Cardiovascular effects of centrally injected melittin in hemorrhaged hypotensive rats: The investigation of peripheral mechanisms

Yalçın, Murat; Savci, Vahide

doi:10.1016/j.npep.2007.07.002

Cited by 23 publications

(15 citation statements)

References 28 publications

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“…Acute hypotensive haemorrhage was induced as described previously 7,9,10,13,16 . Briefly, a total volume of 2.2 mL blood/100 g bodyweight was withdrawn, using the arterial catheter, over a period of 10 min.…”

Section: Methodsmentioning

confidence: 99%

“…Briefly, a total volume of 2.2 mL blood/100 g bodyweight was withdrawn, using the arterial catheter, over a period of 10 min. Approximately 35–40% of the estimated total blood volume was removed during the bleeding procedure; this amount of blood loss causes haemorrhagic shock in animals according to a previously defined procedure 7,9,10,13,16 . Following the haemorrhage procedure, the arterial catheter was flushed with 0.1 mL heparinized saline (100 U/mL) and reconnected to the transducer in order to determine the post‐haemorrhage levels of MAP and HR for a period of 10 min.…”

Section: Methodsmentioning

confidence: 99%

“…In this set of experiments, 48 haemorrhage‐induced hypotensive rats were used. The doses of prazosin, the vasopressin V 1 receptor antagonist and saralasin were based on results reported in previous studies 7,13 …”

Section: Methodsmentioning

confidence: 99%

“…administration of melittin, a PLA 2 activator, affects the cardiovascular system and raises blood pressure under both normal 11–13 and hypotensive conditions 13 . Activation of central TXA 2 receptors contributes to these effects of melittin 11 and increases in plasma catecholamine, vasopressin and renin activity mediate the cardiovascular responses to melittin under both conditions 13 . Taken together, the results of these studies suggest that activation of PLA 2 by melittin may increase AA levels in target cells, leading to increased synthesis of PGs, including TXA 2 .…”

Section: Introductionmentioning

confidence: 99%

“…Taken together, the results of these studies suggest that activation of PLA 2 by melittin may increase AA levels in target cells, leading to increased synthesis of PGs, including TXA 2 . Increased central levels of PGs, at least for TXA 2 , activate the sympathoadrenal, vasopressin and renin–angiotensin systems, 7,13 resulting in cardiovascular effects. In addition, AA can itself provoke a pressor response by activating the peripheral catecholaminergic, vasopressinergic and renin–angiotensin systems in a normotensive setting when injected centrally 14 …”

Section: Introductionmentioning

confidence: 99%

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Cardiovascular Effects of Centrally Administered Arachidonic Acid in Haemorrhage‐induced Hypotensive Rats: Investigation of a Peripheral Mechanism

Yalçın

Aydin

2009

Clin Exp Pharma Physio

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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 microg, 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 microg 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 microg/kg, i.v.), the alpha(1)-adrenoceptor antagonist prazosin (500 microg/kg, i.v.), the non-specific angiotensin II receptor antagonist saralasin (250 microg/kg, i.v.) or a combination of these three antagonists 5 min before injection of AA (150 microg, 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 microg 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.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%