Abstract
We investigated the mechanism of the vasodepressor effect of endokinin A/B. An intravenous (IV) bolus of endokinin A/B (0.05-0.3 nmol/kg) dose-dependently decreased mean arterial pressure in thiobutabarbital-anesthetized rats. The magnitude of the response was unaffected by IV pretreatment with N G-nitro-L-arginine methyl ester (L-NAME, inhibitor of nitric oxide synthase), methylene blue (inhibitor of soluble guanylyl cyclase), indomethacin (cyclooxygenase inhibitor), or tetraethylammonium (TEA, nonspecific K + channel blocker). L-NAME reduced the half-recovery time of the vasodepressor effect of endokinin A/B relative to responses in rats pretreated with either saline or norepinephrine, which caused a similar pressor effect as did L-NAME. Methylene blue, but not TEA or indomethacin, reduced the recovery time of the vasodepressor effect of endokinin A/B. Therefore, the vasodepressor effect of endokinin A/B is mediated via the nitric oxide/L-arginine pathway and activation of soluble guanylyl cyclase but not by production of prostanoids or opening of TEA-sensitive K+ channels.
Original language | English |
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Pages (from-to) | 269-273 |
Number of pages | 5 |
Journal | Journal of Cardiovascular Pharmacology |
Volume | 46 |
Issue number | 3 |
DOIs | |
Publication status | Published - Sept 2005 |
Keywords
- Blood pressure
- Endokinin A/B
- Inhibitor of nitric oxide synthase
- K channel
- Prostanoids
- Soluble guanylyl cyclase
ASJC Scopus subject areas
- Pharmacology
- Cardiology and Cardiovascular Medicine