Central administration of 5‐HT activates 5‐HT1A receptors to cause sympathoexcitation and 5‐HT2/5‐HT1C receptors to release vasopressin in anaesthetized rats

Open Access
Publisher Website
Google Scholar
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 sym pathetic nerve activity, blood pressure, heart rate and phrenic nerve activity were investigated in normotensive rats anaesthetized with α-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, β-mercapto-β,β-cyclopentamethylenepropionyl1, O-Me-Tyr2, Arg8-vasopressin [(d(CH2)5Tyr(Me)AVP, 10 μg 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.

This publication has 53 references indexed in Scilit: