Open AccessMechanisms underlying the biphasic effect of vitamin K 1 (phylloquinone) on arterial blood pressure
Author(s) -
Tirapelli Carlos R.,
Resstel Leonardo B. M.,
Oliveira Ana M.,
Corrêa Fernando M. A.
Publication year - 2008
Publication title -
journal of pharmacy and pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.745
H-Index - 118
eISSN - 2042-7158
pISSN - 0022-3573
DOI - 10.1211/jpp.60.7.0010
Subject(s) - indometacin , blood pressure , nitric oxide , medicine , vasodilation , mean arterial pressure , nitric oxide synthase , anesthesia , heart rate , cyclooxygenase , aorta , pharmacology , chemistry , biochemistry , enzyme , prostaglandin endoperoxide synthase
Phylloquinone (vitamin K 1 , VK 1 ) is widely used therapeutically and intravenous administration of this quinone can induce hypotension. We aimed to investigate the mechanisms underlying the effects induced by VK 1 on arterial blood pressure. With this purpose a catheter was inserted into the abdominal aorta of male Wistar rats for blood pressure and heart rate recording. Bolus intravenous injection of VK 1 (0.5–20 mgkg −1 ) produced a transient increase in blood pressure followed by a fall. Both the pressor and depressor response induced by VK 1 were dose‐dependent. On the other hand, intravenous injection of VK 1 did not alter heart rate. The nitric oxide synthase (NOS) inhibitor N G ‐nitro‐ l ‐arginine methyl ester (L‐NAME, 10 and 20 mgkg −1 ) reduced both the increase and decrease in blood pressure induced by VK 1 (5 mgkg −1 ). On the other hand, indometacin (10 mgkg −1 ), a non‐selective cyclooxygenase inhibitor, did not alter the increase in mean arterial pressure (MAP) induced by VK 1 . However, VK 1 ‐induced fall in MAP was significantly attenuated by indometacin. We concluded that VK 1 induces a dose‐dependent effect on blood pressure that consists of an acute increase followed by a more sustained decrease in MAP. The hypotension induced by VK 1 involves the activation of the nitric oxide (NO) pathway and the release of vasodilator prostanoid(s).