A role for Q type Ca<sup>2+</sup> channels in neurotransmission in the rat urinary bladder

Frew, Robert; Lundy, Paul M.

doi:10.1111/j.1476-5381.1995.tb16378.x

Cited by 37 publications

(26 citation statements)

References 21 publications

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“…However, the residual contraction can be abolished by og-contoxin-MVIIC and co-agatoxin-IVA, blockers of P-and Q-type channels [19,20]. Interestingly, this study suggested that the cholinergic component of contraction was largely abolished .by N-type Ca 2+ channel inhibition, whereas the purinergic component was dependent largely on P and Q-type Ca 2+ channels.…”

Section: Ca 2+ Channels In Detrusor Smooth Musclementioning

confidence: 70%

Electrophysiological properties of the bladder

Fry

Sui

1998

Int Urogynecol J

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The electrophysiological properties of detrusor smooth muscle are described, in particular with regard to their influence on the contractile properties of the tissue. The Ca2+ and K+ channel activities are most important in generating action potentials, but the role of several other ionic currents is described, including Cl-, Ca2+-activated, stretch-activated and ligand-gated channels. The variable appearance and functions of different ionic currents in disease states is discussed, as well as the question of whether electrical activity can transmit between adjacent smooth muscle cells. In addition, the precise role that electrophysiological phenomena play in the regulation of the contractile state of the smooth muscle cells, as well as the generation of bladder electromyograms, is discussed.

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Section: Ca 2+ Channels In Detrusor Smooth Musclementioning

confidence: 70%

Electrophysiological properties of the bladder

Fry

Sui

1998

Int Urogynecol J

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“…Several studies have shown that N-type VDCCs mediate neurotransmitter release from NANC nerves (Maggi et al 1988;De Luca et al 1990;Hata et al 1992;Boeckxstaens et al 1993). Recently, Q-type VDCCs have also been shown to be involved in the release of neurotransmitters, including nitric oxide in the rabbit urethra (Frew and Lundy 1995;Zygmunt et al 1995). In contrast, L, T and P-type VDCCs are believed to play a minor role in transmitter release from NANC nerves (Hata et al 1992;Boeckxstaens et al 1993;Zygmunt et al 1995;Zagorodnyuk and Maggi 1994).…”

Section: Introductionmentioning

confidence: 99%

Involvement of both L- and N-type voltage-dependent Ca2+ channels in KCl- and veratridine-evoked transmitter release from non-adrenergic, non-cholinergic nerves in the rabbit iris sphincter muscle

Kageyama

Fujita

Nakata

et al. 1997

Naunyn-Schmiedeberg's Arch Pharmacol

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To determine which types of voltage-dependent Ca2+ channels mediate tachykinin release in the isolated rabbit iris sphincter muscle, we examined the effects of several Ca2+ channel modulators on contractions induced by either an elevation of the extracellular KCl concentration or application of the Na+ channel activator veratridine. Contractions caused by either 45.9 mM KCl or veratridine (10 microM) were inhibited by spantide (10 microM), a tachykinin receptor antagonist, and capsaicin (10 microM), a tachykinin-depleting agent, but were not changed by atropine. Nicardipine, an L-type Ca2+ channel blocker, inhibited contractions induced by KCl and veratridine in a concentration-dependent manner. omega-Conotoxin GVIA (1 microM), an N-type Ca2+ channel blocker, inhibited only contractions induced by lower concentrations of KCl, both when applied alone and when combined with nicardipine. Bay K 8644, an L-type Ca2+ channel activator, caused a spantide- and nicardipine-sensitive contraction in muscles partially depolarized with 15.9 mM KCl, and enhanced contractions induced by 15.9 mM KCl and veratridine (2 microM). omega-Agatoxin IVA (0.3 microM), a P-type voltage-dependent Ca2+ channel blocker, did not affect contractions induced by either KCl or veratridine. Contractions induced by exogenous substance P were not modified by any of the Ca2+ channel blockers or by Bay K 8644. These results suggest that, in the rabbit iris sphincter muscle. L- and N-type voltage-dependent Ca2+ channels are involved in neurotransmitter release from tachykininergic nerves elicited by high KCl and by veratridine.

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“…Thus, transmitter release from parasympathetic neurons in the mouse bladder involves a combination of N-, P-, and Q-type channels. During preparation of this manuscript, evidence for a role of Q-type channels in transmitter release from parasympathetic neurons in the rat bladder has been published (Frew and Lundy, 1995).…”

Section: Calcium Channel Subtypes Mediating the Whole Contractionmentioning

confidence: 99%

Multiple Subtypes of Voltage-Gated Calcium Channel Mediate Transmitter Release from Parasympathetic Neurons in the Mouse Bladder

Waterman

1996

J. Neurosci.

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Multiple subtypes of voltage-gated calcium channels are coupled to transmitter release from central neurons; however, only N-type channels have been shown to play a role in autonomic neurons. The aim of the present study was to investigate potential roles for other channel subtypes in transmitter release from parasympathetic neurons in the mouse bladder using calcium channel toxins alone and in combination. Transmitter release was measured indirectly by recording the contraction of bladder dome strips in response to electrical stimulation of the neurons by single pulses or trains of 20 pulses at 1-50 Hz.-Conotoxin-GVIA (GVIA) and -conotoxin-MVIIC (MVIIC) inhibited contractions in a concentration-dependent manner, with IC 50 values of ϳ30 and 200 nM, respectively, at low stimulation frequencies. -Agatoxin-IVA (agatoxin) alone did not have any significant effect up to 300 nM. Cumulative addition of the toxins demonstrated that 300 nM agatoxin had a significant effect after N-type channels were blocked with 100 nM GVIA. MVIIC (3 M) reduced the contraction amplitude further. Testing the toxins on the cholinergic or purinergic component of the contraction separately showed that acetylcholine release depends primarily on N-type channels and, to a lesser extent, on P-and Q-type channels, whereas ATP release involves predominantly P-and Q-type channels. In conclusion, parasympathetic neurons in the mouse bladder, like central neurons, use multiple calcium channel subtypes. Furthermore, the release of the two main transmitters in these neurons has differing dependencies on the calcium channel subtypes.

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A role for Q type Ca²⁺ channels in neurotransmission in the rat urinary bladder

Cited by 37 publications

References 21 publications

Electrophysiological properties of the bladder

Electrophysiological properties of the bladder

Involvement of both L- and N-type voltage-dependent Ca2+ channels in KCl- and veratridine-evoked transmitter release from non-adrenergic, non-cholinergic nerves in the rabbit iris sphincter muscle

Multiple Subtypes of Voltage-Gated Calcium Channel Mediate Transmitter Release from Parasympathetic Neurons in the Mouse Bladder

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A role for Q type Ca2+ channels in neurotransmission in the rat urinary bladder

Cited by 37 publications

References 21 publications

Electrophysiological properties of the bladder

Electrophysiological properties of the bladder

Involvement of both L- and N-type voltage-dependent Ca2+ channels in KCl- and veratridine-evoked transmitter release from non-adrenergic, non-cholinergic nerves in the rabbit iris sphincter muscle

Multiple Subtypes of Voltage-Gated Calcium Channel Mediate Transmitter Release from Parasympathetic Neurons in the Mouse Bladder

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A role for Q type Ca²⁺ channels in neurotransmission in the rat urinary bladder