Key result
Central U-46619 reverses hypotension in hemorrhaged rats via TXA2 receptors and increased catecholamines, vasopressin, and renin.
Why the study?
The cardiovascular effects and central and peripheral mechanisms of centrally injected U-46619, a thromboxane A2 analog, in hemorrhagic shock conditions were investigated.
Does centrally injected U-46619 increase blood pressure and reverse hypotension in hemorrhaged hypotensive rats?
Does centrally injected U-46619 increase blood pressure and reverse hypotension in hemorrhaged hypotensive rats?
Centrally administered U-46619 reverses hypotension in hemorrhagic shock via central TXA2 receptors and subsequent increases in plasma catecholamines, vasopressin, and renin activity.
In the present study, we investigated the cardiovascular effects of centrally injected U-46619, a thromboxane A(2) (TXA(2)) analog, and the central and peripheral mechanisms of these effects in hemorrhagic shock conditions. Hemorrhage was performed by withdrawing a total volume of 2.1 ml of blood/100 g body weight over a period of 10 min. Injections were made into the lateral cerebral ventricle (LCV), nucleus tractus solitarius (NTS), rostral ventrolateral medulla (RVLM) and paraventricular nucleus of hypothalamus (PVN). U-46619 (0.1, 1 and 2 microg) increased blood pressure and reversed hypotension in hemorrhagic shock. The pressor effect was dose- and time-dependent in all investigated brain areas. Heart rate changes were not significantly different in all groups. Pretreatment of rats with an injection of SQ-29548 (4 or 8 microg), a TXA(2) receptor antagonist, into the LCV, NTS, RVLM and PVN completely blocked the pressor effect of U-46619 (1 microg) injected into respective brain areas. Hemorrhage itself increased plasma adrenaline, noradrenaline, vasopressIN levels and renin activity. U-46619 (1 microg) injected into the LCV, PVN, RVLM and NTS produced additional increases in these hormone levels and in renin activity. Intravenous pretreatments of rats with prazosin (0.5 mg/kg), an alpha(1)-adrenoceptor antagonist, [beta-mercapto-beta,beta-cyclopentamethylenepropionyl(1), O-Me-Tyr(2),Arg(8)]- vasopressin (10 microg/kg), a vasopressin V(1)-receptor antagonist, or saralasin (250 microg/kg), an angiotensin II receptor antagonist, in hemorrhaged rats partially blocked the pressor response to U-46619 (1 microg) injected into the LCV, PVN, RVLM and NTS. Results show that centrally administered U-46619, a TXA(2) analog, increases blood pressure and reverses hypotension in hemorrhagic shock. Activation of central TXA(2) receptors mediates the pressor effect of the drug. Furthermore, the increases in plasma adrenaline, noradrenaline, vasopressin levels and renin activity are involved in these effects.
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Yalçın et al. (2004) studied Hemorrhagic shock. U-46619 (TXA2 analog) vs. Hemorrhage alone or pretreatment with antagonists was evaluated on Blood pressure and heart rate changes. Centrally administered U-46619 increased blood pressure and reversed hypotension in hemorrhaged rats via central TXA2 receptors and increased plasma catecholamines, vasopressin, and renin activity.
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