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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Deschamps, Kathleen Couture, Réjean |
| Description | Author Affiliation: Deschamps K ( Department of Physiology, Faculty of Medicine, Université de Montréal, CP 6128, Succursale Centre-ville, Montréal, Québec, Canada H3C 3J7.) |
| Abstract | Tachykinin receptor agonists and antagonists were microinjected into the ventral tegmental area (VTA) to study the relative participation of the three tachykinin receptors in cardiovascular regulation in freely behaving rat. Selective agonists (1-100 pmol) for NK1 ([Sar9, Met (O2)11]SP), NK2 ([beta-Ala8]NKA (4-10)) and NK3 (senktide) receptors evoked increases in blood pressure, heart rate (HR) along with behavioural manifestations (face washing, sniffing, head scratching, rearing, wet dog shake). At 1 pmol, NK1 and NK3 agonists did not affect behaviour and blood pressure but only HR. Tachykinin agonists-induced cardiovascular responses were selectively and reversibly blocked by the prior injection of antagonists for NK1 receptors (LY 303870 ((R)-1-[N-(2-methoxybenzyl)acetylamino]-3-(1H-indol-3-yl)-2-[N-(2-(4-(piperidin-1-yl)piperidin-1-yl)acetyl)amino]propane), 5 nmol), NK2 receptors (SR 48968 ([(S)-N-methyl-N-[4-acetylamino-4-phenylpiperidino-2-(3,4-dichlorophenyl)butyl]benzamide]), 250 pmol) and NK3 receptors (SB 235375 ((-)-(S)-N-(alpha-ethylbenzyl)-3-(carboxymethoxy)-2-phenylquinoline-4-carboxamide), 25 nmol). With the exception of the NK2 agonist, most behavioural effects were also blocked by antagonists. Tachykinin agonists-induced cardiovascular responses were inhibited by intravenous (i.v.) treatments with antagonists for D1 dopamine receptor (SCH23390, 0.2 mg kg(-1)) and beta1-adrenoceptor (atenolol, 5 mg kg(-1)) but not for D2 dopamine receptor (raclopride, 0.16 mg kg(-1)). Behavioural responses were blocked by SCH23390 only. The present study provides the first pharmacological evidence that the three tachykinin receptors in the rat VTA can affect the autonomic control of blood pressure and HR by increasing midbrain dopaminergic transmission. This mechanism may be involved in the coordination of behavioural and cardiovascular responses to stress and noxious stimulation. |
| ISSN | 00071188 |
| e-ISSN | 14765381 |
| Journal | British Journal of Pharmacology |
| Issue Number | 6 |
| Volume Number | 145 |
| Language | English |
| Publisher | Wiley Online Library(on behalf of The British Pharmacological Society) |
| Publisher Date | 2005-07-01 |
| Publisher Place | Great Britain (UK) |
| Access Restriction | Open |
| Subject Keyword | Receptors, Neurokinin-1 Receptors, Neurokinin-2 Receptors, Neurokinin-3 Ventral Tegmental Area Drug Effects Acetates Pharmacology Adrenergic Beta-Antagonists Animals Atenolol Behavior, Animal Benzamides Benzazepines Blood Pressure Dopamine D2 Receptor Antagonists Glutamic Acid Heart Rate Indoles Neurokinin A Analogs & Derivatives Neurokinin-1 Receptor Antagonists Peptide Fragments Piperidines Quinolines Rats, Wistar Receptors, Dopamine D1 Antagonists & Inhibitors Agonists Substance P Physiology Research Support, Non-U.S. Gov't |
| Content Type | Text |
| Resource Type | Article |
| Subject | Pharmacology |
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