Please use this identifier to cite or link to this item: http://hdl.handle.net/11452/23043
Title: Cardiovascular effects of centrally administered arachidonic acid in haemorrhage-induced hypotensive rats: Investigation of a peripheral mechanism
Authors: Uludağ Üniversitesi/Veteriner Fakültesi/Fizyoloji Anabilim Dalı.
0000-0002-5600-8162
0000-0002-3090-0099
Yalçın, Murat
Aydın, Cenk
AAG-6956-2021
57192959734
7005426982
Keywords: Alpha (1)-adrenoreceptor
Angiotensin II receptors
Arachidonic acid
Catecholamine
Hypotension
Intracerebroventricular
Renin activity
V 1 receptors
Vasopressin
Sympatho-adrenomedullary outflow
Central cholinergic system
Normotensive conscious rats
Blood-flow autoregulation
Thromboxane a2 analog
Newborn pigs
Vasopressin secretion
Cerebral-circulation
Injected u-46619
Activation
Pharmacology & pharmacy
Physiology
Issue Date: Apr-2009
Publisher: Wiley
Citation: Yalçın, M. ve Aydın, C. (2009). "Cardiovascular effects of centrally administered arachidonic acid in haemorrhage-induced hypotensive rats: Investigation of a peripheral mechanism". Clinical and Experimental Pharmacology and Physiology, 36(4), 447-453.
Abstract: 1. The aims of the present study were to determine the cardiovascular effects of arachidonic acid (AA) and to investigate the peripheral mechanisms mediating these effects in haemorrhage-induced hypotensive rats. 2. Acute haemorrhage was induced by withdrawing a total volume of 2.2 mL blood/100 g bodyweight over a period of 10 min. Rats were then injected with 75-300 mu g, i.c.v., AA and cardiovascular changes were monitored over the next 60 min. Plasma catecholamine and vasopressin levels, as well as plasma renin activity (PRA), were measured 10 min after injection of 150 mu g AA in haemorrhage-induced hypotensive awake rats. In addition, rats were pretreated with saline (1 mL/kg, i.v.), the vasopressin V-1 receptor antagonist [beta-mercapto-beta,beta-cyclopentamethylenepropionyl(1),O-Me-Tyr(2),Arg(8)]-vasopressin (10 mu g/kg, i.v.), the alpha(1)-adrenoceptor antagonist prazosin (500 mu g/kg, i.v.), the non-specific angiotensin II receptor antagonist saralasin (250 mu g/kg, i.v.) or a combination of these three antagonists 5 min before injection of AA (150 mu g, i.c.v.). The effects of these antagonists on responses to AA were determined. 3. Arachidonic acid caused dose- and time-dependent increases in mean arterial pressure and heart rate and reversed hypotension in haemorrhaged rats. Haemorrhage itself produced an increase in plasma catecholamine and vasopressin levels, as well as PRA; injection of AA produced further increases in these parameters, ranging from 39-123%, under hypotensive conditions. Under hypotensive conditions, pretreatment of rats with all three receptor antagonists produced similar partial blockade of the pressor response to AA, but not the increase in heart rate. Moreover, combined administration of all three receptor antagonists prior to the i.c.v. injection of 150 mu g AA completely abolished the pressor response to AA in haemorrhage-induced hypotensive rats. 4. These results indicate that centrally administered AA reverses hypotension by increasing blood pressure and heart rate in the hypotensive setting. The observed increases in plasma catecholamine and vasopressin levels, as well as PRA, mediate the pressor response to AA in haemorrhage-induced hypotensive rats.
URI: https://doi.org/10.1111/j.1440-1681.2008.05087.x
https://onlinelibrary.wiley.com/doi/10.1111/j.1440-1681.2008.05087.x
http://hdl.handle.net/11452/23043
ISSN: 1440-1681
Appears in Collections:Scopus
Web of Science

Files in This Item:
There are no files associated with this item.


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.