α-Adrenergic agonist and antagonist activity of dihydroergotoxine in rats

Roquebert, J; Demichel, P

doi:10.1111/j.2042-7158.1985.tb03026.x

Cited by 18 publications

(22 citation statements)

References 7 publications

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“…In pithed normotensive rats, intravenous administration of DHE caused a dose-de pendent increase in mean arterial blood pressure which was also found by other workers [1,3,13]. The efficacy of DHE was about 60% related to the maximum pressor effect of noradrenaline or 5-HT.…”

Section: Discussionsupporting

confidence: 67%

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Dual Effect of Dihydroergotamine at Vascular 5-Hydroxytryptamine Receptors in Pithed Rats

Müller

Glusa²,

Markwardt³

1988

Pharmacology

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Dihydroergotamine (DHE), administered intravenously to pithed normotensive rats, increased the mean arterial blood pressure dose-dependently. This pressor effect was noncompetitively inhibited by the 5-hydroxytryptamine (5-HT) receptor antagonists pizotifen and cyproheptadine (0.1 mg/kg each). The α₁-adrenoceptor blocker prazosin (1 mg/kg) had no influence on the DHE effect whereas the α₂-adrenoceptor blocker yohimbine, at the same dose, proved to be a noncompetitive inhibitor of this pressor effect. The results indicate that both the 5-HT receptors and α₂-adrenoceptors are involved in the DHE-induced vasoconstriction. On the other hand, in pithed normotensive rats, DHE proved to be a potent inhibitor of the pressor response to 5-HT but it did not inhibit that to noradrenaline. The results obtained characterize DHE as a noncompetitive dualist at vascular 5-HT receptors.

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Section: Discussionsupporting

confidence: 67%

“…In the absence of the neurogenic reflex control in pithed rats or in dogs during high epidural block, DHE produced an in crease in mean arterial pressure [1,3,7,13]. It is now generally accepted that in these ani mals the pressor effect of DHE is due to peripheral vasoconstriction at both the ar terial and venous site.…”

Section: Introductionmentioning

confidence: 99%

Dual Effect of Dihydroergotamine at Vascular 5-Hydroxytryptamine Receptors in Pithed Rats

Müller

Glusa²,

Markwardt³

1988

Pharmacology

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“…In the cat the ergotamine-induced bradycardia is due to an agonist action on presynaptic dopamine receptors located on the cardiac sympathetic nerve terminals (Saxena & Cairo-Rawlins, 1983), but in the rat presynaptic a2-adrenoceptors have been implicated (Roquebert & Grenie, 1986). In both species studied, ergotamine caused a doserelated decrease in carotid blood flow, predominantly by affecting the arteriovenous anastomotic fraction.…”

Section: Effects Ofergotaminementioning

confidence: 99%

Reduction of cephalic arteriovenous shunting by ergotamine is not mediated by 5‐HT₁‐like or 5‐HT₂ receptors

Bom

Heiligers

Saxena

et al. 1989

British J Pharmacology

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1 The potent, antimigraine drug ergotamine has affinity for both 5-HT1 and 5-HT2 binding sites and constricts arteriovenous anastomoses. Since 5-HT also constricts arteriovenous anastomoses (mainly via 5-HT1-like receptors), this study investigates the involvement of 5-HT receptors in the ergotamine-induced reduction of arteriovenous shunting in the carotid circulation of the cat and pig. 2 In the cat, ergotamine (3, 10 and 30 ug kg 1, i.v.) reduced carotid blood flow, predominantly by a reduction in arteriovenous anastomotic blood flow. Pretreatment with ketanserin (0.5 mgkg 1, i.v.) or methiothepin (1 mg kg-', i.v.) did not antagonize the effects of ergotamine.3 In the pig, ergotamine (2.5, 5, 10 and 20pgkg-', i.v.) also reduced carotid blood flow and arteriovenous shunting, which was not affected by pretreatment with methiothepin (1 mg kg-1, i.v.). 4 These results suggest that the reduction by ergotamine in the shunting of carotid arterial blood via cephalic arteriovenous anastomoses is not mediated by 5-HT1-like or 5-HT2 receptors.

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“…In the present investigation, arterial blood pressure was increased by both ergotamine and dihydroergotamine. In the rat, the ergot alkaloids-induced pressor response seems to be mediated partly by x2-adrenoceptors and partly by 5-HT receptors, but probably not by xl-adrenoceptors (Roquebert & Grenie, 1986;Muller et al, 1988). Although the receptor mechanism in the pig is unknown, both the a-adrenoceptor and the 5-HT receptor antagonist potency of methiothepin may be responsible for the attenuation of the pressor responses to the two ergot alkaloids (see Table 1).…”

Section: Systemic Haemodynamicsmentioning

confidence: 99%

Carotid vascular effects of ergotamine and dihydroergotamine in the pig: no exclusive mediation via 5‐HT₁‐like receptors

Boer

Heiligers

Saxena

1991

British J Pharmacology

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1 Though it is well known that the antimigraine drugs ergotamine and dihydroergotamine reduce carotid arteriovenous anastomotic shunting, it is uncertain whether a 5-HT1-like receptor is responsible for this effect. Using a high dose of methiothepin (3 mg kg-1), which completely blocks the carotid vascular effects of sumatriptan, we have attempted to study the role of 5-HT1-like receptors in the carotid vascular effects of ergotamine as well as dihydroergotamine in anaesthetized pigs. 2 Both ergotamine and dihydroergotamine increased arterial blood pressure and decreased heart rate. 3 The ergot alkaloids reduced dose-dependently total carotid blood flow and conductance as a result of a selective decrease in the arteriovenous anastomotic fraction. The nutrient fraction increased, particularly to bones, tongue and salivary glands with ergotamine and to ears, head skin, bones and salivary glands with dihydroergotamine. In contrast, dural vascular conductance tended to decresae. 4 Methiothepin (3mg kg-') partially antagonized the decrease in total carotid and arteriovenous anastomotic blood flow and conductance by the ergot alkaloids; the ED30 for ergotamine and dihydroergotamine (agonist dose eliciting a 30% decrease in arteriovenous anastomotic conductance) was raised by 3.1 and 5.2 fold respectively. 5 These results indicate that the effects of ergotamine and dihydroergotamine are partly mediated by methiothepin-sensitive receptors, which may probably belong to either 5-HT1-like or a2-adrenoceptor category. However, an important part of the effect of ergot alkaloids is left after methiothepin and this could be mediated by other, perhaps novel, receptors.

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α-Adrenergic agonist and antagonist activity of dihydroergotoxine in rats

Cited by 18 publications

References 7 publications

Dual Effect of Dihydroergotamine at Vascular 5-Hydroxytryptamine Receptors in Pithed Rats

Dual Effect of Dihydroergotamine at Vascular 5-Hydroxytryptamine Receptors in Pithed Rats

Reduction of cephalic arteriovenous shunting by ergotamine is not mediated by 5‐HT₁‐like or 5‐HT₂ receptors

Carotid vascular effects of ergotamine and dihydroergotamine in the pig: no exclusive mediation via 5‐HT₁‐like receptors

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α-Adrenergic agonist and antagonist activity of dihydroergotoxine in rats

Cited by 18 publications

References 7 publications

Dual Effect of Dihydroergotamine at Vascular 5-Hydroxytryptamine Receptors in Pithed Rats

Dual Effect of Dihydroergotamine at Vascular 5-Hydroxytryptamine Receptors in Pithed Rats

Reduction of cephalic arteriovenous shunting by ergotamine is not mediated by 5‐HT1‐like or 5‐HT2 receptors

Carotid vascular effects of ergotamine and dihydroergotamine in the pig: no exclusive mediation via 5‐HT1‐like receptors

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Reduction of cephalic arteriovenous shunting by ergotamine is not mediated by 5‐HT₁‐like or 5‐HT₂ receptors

Carotid vascular effects of ergotamine and dihydroergotamine in the pig: no exclusive mediation via 5‐HT₁‐like receptors