushi 1986) and now it was demonstrated that the kinetics of NA-induced depolarization coincided with that of the muscle contraction reflecting cytoplasmic Ca2+ concentration (Fig. 1).…”

Section: Discussionmentioning

confidence: 73%

“…In previous reports (Wakui and Inomata 1985;Wakui and Fukushi 1986), we suggested that through a-adrenergic receptor activation, noradrenaline (NA) reduced the K+ conductance and consequently induced the membrane depolarization in smooth muscle of the guinea-pig vas deferens. This hypothesis has been supported by the following evidence in the experiments using the double sucrosegap method : 1) The NA-induced depolarization is associated with a reduction in the membrane conductance.…”

mentioning

confidence: 94%

See 1 more Smart Citation

Possible relationship between the release of calcium ions and inactivation of the potassium conductance induced by noradrenaline in smooth muscle of the Guinea-pig vas deferens.

Wakui

Fukushi

1986

Tohoku J. Exp. Med.

Self Cite

View full text Add to dashboard Cite

In order to examine whether any change in cytoplasmic Ca2+ concentration occurs during the noradrenaline (NA)-induced change in the membrane potential, the isometric tension of smooth muscle of the guinea-pig vas deferens was recorded together with membrane potentials using the sucrose-gap method. NA induced a depolarization and an increase in cytoplasmic Ca2+ comprising two (initial and second) phases. In time courses, the depolarization and the second phase of the increase in cytoplasmic Ca2+ were similar. Only at the phase around the onset of the depolarization, the membrane conductance was increased but then, it was decreased. Lowering the external Ca2+ concentration and application of D600 suppressed all of the NA-induced responses. In addition, D600 diminished the size of the NA-induced decrement in the membrane conductance. The present results suggest that the initial phase of the increase in the cytoplasmic Ca2+ is due to the influx of Ca2+ and the second phase, probably to the release of Ca2+ from some intracellular stores. It was discussed that the release of Ca2+ might occur at the internal surface of the membrane, and the membrane might be left less permeable to K+ as a result.noradrenaline ; D600; Ca release ; K inactivation ; guinea-pig vas deferensIn previous reports (Wakui and Inomata 1985; Wakui and Fukushi 1986), we suggested that through a-adrenergic receptor activation, noradrenaline (NA) reduced the K+ conductance and consequently induced the membrane depolarization in smooth muscle of the guinea-pig vas deferens. This hypothesis has been supported by the following evidence in the experiments using the double sucrosegap method : 1) The NA-induced depolarization is associated with a reduction in the membrane conductance. 2) The reversal potential of the NA-induced depolarization is negative to the resting membrane potential. 3) The reversal

show abstract

Section: Discussionmentioning

confidence: 73%

mentioning

confidence: 94%

Possible relationship between the release of calcium ions and inactivation of the potassium conductance induced by noradrenaline in smooth muscle of the Guinea-pig vas deferens.

Wakui

Fukushi

1986

Tohoku J. Exp. Med.

Self Cite

View full text Add to dashboard Cite

show abstract

Excitatory and inhibitory actions of norepinephrine on the Ba2+ current through L-type Ca2+ channels of smooth muscle cells of guinea-pig vas deferens

et al. 1996

View full text Add to dashboard Cite

The effect of norepinephrine (NE) was examined on the whole-cell Ba2+ current through L-type Ca2+ channels of freshly isolated smooth muscle cells of guinea-pig vas deferens. The magnitude of maximum Ba2+ current [1Ba(max)] varied in different cells, although the capacitance of the cell membrane was similar (approximately 50 pF). Application of dbcAMP augmented 1Ba(max) by 37%, which was canceled by Rp-cAMPs, while PMA decreased the current by 32%, which was canceled by staurosporine. NE increased 1Ba(max) of the cells which originally showed relatively small 1Ba(max), and decreased the current of the cells which showed larger 1Ba(max). In the presence of phentolamine, NE increased 1Ba(max), and this effect was remarkable in cells showed smaller 1Ba(max). In the presence of propranolol, NE decreased 1Ba(max). The excitatory beta-adrenoceptor activation was canceled by Rp-cAMPs, and the inhibitory alpha-adrenoceptor effect was canceled by staurosporine. It is suggested that NE shows dual (excitatory and inhibitory) actions on the L-type Ca2+ channels of smooth muscle of guinea-pig vas deferens. The excitatory beta-adrenoceptor action mediated through cAMP/PKA is predominant in cells with lower density of the Ca2+ channels, while inhibitory alpha-adrenoceptor action mediated through PKC is predominant in cells with higher channel density.

show abstract

Biophysical Mechanisms of Vaginal Smooth Muscle Contraction: The Role of the Membrane Potential and Ion Channels

Mahapatra,

Kumar

2024

Pathophysiology

View full text Add to dashboard Cite

The vagina is an essential component of the female reproductive system and is responsible for providing female sexual satisfaction. Vaginal smooth muscle contraction plays a crucial role in various physiological processes, including sexual arousal, childbirth, and urinary continence. In pathophysiological conditions, such as pelvic floor disorders, aberrations in vaginal smooth muscle function can lead to urinary incontinence and pelvic organ prolapse. A set of cellular and sub-cellular physiological mechanisms regulates the contractile properties of the vaginal smooth muscle cells. Calcium influx is a crucial determinant of smooth muscle contraction, facilitated through voltage-dependent calcium channels and calcium release from intracellular stores. Comprehensive reviews on smooth muscle biophysics are relatively scarce within the scientific literature, likely due to the complexity and specialized nature of the topic. The objective of this review is to provide a comprehensive description of alterations in the cellular physiology of vaginal smooth muscle contraction. The benefit associated with this particular approach is that conducting a comprehensive examination of the cellular mechanisms underlying contractile activation will enable the creation of more targeted therapeutic agents to control vaginal contraction disorders.

show abstract

Evidence for suppression of potassium conductance by noradrenaline in smooth muscle of guinea-pig vas deferens.

Cited by 3 publications

References 13 publications

Possible relationship between the release of calcium ions and inactivation of the potassium conductance induced by noradrenaline in smooth muscle of the Guinea-pig vas deferens.

Possible relationship between the release of calcium ions and inactivation of the potassium conductance induced by noradrenaline in smooth muscle of the Guinea-pig vas deferens.

Excitatory and inhibitory actions of norepinephrine on the Ba2+ current through L-type Ca2+ channels of smooth muscle cells of guinea-pig vas deferens

Biophysical Mechanisms of Vaginal Smooth Muscle Contraction: The Role of the Membrane Potential and Ion Channels

Contact Info

Product

Resources

About