Drugs online research references
Can J Physiol Pharmacol. 1991 Aug;69(8):1155-62.
Interactions between endothelin and atrial natriuretic factor in the rat aortic ring preparation.
Bolger G, Liard F, Krogsrud R, Welchner E, Jaramillo J.
Department of Pharmacology, Bio-Mega Inc., Laval Quebec, Canada.
The potential interaction (s) between atrial natriuretic factor (ANF) and porcine--human endothelin (ET-1) was investigated in the endothelium-denuded rat aortic ring preparation. ET-1 produced a sustained contraction of aortic rings with an ED50 of 3.6 +/- 0.49 x 10(-9) M. Within the concentration range of 10(-9) to 10(-7) M, both rat ANF 103-126 and rat ANF 99-126 when preincubated with tissues reduced the contractile efficacy of ET-1 especially at low concentrations resulting in a small but significant rightward shift of the dose--response curve to ET-1. In contrast, at a concentration of 10(-10) M, rANF 99-126 but not rANF 103-126 produced a significant leftward shift of the dose--response curve to ET-1 and an increase in the maximal developed tension for the dose--response curve to ET-1. For tissues incubated in the absence of extracellular calcium or in the presence of the calcium channel blocker nifedipine (5 x 10(-7) M), both ANF derivatives produced a dose-dependent decrease in the maximum contraction, but no change in potency to ET-1. Addition of either rANF 103-126 or rANF 99-126 to tissues maximally contracted with ET-1 resulted in relaxation, reaching a maximum of 70%. The ED50 values for relaxation were 2.7 +/- 0.51 x 10(-8) and 3.5 +/- 0.60 +/- 10(-8) M for rANF 103-126 and rANF 99-126, respectively. ET-1 did not interact with biologically responsive and clearance receptors for ANF.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1838297&dopt=Abstract
Eur J Clin Invest. 1991 Oct;21(5):490-6.
Platelet response to the aggregatory effect of platelet activating factor (PAF) ex vivo in patients with acute myocardial infarction.
Tselepis AD, Tsoukatos D, Droudes C, Donas A, Evangelou A.
Department of Chemistry, Faculty of Medicine, University of Ioannina, Greece.
Platelets from patients with acute myocardial infarction exhibit an increased sensitivity to the aggregatory effect of PAF, in vitro, the first 48 h after the onset of the symptoms. This sensitivity, expressed as PAF EC50 values, seems to be transient after the 2 day period. Also, a remarkable decreased sensitivity to the inhibitory effect of PGI2 against the aggregation induced by PAF appears to the platelets of those patients the first hours after the onset of the symptoms, and persists for at least 14 days. Treatment of patients by drugs with a known inhibitory effect on platelet aggregation in vivo and in vitro (aspirin, nifedipine, indomethacin), does not influence the increase in platelet sensitivity to PAF, but inhibits the secondary aggregation induced by the released aggregating factors from the PAF activated platelets. The increase in platelet sensitivity to PAF is not unique to the AMI since it is also observed in patients with acute bacterial pneumonia. However, we cannot support the theory that it is a general phenomenon of acute tissue injury since it is general phenomenon of acute tissue injury since it is not observed in patients with acute muscular injury.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1752288&dopt=Abstract
J Bone Miner Res. 1994 May;9(5):705-14.
Calcium signaling in endothelin- and platelet-derived growth factor-stimulated chondrocytes.
Stojilkovic SS, Vukicevic S, Luyten FP.
Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, Bethesda, Maryland.
In bovine articular chondrocytes, endothelin (ET) and platelet-derived growth factor (PDGF) receptors mediate agonist-induced increases in inositol phosphate hydrolysis, cytoplasmic calcium concentration ([Ca2+]i), and mitogenesis. In most cells, ET stimulated nonoscillatory [Ca2+]i elevations with dose-dependent increases in both spike and plateau amplitudes. However, about 15% of cells showed oscillatory Ca2+ responses with a constant frequency and variable shape and duration of spiking. ET-1 and ET-2 were more potent than ET-3 in stimulating [Ca2+]i responses in inhibiting the specific binding of 125I-ET-1 and 125I-ET-3 and in promoting internalization of the receptor-ligand complex, consistent with actions through endothelin ETA receptors. Similar nonoscillatory and oscillatory patterns of Ca2+ responses were observed in PDGF-stimulated cells. In cells showing nonoscillatory Ca2+ responses to ET-1, subsequent stimulation with PDGF was frequently followed by the development of an oscillatory Ca2+ response. Nonoscillatory responses to both agonists were only slightly reduced in Ca(2+)-deficient medium, but the oscillatory responses were critically dependent on Ca2+ entry. Ca2+ spiking was not altered in the presence of the voltage-sensitive Ca2+ channel blocker, nifedipine; also, depolarization of chondrocytes by high K+ did not induce [Ca2+]i responses, confirming that voltage-sensitive calcium channels are not expressed in these cells. At high agonist concentrations, ET- but not PDGF-stimulated cells underwent rapid desensitization. Activation of ETA and PDGF receptors was associated with differential stimulation of thymidine incorporation; ET-1 induced a low-amplitude bell-shaped dose-response curve; PDGF induced a sustained sigmoidal and dose-dependent rise. These data indicate that two distinct types of Ca(2+)-mobilizing receptors initiate similar patterns of [Ca2+]i responses but have different capacities to maintain and reinitiate the Ca2+ signaling, as well as to promote mitogenesis.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8053400&dopt=Abstract
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