Article date: May 1994
By: Alexandre Prat, Pierre Picard, Réjean Couture, in Volume 112, Issue 1, pages 250-256
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 NK1 ((±)‐CP 96345 and RP 67580), NK2 (SR 48968) and NK3 (R 487) receptors.
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.
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.
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.
These results support the involvement of NK1 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.
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 NK1 ((±)‐CP 96345 and RP 67580), NK2 (SR 48968) and NK3 (R 487) receptors.
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.
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.
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.
These results support the involvement of NK1 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.
DOI: 10.1111/j.1476-5381.1994.tb13059.x
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