Ca2(+)-channel agonist BAY K8644 mimics 1,25(OH)2-vitamin D3 rapid enhancement of Ca2+ transport in chick perfused duodenum
Autor: | Anthony W. Norman, Ana R. de Boland, Ilka Nemere |
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Rok vydání: | 1990 |
Předmět: |
Agonist
Male medicine.medical_specialty Nifedipine medicine.drug_class Duodenum Biophysics chemistry.chemical_element Biological Transport Active Calcium channel blocker Calcium Biochemistry Intestinal absorption Isotopes of calcium chemistry.chemical_compound Calcium Chloride Calcitriol Reference Values Internal medicine medicine Animals Molecular Biology Calcium Radioisotopes Muscle Smooth Cell Biology Membrane transport 3-Pyridinecarboxylic acid 1 4-dihydro-2 6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)- Methyl ester Vitamin D Deficiency Bay K8644 Perfusion Kinetics Endocrinology chemistry Intestinal Absorption Chickens medicine.drug |
Zdroj: | Biochemical and biophysical research communications. 166(1) |
ISSN: | 0006-291X |
Popis: | To further understand the molecular mechanism by which 1,25(OH)2-vitamin D3 (1,25(OH)2D3) rapidly stimulates intestinal calcium transport (termed transcaltachia), the effect of the calcium channel agonist BAY K8644 was studied in vascularly perfused duodenal loops from normal, vitamin D-replete chicks. BAY K8644, 2 mu M, was found to stimulate {sup 45}Ca{sup 2+} transport from the lumen to the vascular effluent to the same extent as physiological levels of 1,25(OH)2D3. The sterol and the Ca{sup 2+} channel agonist both increased {sup 45}Ca{sup 2+} transport 70% above control values within 2 min and 200% after 30 min of vascular perfusion. The effect of the Ca{sup 2+} channel agonist was dose dependent. Also, 1,25(OH)2D3-enhanced transcaltachia was abolished by the calcium channel blocker nifedipine. Collectively, these results suggest the involvement of 1,25(OH)2D3 in the activation of basal lateral membrane Ca{sup 2+} channels as an early effect in the transcaltachic response. |
Databáze: | OpenAIRE |
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