scholarly journals Involvement of central histaminergic system in cardiovascular effects of Y1 receptor antagonist BIBP 3226 in haemorrhagic shock in rats

2017 ◽  
Vol 71 ◽  
pp. 357-362
Author(s):  
Adam Krawiec ◽  
Karolina Jasikowska ◽  
Katarzyna Chojnacka ◽  
Agata Mitera ◽  
Jerzy Jochem
Keyword(s):  
Receptor Antagonist ◽  
Cardiovascular Effects ◽  
Haemorrhagic Shock ◽  
Histaminergic System ◽  
Y1 Receptor

Activation of the central histaminergic system mediates arachidonic-acid-induced cardiovascular effects

2014 ◽  
Vol 92 (8) ◽  
pp. 645-654 ◽  
Author(s):  
Burcin Altinbas ◽  
Bora Burak Topuz ◽  
Tuncay İlhan ◽  
Mustafa Sertac Yilmaz ◽  
Hatice Erdost ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Receptor Antagonist ◽  
Cardiovascular Effects ◽  
Posterior Hypothalamus ◽  
Sprague Dawley ◽  
H2 Receptor Antagonist ◽  
Histaminergic System ◽  
Histaminergic Neurons ◽  
H4 Receptor ◽  
Cox 1

The aim of this study was to explain the involvement of the central histaminergic system in arachidonic acid (AA)-induced cardiovascular effects in normotensive rats using hemodynamic, immunohistochemistry, and microdialysis studies. Intracerebroventricularly (i.c.v.) administered AA (0.25, 0.5, and 1.0 μmol) induced dose- and time-dependent increases in mean arterial pressure and decreased heart rate in conscious normotensive Sprague–Dawley rats. Central injection of AA (0.5 μmol) also increased posterior hypothalamic extracellular histamine levels and produced strong COX-1 but not COX-2 immunoreactivity in the posterior hypothalamus of rats. Moreover, the cardiovascular effects and COX-1 immunoreactivity in the posterior hypothalamus induced by AA (0.5 μmol; i.c.v.) were almost completely blocked by the H2 receptor antagonist ranitidine (50 and 100 nmol; i.c.v.) and partially blocked by the H1 receptor blocker chlorpheniramine (100 nmol; i.c.v.) and the H3–H4 receptor antagonist thioperamide (50 and 100 nmol; i.c.v.). In conclusion, these results indicate that centrally administered AA induces pressor and bradycardic responses in conscious rats. Moreover, we suggest that AA may activate histaminergic neurons and increase extracellular histamine levels, particularly in the posterior hypothalamus. Acting as a neurotransmitter, histamine is potentially involved in AA-induced cardiovascular effects under normotensive conditions.

Cardiovascular effects of histamine H3 receptor antagonist JNJ 5207852 in haemorrhagic shock in rats

2016 ◽  
Vol 70 ◽  
pp. 89-94
Author(s):  
Jerzy Jochem ◽  
Agata Mitera ◽  
Marta Izydorczyk ◽  
Damian Nowak ◽  
Martyna Waliczek
Keyword(s):  
Receptor Antagonist ◽  
Cardiovascular Effects ◽  
Haemorrhagic Shock ◽  
Histamine H3 Receptor ◽  
H3 Receptor ◽  
Histamine H3

NPY Y1 receptor antagonist prevents NPY-induced torporlike hypothermia in cold-acclimated Siberian hamsters

2008 ◽  
Vol 294 (1) ◽  
pp. R236-R245 ◽  
Author(s):  
John Dark ◽  
Kimberly M. Pelz
Keyword(s):  
Body Temperature ◽  
Receptor Antagonist ◽  
Receptor Agonist ◽  
Phodopus Sungorus ◽  
Food Ingestion ◽  
Research Groups ◽  
Ambient Temperatures ◽  
Y1 Receptor ◽  
Siberian Hamsters ◽  
Intracerebroventricular Injections

Siberian hamsters ( Phodopus sungorus) undergo bouts of daily torpor during which body temperature decreases by as much as 20°C and provides a significant savings in energy expenditure. Natural torpor in this species is normally triggered by winterlike photoperiods and low ambient temperatures. Intracerebroventricular injection of neuropeptide Y (NPY) reliably induces torporlike hypothermia that resembles natural torpor. NPY-induced torporlike hypothermia is also produced by intracerebroventricular injections of an NPY Y1 receptor agonist but not by injections of an NPY Y5 receptor agonist. In this research, groups of cold-acclimated Siberian hamsters were either coinjected with a Y1 receptor antagonist (1229U91) and NPY or were coinjected with a Y5 receptor antagonist ( CGP71683 ) and NPY in counterbalanced designs. Paired vehicle + NPY induced torporlike hypothermia in 92% of the hamsters, whereas coinjection of Y1 antagonist + NPY induced torporlike hypothermia in 4% of the hamsters. In contrast, paired injections of vehicle + NPY and Y5 antagonist + NPY induced torporlike hypothermia in 100% and 91% of the hamsters, respectively. Although Y5 antagonist treatment alone had no effect on body temperature, Y1 antagonist injections produced hyperthermia compared with controls. Both Y1 antagonist and Y5 antagonist injections significantly reduced food ingestion 24 h after treatment. We conclude that activation of NPY 1 receptors is both sufficient and necessary for NPY-induced torporlike hypothermia.

Structure-affinity studies of C-terminally modified analogs of neuropeptide Y led to a novel class of peptidic Y1 receptor antagonist

1996 ◽  
Vol 65 (1) ◽  
pp. 61-70 ◽  
Author(s):  
Susanne Hoffmann ◽  
Beate Rist ◽  
Georgi Videnov ◽  
Günther Jung ◽  
Annette G. Beck-Sickinger
Keyword(s):  
Neuropeptide Y ◽  
Receptor Antagonist ◽  
Y1 Receptor
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