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Microinjections of 5‐HT 1A agonists into the dorsal motor vagal nucleus produce a bradycardia in the atenolol‐pretreated anaesthetized rat
Author(s) -
Sporton Simon C.E.,
Shepheard Sara L.,
Jordan David,
Ramage Andrew G.
Publication year - 1991
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1991.tb12452.x
Subject(s) - microinjections , agonist , atenolol , chemistry , endocrinology , bradycardia , medicine , heart rate , blood pressure , receptor
1 The effects of microinjections (100 nl) into the dorsal motor vagal nucleus of the 5‐HT 1A receptor agonists 8‐hydroxy‐2‐(di‐n‐propylamino)tetralin (8‐OH‐DPAT) and flesinoxan, the 5‐HT 2 receptor agonist (±)‐1‐(2,5‐dimethoxy‐4‐iodophenyl)‐2‐aminopropane hydrochloride (DOI), the 5‐HT 3 receptor agonist phenylbiguanide (PBG), the α 2 ‐adrenoceptor agonist clonidine and the excitatory amino acid glutamate on heart rate, blood pressure, tracheal pressure and phrenic nerve activity were investigated in atenolol‐pretreated rats anaesthetized with sodium pentobarbitone. 2 Microinjections of glutamate (2.5 nmol) caused decreases in blood pressure, heart rate and phrenic nerve activity. In contrast, microinjections of 5‐HT (1.2 nmol), 8‐OH‐DPAT (1.2 nmol) and flesinoxan (1.3 nmol) all caused a bradycardia but had no effect on blood pressure. In addition, 8‐OH‐DPAT and flesinoxan caused an increase in phrenic nerve activity. 3 Microinjections of DOI, PBG and clonidine had no significant effect on any of the variables recorded. None of the drugs used had any significant effect on tracheal pressure. 4 These results support the hypothesis that activation of 5‐HT 1A receptors causes excitation of cardiac vagal motoneurones and suggest that these receptors are also important in the control of central respiratory drive.