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Publications (7)12.08 Total impact

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    ABSTRACT: The sympathetic nervous system that innervates the peripheral circulation is regulated by several mechanisms/receptors. It has been reported that prejunctional 5-HT1A, 5-HT1B, 5-HT1D, D2-like receptors and α2-adrenoceptors mediate the inhibition of the vasopressor sympathetic outflow in pithed rats. In addition, ergotamine, an antimigraine drug, displays affinity at the above receptors and may explain some of its adverse/therapeutic effects. Thus, the aims of this study were to investigate in pithed rats: (i) whether ergotamine produces inhibition of the vasopressor sympathetic outflow; and (ii) the major receptors involved in this effect. For this purpose, male Wistar pithed rats were pre-treated with gallamine (25mg/kg; i.v.) and desipramine (50µg/kg) and prepared to stimulate the vasopressor sympathetic outflow (T7-T9; 0.03-3Hz) or to receive i.v. bolus of exogenous noradrenaline (0.03-3µg/kg). I.v. continuous infusions of ergotamine (1 and 1.8μg/kg·min) dose-dependently inhibited the vasopressor responses to sympathetic stimulation but not those to exogenous noradrenaline. The sympatho-inhibition elicited by 1.8μg/kg·min ergotamine was: (i) unaffected by saline (1ml/kg); (ii) partially antagonised by WAY 100635 (5-HT1A; 30μg/kg) and rauwolscine (α2-adrenoceptor; 300μg/kg), and (iii) dose-dependently blocked by GR 127935 (5-HT1B/1D; 100 and 300μg/kg) or raclopride (D2-like; 300 and 1000μg/kg), The above doses of antagonists did not modify per se the sympathetically-induced vasopressor responses. The above results suggest that ergotamine induces inhibition of the vasopressor sympathetic outflow by activation of prejunctional 5-HT1A, 5-HT1B/1D, α2-adrenoceptors and D2-like receptors in pithed rats.
    European journal of pharmacology. 06/2014;
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    Dataset: 123 13104FP
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    ABSTRACT: It has been suggested that N,N-di-n-propyl-dopamine (dopamine analogue) decreased heart rate in rats through stimulation of dopamine receptors. Nevertheless, the role of prejunctional dopamine D1/2-like receptors or even α2-adrenoceptors to mediate cardiac sympatho-inhibition induced by dopamine remains unclear. Hence, this study identified the pharmacological profile of the cardiac sympatho-inhibition to dopamine in pithed rats. Male Wistar rats were pithed and prepared to stimulate the cardiac sympathetic outflow or to receive i.v. bolus of exogenous noradrenaline. I.v. continuous infusions of dopamine (endogenous ligand) or quinpirole (D2-like agonist) dose-dependently inhibited the tachycardic responses to sympathetic stimulation, but not those to exogenous noradrenaline. In contrast, SKF-38393 (100 μg/kg∙min, D1-like agonist) failed to modify both of these responses. The sympatho-inhibition to dopamine (1.8 μg/kg∙min) or quinpirole (100 μg/kg∙min): i) remained unaltered after saline or the antagonists SCH-23390 (D1-like, 300 μg/kg) and rauwolscine (α2-adrenoceptors, 300 μg/kg); and ii) was significantly antagonized by raclopride (D2-like, 300 μg/kg). These antagonists, at the above doses, failed to modify the sympathetically-induced tachycardic responses. The above results suggest that the inhibition of the cardiac sympathetic outflow to dopamine and quinpirole is primarily mediated by prejunctional D2-like receptors but not D1-like receptors or α2-adrenoceptors.
    Journal of Pharmacological Sciences 11/2013; · 2.15 Impact Factor
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    ABSTRACT: α2-adrenoceptors were first described as presynaptic receptors inhibiting the release of various transmitters from neurons in the central and peripheral nervous systems. In vitro studies have confirmed that α2A, α2B and α2C subtypes inhibited noradrenaline release from postganglionic sympathetic neurons but no study has been reported their involvement in the vasopressor sympathetic outflow in vivo. Thus, this study analysed the subtype(s) involved in the inhibition produced by the α2-adrenoceptor agonist, B-HT 933, on the vasopressor sympathetic outflow. Male Wistar pithed rats were pre-treated with i.v. bolus injections of gallamine (25mg/kg) and desipramine (50µg/kg) and prepared to stimulate the vasopressor sympathetic outflow (T7-T9) or to receive i.v. bolus of exogenous noradrenaline. Sympathetic stimulation or exogenous noradrenaline produced, respectively, frequency-dependent and dose-dependent vasopressor responses. I.v. continuous infusion of B-HT 933 (30μg/kg.min) failed to modify the vasopressor responses to exogenous noradrenaline and inhibited those induced by preganglionic stimulation of the vasopressor sympathetic outflow at all frequencies of stimulation (0.03-3Hz). The sympatho-inhibition elicited by B-HT 933 was: (i) unaffected by vehicles (1ml/kg); (ii) partially antagonised by BRL44408 (300μg/kg; α2A), imiloxan (3000μg/kg; α2B) and/or JP-1302 (300μg/kg; α2C) given separately; and (iii) completely blocked by rauwolscine (300μg/kg) or the combination of BRL44408 (300μg/kg)+imiloxan (3000μg/kg)+JP-1302 (300μg/kg). The above doses of antagonists did not modify per se the sympathetically-induced vasopressor responses. These results suggest that the vasopressor sympatho-inhibition to B-HT 933 is primarily mediated by activation of α2A/2B/2C-adrenoceptors in pithed rats.
    European journal of pharmacology 09/2013; · 2.59 Impact Factor
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    ABSTRACT: Ergotamine has been used in clinical practice for the acute treatment of migraine for over 90 years. So far, it is known that ergotamine interacts with diverse receptors (including α1/2-adrenoceptors, 5-HT1, 5-HT2 and D2-like receptors) and that produces increases in mean blood pressure which are significantly blocked by yohimbine, a classical α2-adrenoceptor antagonist with a moderate affinity for α1-adrenoceptors. Since α1/2-adrenoceptors mediate vasopressor and vasoconstrictor responses in the cardiovascular system, this study was designed to identify the α-adrenoceptor subtypes (α1A, α1B, α1D, α2A, α2B and α2C) involved in ergotamine-induced vasopressor responses in pithed rats. In male Wistar pithed rats baseline heart rate and blood pressure were recorded. Then, the vasopressor responses to intravenous (i.v.) bolus injections of ergotamine were determined after administration of vehicle or several α1⧸2-adrenoceptor antagonists. I.v. administration of the antagonists prazosin (α1, 0.1-30µg/kg), rauwolscine (α2, 0.3-300µg/kg), prazosin (0.1µg/kg) plus rauwolscine (0.3µg/kg), 5-methylurapidil (α1A, 100 and 300µg/kg), L-765,314 (α1B, 100 and 300µg/kg), BMY 7378 (α1D, 100 and 300µg/kg), BRL44408 (α2A, 300 and 1000µg/kg) and JP-1302 (α2C, 300µg/kg), significantly blocked the vasopressor responses to ergotamine, whereas imiloxan (α2B, 1000 and 3000µg/kg), JP-1302 (100µg/kg) or the corresponding vehicles (saline 0.9%, propylene glycol 20% or dimethyl sulfoxide 10%; 1ml/kg) failed to modify the responses to ergotamine. The above results suggest that the vasopressor responses to ergotamine in pithed rats are mainly mediated by α1A-, α1B-, α1D-, α2A- and α2C-adrenoceptors and may explain its adverse/therapeutic effects.
    European journal of pharmacology 05/2013; · 2.59 Impact Factor
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    ABSTRACT: It has been shown that α(2)-adrenoceptors mediate vasopressor responses in pithed rats. However, the corresponding α(2)-adrenoceptor subtypes have not been pharmacologically identified. Thus, this study set out to identify the specific subtypes (α(2A), α(2B) and α(2C)) mediating the vasopressor responses to the α(2)-adrenoceptor agonist, B-HT 933, by using the antagonists prazosin (α(1A/1B/1D)), rauwolscine (α(2A/2B/2C)), BRL44408 (α(2A)), imiloxan (α(2B)) and/or JP-1302 (α(2C)). In pithed rats, consecutive i.v. bolus injections of B-HT 933 produced dose-dependent increases in diastolic blood pressure, without affecting heart rate. The vasopressor responses to B-HT 933: (1) remained unaltered after, i.v., bolus injections of vehicles (1 ml/kg) or prazosin (10, 30, 100 and 300 μg/kg); (2) were dose-dependently blocked by rauwolscine (100 and 300 μg/kg), BRL44408 (100 and 300 μg/kg), imiloxan (1000 and 3000 μg/kg) and/or JP-1302 (10, 30, 100, and 300 μg/kg); and (3) were abolished by the combination BRL44408 (300 μg/kg)+imiloxan (1000 μg/kg)+JP-1302 (300 μg/kg). The above results support our contention that the α(2)-adrenoceptors mediating the vasopressor responses to B-HT 933 in pithed rats pharmacologically correlate with the α(2A), α(2B) and α(2C)-adrenoceptor subtypes.
    European journal of pharmacology 06/2012; 691(1-3):118-24. · 2.59 Impact Factor
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    ABSTRACT: This study investigated in pithed rats whether dopamine can inhibit the sympathetic vasopressor outflow and analysed the pharmacological profile of the receptors involved. Male Wistar pithed rats were pre-treated with intravenous (i.v.) bolus injections of gallamine (25 mg/kg) and desipramine (50 μg/kg). The vasopressor responses to electrical stimulation of the sympathetic vasopressor outflow (0.03-3 Hz; 50 V and 2 msec.) were analysed before and during i.v. continuous infusions of the agonists dopamine (endogenous ligand), SKF-38393 (D(1) -like) or quinpirole (D(2) -like). If inhibition was produced by any agonist, then its capability to inhibit the vasopressor responses to i.v. bolus injections of exogenous noradrenaline (0.03-3 μg/kg) was also investigated. Dopamine (3-100 μg/kg min.) inhibited the vasopressor responses to both electrical stimulation and noradrenaline. In contrast, SKF-38393 (10-100 μg/kg min.) failed to inhibit the vasopressor responses to electrical stimulation; whereas quinpirole (0.1-30 μg/kg min.) inhibited the vasopressor responses to electrical stimulation but not those to noradrenaline. The sympatho-inhibition by quinpirole (1 μg/kg min.) remained unaltered after i.v. SCH 23390 (300 and 1000 μg/kg; D(1) -like receptor antagonist), but was abolished after i.v. raclopride (1000 μg/kg; D(2) -like receptor antagonist). These doses of antagonists did not modify per se the sympathetically-induced vasopressor responses. In conclusion, quinpirole-induced inhibition of the sympathetic vasopressor outflow is primarily mediated by activation of dopamine D(2) -like receptors.
    Basic & Clinical Pharmacology & Toxicology 07/2011; 109(6):506-12. · 2.18 Impact Factor