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Neurol Med Chir (Tokyo). 1993 Oct;33(10):675-81.
Characteristics of histamine receptors in human cerebral arteries.

Takagi T, Tan EC, Shibata S.

Department of Neurosurgery, Nagoya City Higashi General Hospital.

Histamine and 2,2-pyridylethylamine, an H1-receptor agonist, (both 10(-8)-10(-3) M) caused contraction of human cerebral artery preparations in the absence of active tension, while dimaprit, an H2-receptor agonist, caused vasorelaxation. The histamine-induced vasoconstriction was blocked non-competitively by tripelennamine, an H1-receptor antagonist. In the presence of cimetidine, an H2-receptor antagonist, histamine-induced contraction was enhanced. The histamine-induced contraction was not affected by phentolamine or propranolol, but abolished by nifedipine. In prostaglandin F2 alpha-precontracted arteries, histamine and dimaprit caused relaxation, while 2,2-pyridylethylamine had no apparent effect. Histamine-induced relaxation was much greater in the presence than in the absence of an H1-antagonist. The vasorelaxation induced by histamine in the presence of an H1-antagonist was also inhibited by an H2-antagonist. Histamine caused no apparent relaxation in precontracted preparations without endothelium. The present results provide further evidence that histamine causes either vasocontraction or vasodilation in human cerebral arteries, and suggest that vasocontraction and vasorelaxation are due to the activation of H1- and H2-receptors, respectively. The relaxation induced by histamine may also be related to the endothelium-derived relaxing factors released from endothelial cells.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7505894&dopt=Abstract




Int J Parasitol. 1993 Sep;23(6):803-7.
Expression of a channel-like pathway for adenosine transport in Leishmania donovani promastigotes.

Ogbunude PO, Dzimiri MM.

Biological and Medical Research (MBC-03), King Faisal Specialist Hospital and Research Centre, Riyadh, Kingdom of Saudi Arabia.

L. donovani promastigotes (MHOM/ET/67/HA3) transport adenosine by a route that is sensitive to inhibition by a nonspecific channel blocker, propranolol. At the logarithmic and stationary phases of growth, the transport of 1 microM-3H-adenosine was significantly inhibited (40-50%) by 100 microM-propranolol. In contrast, a strain of Leishmania donovani promastigotes clonally selected to grow in defined medium was only slightly (approximately 10%) inhibited at the logarithmic but not at the stationary phase. These results suggest that the differences in expression of adenosine in the parasites previously reported, may be related to uptake by a channel-like pathway in the promastigotes.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7507902&dopt=Abstract




Prostaglandins. 1985 Jul;30(1):99-107.
Effect of prostaglandin E2 on the electrical activity of cat isolated stomach muscle.

Kim MS, Lee YL, Jo YH, Sim SS, Choi H.

Prostaglandins (PGs) are believed to be present in the gastrointestinal tract and to increase the tone of longitudinal muscle layer. However the influence of PGs on the gastric slow wave (SW) is not clarified yet. We therefore investigated the effect of prostaglandin E2 (PGE2) on the electrical and the mechanical activities of feline isolated stomach muscle strips (7 X 1.5 cm), using five capillary electrodes (Ag-AgCl) and an isometric force transducer connected to the antral edge. One hundred and ninety-six strips, obtained from the corpus and antrum of 196 anaesthetized cats, were studied in a muscle chamber filled with Krebs solution (pH 7.4, temperature 36 degrees C) bubbled with 5% CO2 in O2. Exogenous PGE2 concentration-dependently increased the gastric SW frequency without affecting the spike and mechanical activities. Indomethacin decreased the SW frequency. These responses to PGE2 or indomethacin were not blocked by phentolamine, propranolol, hexamethonium, atropine or tetrodotoxin. It is therefore suggested that PGE2 facilitates the development of the gastric SW by an action on the muscle that does not involve cholinergic or adrenergic mechanism.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3863196&dopt=Abstract













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