Drugs online research references
Am J Physiol. 1992 Feb;262(2 Pt 1):G298-307.
Electrical and mechanical effects of acetylcholine and substance P in subregions of canine colon.
Keef KD, Ward SM, Stevens RJ, Frey BW, Sanders KM.
Department of Physiology, University of Nevada School of Medicine, Reno 89557-0046.
Effects of acetylcholine (ACh) and substance P on the electrical and mechanical activities of the circular muscle layer of the canine proximal colon were studied. Because this muscle layer is bordered by two different pacemaker regions, responses from segments containing either a single pacemaker region or no pacemaker region were compared with responses of the complete muscle layer. Concentration-response relationships for ACh and substance P were similar between the various segments, suggesting that receptors for these agonists are expressed throughout the layer. The dominant contractile pattern induced by ACh and substance P in each segment was a 1- to 3-cycle/min rhythm. In a like manner, these agonists also elicited an electrical pattern in which a long-duration slow wave occurred one to three times per minute between short-duration slow waves. Low concentrations of nifedipine (0.01 microM) selectively antagonized the 1- to 3-cycle/min rhythm. In circular muscles with no pacemaker region, ACh (1 microM) caused depolarization, induced oscillations in membrane potential averaging 24 +/- 5 mV in amplitude and 2.9 +/- 0.9 cycles/min in frequency, and generated rhythmic contractions at the same frequency. This "interior" circular muscle was functionally innervated by cholinergic excitatory nerves. Exposure to ACh (1 microM) did not alter the conduction of slow waves through the thickness of the circular layer. In summary, the excitatory neurotransmitters, ACh and substance P, induce a dominant electrical and contractile rhythm throughout the circular muscle layer that is different from the spontaneous rhythms produced at either the myenteric or submucosal border.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1371648&dopt=Abstract
Methods Find Exp Clin Pharmacol. 1992 Jul-Aug;14(6):437-9.
Comparison of vasodilator effects on human middle cerebral artery constriction induced by vasoconstrictors or activated platelets.
Akopov SE, Balayan BG, Gabrielian ES.
Department of Pharmacology, Yerevan Medical Institute, Armenia, USSR.
Experiments were performed on de-endothelized perfused human middle cerebral artery constricted with noradrenaline, serotonin, prostaglandin F2 alpha and collagen-aggregated platelets, all of which provoked similar vasoconstriction; however, the ability of dipyridamole, prostacyclin and nifedipine to reduce the constriction was significantly less marked when induced by activated platelets. The decrease in drug antispasmatic effects was less marked for nifedipine than for other vasodilators. It was suggested that the resistance of platelet-induced vasoconstriction to vasodilator action depends on platelets ability to release several vasoactive substances simultaneously.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1469952&dopt=Abstract
Invest Ophthalmol Vis Sci. 1991 Sep;32(10):2689-95.
Mitogenic and chemotactic effects of platelet-derived growth factor on human retinal glial cells.
Uchihori Y, Puro DG.
Department of Ophthalmology, University of Michigan School of Medicine, Ann Arbor.
Glial cell migration and proliferation appear to play a role in many of the proliferative retinopathies. Knowledge concerning the regulation of the migratory and proliferative responses of glial cells to pathophysiologic conditions in the human retina is limited. Here, we report that platelet-derived growth factor (PDGF) has both mitogenic and chemotactic effects on human retinal glial cells in culture. These effects of PDGF support the idea that this growth factor may be one of the molecules influencing glial cell activities in the proliferative retinopathies. Both the mitogenic and chemotactic responses of retinal glial cells to PDGF could be inhibited by the calcium-channel blocker, nifedipine. Although this finding suggests that nifedipine-sensitive calcium channels may help mediate these responses to PDGF, an electrophysiologic effect of PDGF on voltage-gated calcium channels was not detected. Also, the concentration of nifedipine required to inhibit proliferation was higher than the dose needed to block calcium channels. It seems likely that nifedipine inhibits the mitogenic and chemotactic responses of human retinal glial cells to PDGF by affecting cellular processes in addition to calcium channels.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1654308&dopt=Abstract
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