Effects of prolonged exposure to α,β‐methylene ATP on non‐adrenergic, non‐cholinergic excitatory transmission in the rectum of the chicken

Komori, Seiichi; Kwon, Seong-Chun; Ohashi, Hidenori

doi:10.1111/j.1476-5381.1988.tb11494.x

Cited by 11 publications

(4 citation statements)

References 29 publications

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“…It is therefore possible that a,J-me-ATP may act as a slowly equilibrating P2l receptor antagonist. In avian smooth muscle, however, this compound can inhibit responses to ATP by causing alterations in membrane properties rather than by interacting with a specific receptor (Komori, Kwon & Ohashi, 1988) and a similar action may well underlie the inhibitory effects of a,,d-me-ATP that were seen in the present experiments.…”

Section: Effects Of Adrenergic Agentsmentioning

confidence: 51%

The regulation of membrane 125I‐ and 86Rb+ permeability in a virally transformed cell line (NCL‐SG3) derived from the human sweat gland epithelium

Wilson¹,

Whiteford²,

Bovell³

et al. 1994

Experimental Physiology

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SUMMARYWe have explored the factors that may regulate membrane permeability in a cell line (NCL-SG3) derived from the human sweat gland epithelium. lonomycin increased the rate of 1251-efflux from preloaded cells and this action appeared to be due to an increase in intracellular free calcium ([Ca2+]). The ionomycin-evoked increase in 1251-efflux was reduced in cells that were exposed either to barium or to valinomycin in the presence of a high concentration of external potassium. It thus appears that a fraction of the ionomycin-evoked increase in 1251-efflux is due to the activation of potassium channels and experiments using 8"Rb+ also suggested that ionomycin increased the rate of potassium efflux, an effect which was totally abolished by barium. Blockade of Na+-K+-2Cl1-cotransport and of Cl--HCO exchange reduced the basal rate of 1251-efflux and the ionomycin-evoked increase in 1251-efflux from control cells and from cells depolarized by valinomycin. These transport systems thus contribute to anion efflux, although [Ca2+]-dependent chloride channels also appear to be present. Acetylcholine increases [Ca2+] [Ca2+]i, but this hormone did evoke cyclic-3',5'-adenosine monophosphate (cyclic AMP) production. However, membrane permeability was riot under adrenergic control, as the cells did not appear to express functional, cyclic AMP-dependent anion channels. This may be because they were not fully differentiated under the culture conditions. ATP consistently evoked a dose-dependent increase in anion efflux that appeared to be mediated by [Ca2+]i. The increase in [Ca2+]i was initiated by the release of calcium from a limited internal store and was subsequently sustained by calcium influx. UTP and ADP also increased [Ca2+]i, whereas adenosine, AMP and x,/i-methylene ATP were without effect. These data thus suggest that a subclass of type 2 purine receptor, which is functionally coupled to phosphoinositidase C, is present in these cells.

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Section: Effects Of Adrenergic Agentsmentioning

confidence: 51%

The regulation of membrane 125I‐ and 86Rb+ permeability in a virally transformed cell line (NCL‐SG3) derived from the human sweat gland epithelium

Wilson¹,

Whiteford²,

Bovell³

et al. 1994

Experimental Physiology

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“…Although purinergic cotransmission has been described in other vascular beds such as the urinary bladder (Kasakov & Burnstock, 1983), vas deferens (Sneddon & Burnstock, 1984) and colon (Hedlund et al, 1983), no evidence was obtained in the present study to indicate that ATP has a role to play in mediating the actions of sympathetic vasoconstrictor fibres innervating the joint. The pronounced constrictor effect of the first injection of a, methylene ATP (Figure la) suggests the presence of P2,Xpurinoceptors in these knee joint blood vessels, although this could also have resulted from a direct depolarizing effect of cz methylene ATP on smooth muscle cells (Komori et al, 1988). However, previous experiments in an isolated knee joint preparation showed both P1-and P2x-purinoceptors to be present, although relatively high doses of purines were required (Ferrell & Khoshbaten, 1990b).…”

Section: Discussionmentioning

confidence: 87%

Sympathetic innervation and α‐adrenoceptor profile of blood vessels in the posterior region of the rabbit knee joint

Najafipour

Ferrell

1993

British J Pharmacology

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1 Experiments were performed to determine the nature of adrenoceptors mediating neurally-induced vasoconstriction of blood vessels in the posterior region of the rabbit knee joint capsule. 2 Electrical stimulation of the posterior articular nerve resulted in frequency-dependent vasoconstriction which was maximal at 10 Hz. This response was mediated predominantly by a2-adrenoceptors as it was only slightly reduced by prazosin administration and was not only abolished but converted into a dilator response by the a2-adrenoceptor antagonist rauwolscine. Further experiments with another specific al-adrenoceptor antagonist YM-12617 showed that the frequency-response curve in the presence of this antagonist did not differ significantly from control. 3 Neurally-induced vasoconstriction did not appear to have a purinergic component as it was unaffected by the P2x-purinoceptor desensitiser a, methylene ATP. 4 The rank-order of potency of a-adrenoceptor agonists given as a bolus by close intra-arterial injection was: adrenaline = UK-14304 > clonidine> phenylephrine, suggesting that the vasoconstrictor effects were mediated predominantly by postjunctional a2-adrenoceptors. 5 The M2-adrenoceptor antagonist rauwolscine converted the constrictor response to close intra-arterial injection of adrenaline into a dilator response. The vasoconstrictor responses to UK-14304, clonidine and phenylephrine were substantially inhibited by rauwolscine. The a,-adrenoceptor antagonist prazosin failed to inhibit the vasoconstrictor responses to adrenaline, clonidine and UK-14304 and resulted in enhancement of their constrictor effects. 6 The enhancement of the responses to the a, and a2 agonists by prazosin appeared to be specifically related to this agent as administration of YM-12617 did not show such enhancement. The dose-response curves to both clonidine and UK-14304 in the presence of YM-12617 did not differ significantly from control responses. Responses to phenylephrine were significantly reduced by YM-12617, indicating the presence of post-junctional a,-adrenoceptors. 7 These results show almost complete reversal of the adrenoceptor profile compared to results obtained in an earlier in vitro study, where responses were mediated predominantly by ax,-adrenoceptors with a small population of postjunctional a2-adrenoceptors (Ferrell & Khoshbaten, 1989). This suggests that the differing environment in vitro may not completely reflect the conditions prevailing in vivo.

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“…The pronounced constrictor effect of the first injection of a, methylene ATP (Figure la) suggests the presence of P2,Xpurinoceptors in these knee joint blood vessels, although this could also have resulted from a direct depolarizing effect of cz methylene ATP on smooth muscle cells (Komori et al, 1988). However, previous experiments in an isolated knee joint preparation showed both P1and P2x-purinoceptors to be present, although relatively high doses of purines were required (Ferrell & Khoshbaten, 1990b).…”

Section: Discussionmentioning

confidence: 88%

Sympathetic innervation and beta‐adrenoceptor profile of blood vessels in the posterior region of the rabbit knee joint

Najafipour

Ferrell²

1993

Experimental Physiology

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SUMMARYExperiments were performed to investigate the presence and nature of f-adrenoceptors in blood vessels supplying the posterior capsule of the rabbit knee joint. Electrical stimulation of the posterior articular nerve (PAN) and close intra-arterial injection of adrenaline produced vasoconstriction which reversed to vasodilatation with administration of the a-adrenoceptor antagonist phenoxybenzamine. In almost all animals close intra-arterial injection of the /,-adrenoceptor agonist isoprenaline resulted in vasodilatation. Injection of the more selective ,1-agonists dobutamine, salbutamol and terbutaline also produced vasodilatation with a rank potency order of isoprenaline > dobutamine > salbutamol > terbutaline. The /-adrenoceptor antagonist propranolol abolished the dilator responses to adrenaline and isoprenaline, and significantly reduced the dilator responses to PAN stimulation in phenoxybenzamine-treated animals. Nerve-mediated vasodilatation was also reduced by the substance P antagonist D-Pro4 D-Trp7'9'10 SP4 -1, suggesting that substance P contributes to this dilatation. Dobutamine, a selective /31-agonist, produced vasodilatation which was abolished by administration of the selective /ll-antagonist atenolol. Isoprenaline-induced vasodilatation was substantially reduced by atenolol. The dilator response to isoprenaline appeared to be unaffected by the selective I82-antagonist ICI1 18551, but the weak dilator responses to the selective fl2-agonists salbutamol and terbutaline were significantly reduced by this antagonist. The results of this study suggest that /-adrenoceptors appear to be involved in the sympathetic regulation of rabbit knee joint blood flow, and that this is predominantly mediated via fll-adrenoceptors.

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Effects of prolonged exposure to α,β‐methylene ATP on non‐adrenergic, non‐cholinergic excitatory transmission in the rectum of the chicken

Cited by 11 publications

References 29 publications

The regulation of membrane 125I‐ and 86Rb+ permeability in a virally transformed cell line (NCL‐SG3) derived from the human sweat gland epithelium

The regulation of membrane 125I‐ and 86Rb+ permeability in a virally transformed cell line (NCL‐SG3) derived from the human sweat gland epithelium

Sympathetic innervation and α‐adrenoceptor profile of blood vessels in the posterior region of the rabbit knee joint

Sympathetic innervation and beta‐adrenoceptor profile of blood vessels in the posterior region of the rabbit knee joint

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