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The possibility that the anandamide transport inhibitor N-(4-hydroxyphenyl)-5,8,11,14-eicosatetraenamide (AM404), structurally similar to the vanilloid receptor agonists anandamide and capsaicin, may also activate vanilloid receptors and cause vasodilation was examined. AM404 evoked concentration-dependent relaxations in segments of rat isolated hepatic artery contracted with phenylephrine. Relaxa
1. In the rat hepatic artery, the SK(Ca) inhibitors UCL 1684 (300 nM) completely blocked, and scyllatoxin (1 μM) and d-tubocurarine (100 μM) partially inhibited EDHF relaxations when each of them was combined with charybdotoxin (300 nM). 2. The IK(Ca) inhibitors clotrimazole (3 μM) and 2-chlorophenyl-bisphenyl-methanol (3 μM) strongly depressed EDHF relaxations when each of them was combined with
In the presence of ouabain (1 mM), acetylcholine and KCl (5 mM) evoked endothelium-independent relaxations in rat hepatic arteries. Treatment with capsaicin (10 μM), scopolamine (1 μM) or CGRP8-37 (3 μM) prevented these relaxations. Acetylcholine-induced relaxations in intact arterial segments in the presence of indomethacin (10 μM) and N(G)-nitro-L-arginine (0.3 mM) were only partially inhibited
Vasodilator responses to anandamide (arachidonylethanolamide) and potassium ions were compared with those mediated by endothelium-derived hyperpolarizing factor (EDHF) in guinea-pig isolated basilar artery contracted with prostaglandin F(2α). In this artery, EDHF-mediated responses can be evoked by acetylcholine in the presence of both indomethacin (10 μM) and N(G)-nitro-L-arginine (0.3 mM). In en
1. In the present study, the vasodilator actions of methanandamide and capsaicin in the rat isolated mesenteric arterial bed and small mesenteric arterial segments were investigated. 2. Methanandamide elicited concentration-dependent relaxations of preconstricted mesenteric arterial beds (pEC 50 = 6.0 ± 0.1, E(max) = 87 ± 3%) and arterial segments (pEC 50 = 6.4 ± 0.1, E(max) = 93 ± 3%). 3. In art
The endogenous cannabinoid receptor agonist anandamide is a powerful vasodilator of isolated vascular preparations, but its mechanism of action is unclear. Here we show that the vasodilator response to anandamide in isolated arteries is capsaicin-sensitive and accompanied by release of calcitonin- gene-related peptide (CGRP). The selective CGRP-receptor antagonist 8-37 CGRP (ref. 5), but not the c
1. In rat isolated hepatic arteries contracted with phenylephrine, acetylcholine and the calcium ionophore A23187 each elicit endothelium-dependent relaxations, which involve both nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF). However, the contribution of prostanoids to these responses, and the potential interaction between EDHF and other endothelium-derived relaxing fact
A blog-post on a performance of The Taming of the Shrew by LU students.
In the guinea pig basilar artery, acetylcholine and the calcium ionophore A23187 induced endothelium-dependent relaxations, which were not significantly affected by the nitric oxide (NO) synthase inhibitor N(ω)- nitro-L-arginine (L-NOARG; 0.3 mM) or the guanylate cyclase inhibitor ODQ (1H-[1,2,4]oxadiazolo[4,3-a]quinoxaline-1-one; 1-10 μM), or by these inhibitors combined. However, acetylcholine (
1. The effects of anandamide on K+ currents and membrane potential have been examined in freshly-isolated smooth muscle cells from rat hepatic artery and the results compared with the effects of this arachidonic acid derivative on tension and membrane potential changes in segments of whole artery. 2. In the presence of 0.3 mM L-NOARG and 10 μM indomethacin, anandamide (0.1-100 μM) and endothelium-
1. In the rat hepatic artery, the acetylcholine-induced relaxation mediated by endothelium-derived hyperpolarizing factor (EDHF) is abolished by a combination of apamin and charybdotoxin, inhibitors of small (SK(Ca)) and large (BK(Ca)) conductance calcium-sensitive potassium (K)-channels, respectively, but not by each toxin alone. The selective BK(Ca) inhibitor iberiotoxin cannot replace charybdot
1. In the presence of N(G)-nitro-L-arginine (L-NOARG, 0.3 mM) and indomethacin (10 μM), the relaxations induced by acetylcholine and the calcium (Ca) ionophore A23187 are considered to be mediated by endothelium-derived hyperpolarizing factor (EDHF) in the guinea-pig basilar artery. 2. Inhibitors of adenosine 5'-triphosphate (ATP)-sensitive potassium (K)-channels (K(ATP); glibenclamide, 10 μM), vo
1. The possibility that the endothelium-derived hyperpolarising factor (EDHF) in the rat hepatic artery is a cytochrome P450 mono-oxygenase metabolite of arachidonic acid was examined in the present study. In this preparation, acetylcholine elicits EDHF-mediated relaxations in the presence of the nitric oxide (NO) synthase and cyclo-oxygenase inhibitors N(ω)-nitro-L-arginine (L-NOARG) and indometh
1. In the presence of indomethacin (IM, 10 μM) and N(ω)-nitro-L-arginine (L-NOARG, 0.3 mM), acetylcholine (ACh) induces an endothelium-dependent smooth muscle hyperpolarization and relaxation in the rat isolated hepatic artery. The potassium (K) channel inhibitors, tetrabutylammonium (TBA, 1 mM) and to a lesser extent 4-aminopyridine (4-AP, 1 mM) inhibited the L-NOARG/IM-resistant relaxation induc
1. The effects of the cytochrome P450 inhibitors, proadifen, clotrimazole and 17-octadecynoic acid (17-ODYA) on K-currents in freshly-isolated single cells derived from rat portal vein and on mechanical activity in whole veins were studied. 2. When cells were stepped from -90 mV to a series of test potentials (from -80 to +50 mV), a delayed rectifier current (I(K(V))) and an A-type current ((IK(A)
Electrical field stimulation (EFS) of the rabbit urethral lamina propria elicited a frequency‐dependent non‐adrenergic, non‐cholinergic (NANC) relaxation, which was abolished by NΩ–nitro‐L‐arginine (l‐NOARG). Ω‐Conotoxin GVIA, a selective blocker of N‐type voltage‐operated calcium channels (VOCCs), and Ω‐conotoxin MVIIC (blocker of N‐ and Q‐type VOCCs) inhibited the NANC relaxation, and the inhibi
Relaxant effects of acetylcholine (ACh), histamine, calcitonin gene‐related peptide (CGRP) and the calcium ionophore A23187 were examined in rat femoral (Ø ≅ 0.2 mm), mesenteric (0.2 mm), intrarenal (0.2 mm) and hepatic (0.3 mm) arteries, and aorta (2 mm). Acetylcholine elicited an endothelium‐dependent relaxation in all arteries. Histamine induced an endothelium‐dependent relaxation in aorta, and
Nitric oxide (NO)‐independent pathways contributing to acetylcholine (ACh)‐induced relaxation were examined in the rat isolated hepatic artery and aorta at low and high levels of precontraction induced by phenylephrine (PhE). In the hepatic artery, the ACh‐induced relaxation was unaffected by the NO synthase inhibitors Nw‐nitro‐L‐arginine (L‐NOARG, 0.3 mM) and Nω‐nitro‐L‐arginine methyl ester (0.1
Acetylcholine (ACh) induces an Nω–nitro–L–arginine (L–NOARG)–resistant relaxation and hyperpolarization in the rat isolated hepatic artery. The possibility that carbon monoxide (CO) produced by haem oxygenase (HO) is an endogenous mediator of this response was investigated. Exogenously applied CO evoked a concentration–dependent relaxation, and the CO ‘scavenger’ oxyhaemoglobin (10μM) reduced the
