Differential effect of ω‐conotoxin on release of the adrenergic transmitter and the vasoconstrictor response to noradrenaline in the rat isolated kidney

El-Din, Mahmoud M. Mohy; Malik, Kafait U.

doi:10.1111/j.1476-5381.1988.tb11537.x

Cited by 57 publications

(29 citation statements)

References 21 publications

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“…The peptide co-conotoxin has been shown in certain preparations to attenuate depolarizationevoked release of neurotransmitter (Olivera et al, 1984;Kerr & Yoshikama, 1984;Reynolds et al, 1986;Rivier et al, 1987;Sano et al, 1987;Dooley et al, 1987;Mohy El-Din & Malik, 1988;Maggi et al, 1988;Herdon & Nahorski, 1988). On the basis of electrophysiological evidence it has been suggested that this toxin blocks both L and N type neuronal VSCC (McCleskey et al, 1987;Cruz et al, 1987), consistent with the suggestion that release is mediated principally by these two channel types (Miller, 1987).…”

Section: Introductionsupporting

confidence: 55%

“…Heterogeneity of L type channels with respect to co-conotoxin-sensitivity has always been recognised in the comparison between neurones and muscle cells. No conotoxin binding or calcium channel activity is apparent on smooth, cardiac or skeletal muscle (Yeager et al, 1987;McCleskey et al, 1987;Cruz et al, 1987;Barhanin et al, 1988;Mohy El-Din & Malik, 1988) despite the presence of DHP-sensitive L type channels. Indeed Cruz et al (1987) have proposed two types of L channel, L. (neuronal and co-conotoxin-sensitive) and Lm (co-conotoxin-insensitive).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Evidence for a dihydropyridine‐sensitive and conotoxin‐insensitive release of noradrenaline and uptake of calcium in adrenal chromaffin cells

Owen¹,

Marriott²,

Boarder³

1989

British J Pharmacology

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Section: Introductionsupporting

confidence: 55%

Section: Discussionmentioning

confidence: 99%

Evidence for a dihydropyridine‐sensitive and conotoxin‐insensitive release of noradrenaline and uptake of calcium in adrenal chromaffin cells

Owen¹,

Marriott²,

Boarder³

1989

British J Pharmacology

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“…N-type calcium channels have been shown to be predominant in controlling neurotransmitter release in sympathetically innervated preparations from animal species in vitro [11][12][13] (for brief review, see Reference 7) and in vivo. 14,15 In agreement with those findings, norepinephrine release from the sympathetic nerves of the human heart was prevented by the highly selective N-type channel blocker -conotoxin GVIA (present study).…”

Section: Discussionmentioning

confidence: 99%

N-Type Calcium Channels Control Sympathetic Neurotransmission in Human Heart Atrium

2000

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Background-Because knowledge about the type of calcium channels involved in action potential-induced norepinephrine release from the human peripheral sympathetic nervous system is sparse, we investigated which types of calcium channels are functionally important in the sympathetic nerves of human cardiac tissue. Methods and Results-In superfused segments of human right atrial appendages, the type of calcium channels that control [ 3 H]norepinephrine release evoked by transmural electrical stimulation was determined.[ 3 H]norepinephrine release was almost abolished by 0.2 mol/L -conotoxin GVIA (a selective blocker of N-type channels) but was not modified by 0.1 mol/L -agatoxin IVA (a selective blocker of P-and Q-type channels). Mibefradil (a T-type and N-type calcium channel blocker) at concentrations of 0.3 to 3 mol/L reduced the evoked tritium overflow in a frequency-and calcium-dependent manner, whereas 0.1 to 10 mol/L amlodipine, diltiazem, and verapamil (selective blockers of L-type channels) were ineffective. Conclusions-Norepinephrine release from cardiac sympathetic nerves is triggered by Ca 2ϩ influx via N-type but not L-and P/Q-type calcium channels. The inhibitory effect of mibefradil on norepinephrine release at clinically relevant concentrations is probably due to its blocking action on N-type Ca 2ϩ channels. This property of mibefradil is unique among the calcium channel blockers that have been or still are therapeutically applied and may considerably contribute to its slight negative chronotropic effect in vivo. (Circulation. 2000;101:403-407.)

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“…These differences in sensitivity to conotoxin do not appear to be related to differences in the stimulation parameters (see Table 2), and presumably reflect differences in the susceptibility to conotoxin between species and tissues. It has been demonstrated previously that conotoxin inhibits electrical stimulation-induced release of noradrenaline from rat perfused kidneys (Mohy El-Din & Malik, 1988), tail artery (Clasbrummel et al, 1989) and anococcygeus muscle (McKnight et al, 1989).…”

Section: Effects Ofconotoxin On Noradrenergic Transmissionmentioning

confidence: 99%

“…Conotoxin has been shown to block responses, in autonomically innervated tissues, to stimulation of noradrenergic (Maggi et al, 1988b;Mohy El-Din & Malik, 1988;Brock et al, 1989;Clasbrummel et al, 1989;Keith et al, 1989;McKnight et al, 1989), cholinergic (Lundy & Frew, 1988;Keith et al, 1989) and non-adrenergic, non-cholinergic ' Author for correspondence.…”

Section: Introductionmentioning

confidence: 99%

Effects of ω‐conotoxin GVIA on autonomic neuroeffector transmission in various tissues

Luca

Rand

et al. 1990

British J Pharmacology

101

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1 The effects of co-conotoxin GVIA (conotoxin), a potent inhibitor of neuronal N-type Ca2+ channels, have been examined on responses to stimulation of noradrenergic, cholinergic and non-adrenergic, noncholinergic (NANC) nerves in a range of isolated tissues to investigate the role of conotoxin-sensitive Ca2 + channels in neurotransmission. 2 Contractions elicited by field stimulation of noradrenergic nerves in rat and mouse anococcygeus muscles, rabbit ear artery and rat vas deferens (epididymal portion) were inhibited by conotoxin. Responses to noradrenaline, and to adenosine triphosphate in the vas deferens, were not affected. 3 Positive chronotropic responses to field stimulation of noradrenergic nerves were inhibited by conotoxin in rat and mouse atria, but responses to noradrenaline and tyramine were not affected. 4 The stimulation-induced release of noradrenaline was inhibited by conotoxin in the rabbit ear artery and in rat and mouse atria. 5 Relaxations in response to stimulation of the noradrenergic perivascular mesenteric nerves were reduced or abolished by conotoxin in rat and rabbit jejunum. The response to noradrenaline in rat jejunum was not affected. 6 Contractions elicited by stimulation of cholinergic nerves were inhibited by conotoxin in rat jejunum and mouse ileum (perivascular mesenteric nerves), and in guinea-pig taenia caeci (field stimulation). Responses to acetylcholine in rat jejunum and mouse ileum were not affected. 7 Contractions elicted by stimulation of the cholinergic plus NANC pelvic nerves were inhibited by conotoxin in rabbit colon, and to a lesser extent in guinea-pig colon. The stimulation-induced contraction of the guinea-pig colon was inhibited by conotoxin by a greater proportion in the presence than in the absence of atropine. Responses to acetylcholine were not affected in the rabbit colon but were slightly reduced in the guinea-pig colon. 8 Relaxations in response to field stimulation of NANC nerves were inhibited by conotoxin in guineapig taenia caeci and rat gastric fundus strips, and in rat anococcygeus muscle when the tone was raised by guanethidine but not when it was raised by carbachol. The relaxations produced by sodium nitroprusside in the rat gastric fundus and anococcygeus were not affected. 9 Contractions of the rat bladder elicited by stimulation of the peri-urethral nerves, which are NANCand cholinergically mediated, were relatively insensitive to inhibition by conotoxin. The responses were almost completely abolished by tetrodotoxin. 10 The conotoxin-induced inhibitions of responses to nerve stimulation developed slowly and persisted after removal of conotoxin.11 The inhibitory effect of conotoxin was inversely proportional to the frequency of stimulation (in several preparations) and to the Ca2+ concentration in the bathing solution (in rat vas deferens). These observations suggest that the inhibition by conotoxin of the Ca2+ influx required for excitation-secretion coupling in autonomic nerve terminals is not absolute, and can be overcome by repeated st...

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Differential effect of ω‐conotoxin on release of the adrenergic transmitter and the vasoconstrictor response to noradrenaline in the rat isolated kidney

Cited by 57 publications

References 21 publications

Evidence for a dihydropyridine‐sensitive and conotoxin‐insensitive release of noradrenaline and uptake of calcium in adrenal chromaffin cells

Evidence for a dihydropyridine‐sensitive and conotoxin‐insensitive release of noradrenaline and uptake of calcium in adrenal chromaffin cells

N-Type Calcium Channels Control Sympathetic Neurotransmission in Human Heart Atrium

Effects of ω‐conotoxin GVIA on autonomic neuroeffector transmission in various tissues

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