Drugs online research references
Life Sci. 2001 Jul 27;69(10):1143-54.
Actions of NO donors and endogenous nitrergic transmitter on the longitudinal muscle of rat ileum in vitro: mechanisms involved.
Tanovic A, Jimenez M, Fernandez E.
Department of Cell Biology, Physiology and Immunology, Universitat Autonoma de Barcelona, Spain.
The aim of this work has been to characterize and to compare the responses of the rat ileal longitudinal muscle to the nitric oxide (NO) donors, sodium nitroprusside (SNP) and morpholinosydnonimine hydrochloride (SIN-1). SNP (10(-5)-10(-3) M) caused a contraction followed by a relaxation, both components being concentration-dependent. In contrast, SIN-1 (10(-5)-10(-4) M) caused a relaxation followed by a contraction. Neither the neural blocker tetrodotoxin (TTX) nor atropine were able to change the response to SNP, whereas nifedipine abolished its contractile component. In contrast, TTX and nifedipine diminished both the relaxation and the contraction in response to SIN-1, whereas atropine decreased only the contractile component. The specific guanylate cyclase inhibitor oxadiazolo-quinoxalin-1-one (ODQ) decreased the relaxation induced by SNP but did not modify that caused by SIN-1. The K+ channel blockers charybdotoxin, apamin and tetraethylamonium were unable to modify the response to SNP. In contrast, both TEA and apamin significantly decreased the relaxation induced by SIN- 1. The relaxation resulting from electrical field stimulation (EFS) of enteric nerves in non-adrenergic non-cholinergic conditions is mainly but not exclusively nitrergic, as incubation with the NO synthase inhibitor L-NNA markedly decreases such relaxation. EFS-induced relaxation is also sensitive to ODQ. We conclude that SNP acts mainly on smooth muscle cells activating L-type Ca2+ channels, which result in contraction, and activates the soluble guanylate cyclase, which results in relaxation. In contrast SIN-1 has mixed--neuronal and muscular--effects, the contraction being caused both by acetylcholine release from neurons and by direct activation of L-type Ca2+ channels on smooth muscle cells. SIN-1-induced relaxation is cGMP-independent and it is likely to occur as a consequence of both, neuronal release of inhibitory transmitter(s) and by activation of apamin sensitive K+ channels. The effect of the nitrergic transmitter released from enteric nerves is different from those caused by SIN-1 but shows similarities with those caused by SNP.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11508347&dopt=Abstract
J Vasc Res. 1992 May-Jun;29(3):270-80.
Eicosanoid-dependent and endothelium-independent oscillations of rat aorta.
Chemtob S, Inayatulla A, Varma DR.
Department of Pharmacology and Therapeutics, McGill University, Montreal, Canada.
We studied the role of endothelium and eicosanoids in rhythmic contractions of rat thoracic aorta. Spontaneous oscillations were observed in 35% of 385 endothelium-intact and in 46% of 22 endothelium-denuded aortic strips from normotensive Sprague-Dawley male rats. Vasoactive agents (norepinephrine, epinephrine, phenylephrine, isoproterenol, arachidonic acid, PGF2 alpha, serotonin, potassium, endothelin, atrial natriuretic factor and angiotensin II) induced rhythmic contractions in the majority of tissues. Rhythmic activity was also observed in aortic strips from adult female, pregnant and old male rats. Aortic oscillations were partially inhibited by indomethacin, ibuprofen and nordihydroguaiaretic acid (NDGA), and completely inhibited by indomethacin plus NDGA, nifedipine, low external calcium (less than 1 mM) and pretreatment with dexamethasone. Indomethacin, NDGA and arachidonic acid did not affect oscillations of the portal vein. Rhythmic contractions were observed in thoracic aortic strips from neonatal but not from adult rabbits. However, oscillations could be induced in strips of the mesenteric artery and terminal abdominal aorta of adult rabbits. Also, adult rabbit thoracic aortic strips exhibited oscillations when set up in close proximity of rat aorta. It is suggested that rhythmic contractions are physiological characteristics of many and perhaps all blood vessels and may play a role in blood flow and turbulence; the likely cause of these oscillations is the cyclic release of one or more eicosanoids.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1387009&dopt=Abstract
Gen Pharmacol. 1991;22(6):1005-9.
Inhibitory effect of the endothelium on thrombin-induced contraction in rabbit aorta.
Sakiyama N, Wakabayashi I, Hatake K, Kakishita E.
Second Department of Internal Medicine, Hyogo College of Medicine, Japan.
1. Thrombin caused a tonic contractile response in rabbit aortic strips which showed tachyphylaxis. 2. Thrombin-induced contraction was partially dependent upon extracellular calcium. 3. Contractile response by lower concentrations of thrombin was suppressed by the endothelium. This endothelial effect was blocked by methylene blue, hemoglobin, bromophenacyl bromide or removal of extracellular calcium but not by indomethacin, nordihydroguaiaretic acid or nifedipine. 4. Cyclic GMP levels were not different between the thrombin-stimulated and control strips. 5. Thrombin could not stimulate prostacyclin release from the aortic strips. 6. These results suggest that thrombin possesses a contractile action in rabbit aortic smooth muscle which is attenuated by endothelium-derived relaxing factor (EDRF) spontaneously released from the endothelium during the contraction.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1667300&dopt=Abstract
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