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Cardiovascular and behavioural effects of centrally administered neuropeptide K in the rat: receptor characterization
Author(s) -
Prat Alexandre,
Picard Pierre,
Couture Réjean
Publication year - 1994
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.1476-5381.1994.tb13059.x
Subject(s) - scratching , medicine , endocrinology , receptor , neuropeptide , antagonist , blood pressure , desensitization (medicine) , physics , acoustics
1 The cardiovascular and behavioural responses to intracerebroventricularly (i.c.v.) administered neuropeptide K (NPK) were studied in conscious rats. The central effects of NPK were characterized by pretreatment (i.c.v.) with selective antagonists for the NK 1 ((±)‐CP 96345 and RP 67580), NK 2 (SR 48968) and NK 3 (R 487) receptors. 2 NPK (10–65 pmol) induced tachycardia and dose‐dependent increases of mean arterial blood pressure. The cardiovascular responses reached a maximum within 3 min post‐injection and lasted for more than 1 h. Concurrently, NPK produced dose‐dependent increases of face washing, head scratching, grooming, walking and wet dog shakes. 3 A desensitization of most of the behavioural responses (except head scratching) but not of the cardiovascular response was shown when two consecutive injections of 25 pmol NPK were given 24 h apart. 4 Both the cardiovascular and behavioural responses (except the head scratching) to 25 pmol NPK were blocked by pre‐administration (i.c.v.) of 6.5 nmol (±)‐CP 96345 or RP 67580 given 5 min earlier. No inhibition of NPK responses was observed when 6.5 nmol SR 48968 or R 487 were used in a similar study. Additionally, NPK effects were significantly reduced 24 h after the prior injection of (±)‐CP 96345 but not of RP 67580. 5 These results support the involvement of NK 1 receptors in the cardiovascular and behavioural effects of i.c.v. NPK. Thus, this peptide may play a putative role in central cardiovascular regulation as it is the most potent endogenous tachykinin described centrally, to date.