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CENTRAL ADMINISTRATION OF 5-HT ACTIVATES 5-HT1A RECEPTORS TO CAUSE SYMPATHOEXCITATION AND 5-HT2/5-HT1C RECEPTORS TO RELEASE VASOPRESSIN IN ANESTHETIZED RATS

ANDERSON, IK; MARTIN, GR; RAMAGE, AG; (1992) CENTRAL ADMINISTRATION OF 5-HT ACTIVATES 5-HT1A RECEPTORS TO CAUSE SYMPATHOEXCITATION AND 5-HT2/5-HT1C RECEPTORS TO RELEASE VASOPRESSIN IN ANESTHETIZED RATS. BRIT J PHARMACOL , 107 (4) 1020 - 1028.

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Abstract

1 The effects of intracerebroventricular injections to the right lateral ventricle (i.c.v.) of 5-hydroxytryptamine (5-HT, 40 and 120 nmol kg-1), N,N-di-n-propyl-5-carboxamidotryptamine (DP-5-CT; 3 nmol kg-1), 5-carboxamidotryptamine (5-CT; 3 nmol kg-1), 8-hydroxy-2-(di-N-propylamino) tetralin (8-OH-DPAT; 3, 40 and 120 nmol kg-1) and 1-(2,5-di-methoxy-4-iodophenyl)-2-aminopropane (DOI; 40 and 120 nmol kg-1) on renal sympathetic nerve activity, blood pressure, heart rate and phrenic nerve activity were investigated in normotensive rats anaesthetized with alpha-chloralose.2 5-HT caused a long lasting pressor response which was associated with an initial bradycardia and renal sympathoinhibition followed by a tachycardia and renal sympathoexcitation. Pretreatment with the 5-HT2/5-HT1C receptor antagonists, cinanserin (300 nmol kg-1, i.c.v.) or LY 53857 (300 nmol kg-1, i.c.v.) reversed the initial bradycardia and sympathoinhibition to tachycardia and sympathoexcitation. Combined pretreatment with LY 53857 (300 nmol kg-1, i.c.v.) and the 5-HT1A antagonist, spiroxatrine (300 nmol kg-1, i.c.v.), blocked the effects of 5-HT on all the above variables.3 Pretreatment with the vasopressin V1-receptor antagonist, beta-mercapto-beta,beta-cyclopentamethylene-propionyl1, O-Me-Tyr2, Arg8-vasopressin [(d(CH2)5Tyr(Me)AVP, 10 mug kg-1, i.v.] did not affect the magnitude but reduced the duration of the pressor response produced by i.c.v. 5-HT and reversed the initial bradycardia and renal sympathoinhibition to tachycardia and sympathoexcitation.4 1-(2,5-Di-methoxy-4-iodophenyl)-2-aminopropane (DOI) caused a pressor effect which was associated with a bradycardia and sympathoinhibition. These effects were blocked by pretreatment with BW501C67 (0.1 mg kg-1, i.v.), a peripherally acting 5-HT2/5-HT1C receptor antagonist. However, BW501C67 (0.1 mg kg-1, i.v.) failed to block the effects of i.c.v. 5-HT.5 DP-5-CT, 5-CT and 8-OH-DPAT (3 nmol kg-1, i.c.v.) caused sympathoexcitation, tachycardia and a rise in blood pressure. Pretreatment with methiothepin (1 mg kg-1, i.v.) or spiroxatrine (300 nmol kg-1, i.c.v.) attenuated the response to i.c.v. DP-5-CT.6 It is concluded that i.c.v. administration of 5-HT activates 5-HT1A receptors to cause sympathoexcitation and 5-HT2 or 5-HT1C receptors to cause the release of vasopressin.

Type: Article
Title: CENTRAL ADMINISTRATION OF 5-HT ACTIVATES 5-HT1A RECEPTORS TO CAUSE SYMPATHOEXCITATION AND 5-HT2/5-HT1C RECEPTORS TO RELEASE VASOPRESSIN IN ANESTHETIZED RATS
Keywords: 5-HT1A RECEPTORS, 5-HT2 OR 5-HT1C RECEPTORS, VASOPRESSIN V1-RECEPTORS, 8-OH-DPAT, DP-5-CT, 5-HT, DOI, BLOOD PRESSURE, SYMPATHETIC NERVE ACTIVITY, ANESTHETIZED RAT, 8-HYDROXY-2-(DI-N-PROPYLAMINO) TETRALIN 8-OH-DPAT, SYMPATHETIC-NERVE ACTIVITY, CONSCIOUS RATS, ANESTHETIZED RAT, BLOOD-PRESSURE, RAPHE OBSCURUS, 1-(2,5-DIMETHOXY-4-IODOPHENYL)-2-AMINOPROPANE DOI, CARDIOVASCULAR-RESPONSES, HYPERTENSIVE RAT, ANGIOTENSIN-II
UCL classification: UCL > Provost and Vice Provost Offices
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Life Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Life Sciences > Div of Biosciences
URI: http://discovery.ucl.ac.uk/id/eprint/167133
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