Corticotrophin releasing factor attenuates NG-Nitro-L-arginine Methyl Ester induced increases in blood pressure in the anaesthetised rat

Corder, Roger; Dm, Barker

doi:10.1038/sj.jhh.1000903

Cited by 1 publication

(1 citation statement)

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“…bolus) did not affect the depressor effect of urocortin. In conclusion, the depressor effect of urocortin in anesthetized rats is not mediated via the NO/ L -arginine When injected i.v., CRF causes a long-lasting depressor response which is not attenuated by pretreatment with N G -nitro-L -arginine methyl ester (L-NAME), thereby suggesting that its action is independent of the nitric oxide (NO)/ L -arginine pathway [7] . Urocortin also induces in vitro relaxation of blood vessels via the activation of endothelium-dependent [8] as well as endothelium-independent [8][9][10][11][12] mechanisms.…”

Section: Introductionmentioning

confidence: 99%

Analysis of the Mechanism of the Vasodepressor Effect of Urocortin in Anesthetized Rats

et al. 2005

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The aim was to examine if the depressor effect of urocortin involves activation of the nitric oxide (NO)/L-arginine pathway, production of prostanoids or opening of K⁺-channels. I. v. bolus urocortin (0.1–3 nmol/kg) dose-dependently decreased mean arterial pressure in thiobutabarbital-anesthetized rats. The depressor effect of urocortin was unaffected by pretreatment with N^G-nitro-L-arginine methyl ester (L-NAME, inhibitor of NO synthase, i.v. bolus) or noradrenaline (i.v. infusion), which increased arterial pressure to a similar level as that produced by L-NAME. In addition, methylene blue (inhibitor of soluble guanylyl cyclase, i.v. infusion), indomethacin (cyclooxygenase inhibitor, i.v. bolus), glibenclamide (blocker of ATP-sensitive K⁺-channels, i.v. bolus) or tetraethylammonium (a non specific K⁺-channel blocker, i.v. bolus) did not affect the depressor effect of urocortin. In conclusion, the depressor effect of urocortin in anesthetized rats is not mediated via the NO/L-arginine pathway, activation of soluble guanylyl cyclase, production of prostanoids, opening of TEA sensitive K⁺-channels nor opening of ATP sensitive K⁺-channels.

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