Blockade of vasopressor and vas deferens responses by α, β‐methylene ATP in the pithed rat

Bulloch, J.M.; McGrath, J.C.

doi:10.1111/j.1476-5381.1988.tb11504.x

Cited by 58 publications

(38 citation statements)

References 22 publications

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“…No NA release was detected upon nerve stimulation, and reserpine in the dosage used in this study is known to cause a marked (>90%) depletion of tissue NA in the pig (see Lundberg et al, 1990). The presumably non-adrenergic vascular effects of sympathetic stimulation in reserpine-treated pigs in the presence of a Y. receptor antagonist may therefore be caused by some rapidly acting and quickly metabolized transmitter, like ATP, especially at low frequency stimulation (von Kigelgen & Starke, 1985;Bulloch & McGrath, 1988). Rapid, presumably ATPmediated nerve stimulation-evoked contractions of isolated blood vessels in vitro thus remain after reserpine (Muramatsu, 1987).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of sympathetic vasoconstriction in pigs in vivo by the neuropeptide Y‐Y₁ receptor antagonist BIBP 3226

Lundberg

Modin

1995

British J Pharmacology

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4 High frequency stimulation of the sympathetic trunk in control pigs caused a biphasic vasoconstrictor response in nasal mucosa, hind limb and skin: there was an immediate, peak response, followed by a long-lasting vasoconstriction. BIBP 3226 (1 and 3 mg kg-1) reduced the second phase by about 50% but had no effect on the-peak response. In the spleen, kidney and mesenteric circulation (which lack the protracted response) BIBP 3226 was likewise without effect on the maximal vasoconstriction, and did not influence noradrenaline overflow from spleen and kidney. pressure (by about 5 and 15 mmHg at 1 mg kg-' and 3 mg kg-', respectively), accompanied by splenic and mesenteric vasodilatation, suggesting that this effect was unrelated to Y, receptor blockade. 6 The peptide YY (PYY)-and NPY-evoked vasoconstriction in the kidney of reserpine-treated pigs was markedly reduced (by 95%) by BIBP 3226 while the vasoconstrictor effect in the spleen was attenuated by only 20%. BIBP 3226 did not influence stimulation-evoked NPY release. The vasoconstrictor response in reserpine-treated pigs to single impulse stimulation, which is observed only in nasal mucosa and hind limb, was unchanged regarding maximal amplitude and the integrated effect was only moderately reduced (by about 25%) in the presence of BIBP 3226 (1 mg kg-'). BIBP 3226 (1 mg kg-') markedly reduced (by 55-70%) the long-lasting vascular response (total integrated blood flow reduction) evoked by sympathetic nerve stimulation at high frequency (40 impulses at 20 Hz) in spleen, kidney, nasal mucosa and hind limb. Furthermore, the maximal amplitude of the vasoconstriction was reduced mainly in the kidney (by 60%) and also in the spleen (by 40%). 7 It is concluded that BIBP 3226 can act as a selective Y, receptor antagonist in the pig. Endogenous NPY via Y, receptor activation may play a role in evoking the long-lasting vasoconstriction seen in nasal mucosa, hind limb and skin after high frequency stimulation of sympathetic nerves in control pigs. Furthermore, NPY via Y, receptor mechanisms seems to be of major importance for the long-lasting component of the reserpine resistant sympathetic vasoconstriction in many vascular beds, and for the maximal vasoconstrictor response in the kidney. Circulating NPY and PYY induce splenic vasoconstriction via Y2-receptors in contrast to neuronally released NPY which mainly activates Y1 receptors.

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Section: Discussionmentioning

confidence: 99%

Inhibition of sympathetic vasoconstriction in pigs in vivo by the neuropeptide Y‐Y₁ receptor antagonist BIBP 3226

Lundberg

Modin

1995

British J Pharmacology

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“…, 1988), but there are no pre vious reports on the "in vivo" effects of a,r3-methy lene-ATP. However, the vasoconstrictor action of this compound in the cerebral circulation is consis tent with the pressor response recorded during its intravascular administration in rats Bulloch and McGrath, 1988) and cats (Ribeiro and Lima, 1985).…”

Section: Discussionmentioning

confidence: 57%

Heterogeneity of P₂-Purinoceptors in Brain Circulation

Torregrosa

Miranda

Salom

et al. 1990

J Cereb Blood Flow Metab

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Summary:The existence of P2-purinoceptors in the cere brovascular bed was examined by testing the effects of ATP and its stable analog, u,p-methylene-ATP, on CBF in the unanesthetized goat as well as on isometric tension in isolated goat middle cerebral artery. When injected directly into the cerebral circulation, A TP increased and u,p-methylene-ATP decreased CBF. Indomethacin did not modify either of these effects. The vasoconstrictor action of u,p-methylene-ATP was reduced by nicar dipine. "In vitro," both ATP and u,p-methylene-ATP contracted the cerebral arteries at resting tone, but the analog was more potent than A TP. 572cantly reduced the ATP-induced contractions. Nicar dipine inhibited both the u,p-methylene-ATP-and the ATP-induced contractile response. In preconstricted ar teries, ATP produced relaxation and u,p-methylene-ATP induced further contraction. The relaxant response to ATP was not modified by indomethacin. These results show the existence of two subtypes of P2-purinoceptors in brain circulation: P2x, more sensitive to u,P methylene-ATP than to ATP, which elicits cerebral vas oconstriction; and P2y, sensitive to ATP, which elicits cerebral vasodilation.

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“…More recently, it was found that a novel administration regime of mATP in the pithed rat avoided the cardiotoxic effects of the drug. This modified regime of administration of mATP reduced the sympathetic pressor response to spinal stimulation by 60% in the absence of xadrenoceptor blockade, and completely abolished the residual response after a-adrenoceptor antagonism (Bulloch & McGrath, 1988). The previous inability of mATP to affect the pressor response before a-antagonism, or to abolish the residual response after a-antagonism completely (Flavahan et al, 1985), was attributed to the transient nature of its action.…”

Section: Introductionmentioning

confidence: 97%

“…Thus, the effects of mATP and a-adrenoceptor antagonists appeared to be additive, and dissect the sympathetic pressor response of the pithed rat into a-adrenergic (40%) and purinergic (60%) components. The use of mATP was demonstrated to be selective in that it had no effect on the pressor response to intravenously administered NA (Bulloch & McGrath, 1988).…”

Section: Introductionmentioning

confidence: 99%

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Investigation of the selectivity of α, β‐methylene ATP in inhibiting vascular responses of the rat in vivo and in vitro

Dalziel

Gray

Drummond

et al. 1990

British J Pharmacology

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1 The proposal that a,fi-methylene adenosine 5'-triphosphate (mATP) inhibits pressor responses in the pithed rat by selective desensitization of P2.-purinoceptors was examined by comparing the selectivity of its inhibitory effect on vascular responses in vitro and in vivo.2 In isolated ring preparations of rat femoral and tail artery, which had been denuded of endothelium, mATP markedly reduced the contractile response to exogenous ATP but had no effect on the response of the arteries to exogenous noradrenaline (NA). 3 In the pithed rat a substantial proportion of the pressor response to sympathetic nerve stimulation was resistant to a-adrenoceptor blockade, suggesting a non-adrenergic component to the sympathetic vasoconstriction. 4 In the pithed rat, repeated administration of desensitizing doses of mATP attenuated the pressor response to sympathetic nerve stimulation by approximately 80%, suggesting that a component of the sympathetic vasoconstriction is mediated by ATP acting on vascular P21-purinoceptors. However, the same mATP treatment also attenuated, to a similar degree, the pressor responses to intravenous NA, angiotensin II and vasopressin, indicating that the desensitization procedure was non-selective.5 These results demonstrate that while mATP can be used to desensitize selectively P2.-purinoceptors in vitro, its attenuation of the sympathetic nerve-mediated pressor response in vivo is non-selective.

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Blockade of vasopressor and vas deferens responses by α, β‐methylene ATP in the pithed rat

Cited by 58 publications

References 22 publications

Inhibition of sympathetic vasoconstriction in pigs in vivo by the neuropeptide Y‐Y₁ receptor antagonist BIBP 3226

Inhibition of sympathetic vasoconstriction in pigs in vivo by the neuropeptide Y‐Y₁ receptor antagonist BIBP 3226

Heterogeneity of P₂-Purinoceptors in Brain Circulation

Investigation of the selectivity of α, β‐methylene ATP in inhibiting vascular responses of the rat in vivo and in vitro

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Blockade of vasopressor and vas deferens responses by α, β‐methylene ATP in the pithed rat

Cited by 58 publications

References 22 publications

Inhibition of sympathetic vasoconstriction in pigs in vivo by the neuropeptide Y‐Y1 receptor antagonist BIBP 3226

Inhibition of sympathetic vasoconstriction in pigs in vivo by the neuropeptide Y‐Y1 receptor antagonist BIBP 3226

Heterogeneity of P2-Purinoceptors in Brain Circulation

Investigation of the selectivity of α, β‐methylene ATP in inhibiting vascular responses of the rat in vivo and in vitro

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Inhibition of sympathetic vasoconstriction in pigs in vivo by the neuropeptide Y‐Y₁ receptor antagonist BIBP 3226

Inhibition of sympathetic vasoconstriction in pigs in vivo by the neuropeptide Y‐Y₁ receptor antagonist BIBP 3226

Heterogeneity of P₂-Purinoceptors in Brain Circulation