Sulfonylurea receptor ligands modulate stretch-induced ANF secretion in rat atrial myocyte culture
Autor: | Jin-Hua Jiao, Alex J. Baertschi, Angela Roatti, Philippe Baumann, Anne Baron, Richard A. Pence |
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Přispěvatelé: | University of Virginia [Charlottesville], Centre médical universitaire de Genève (CMU) |
Jazyk: | angličtina |
Rok vydání: | 2000 |
Předmět: |
medicine.medical_specialty
Potassium Channels Physiology Receptors Drug Deoxyglucose 030204 cardiovascular system & hematology Ligands Sulfonylurea Receptors Rats Sprague-Dawley 03 medical and health sciences Adenosine Triphosphate 0302 clinical medicine Tolbutamide Atrial natriuretic peptide [SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system Physical Stimulation Physiology (medical) Internal medicine adenosine 58-triphosphate-sensitive potassium channels [SDV.BC.IC]Life Sciences [q-bio]/Cellular Biology/Cell Behavior [q-bio.CB] Potassium Channel Blockers medicine Diazoxide Animals Myocyte Heart Atria Potassium Channels Inwardly Rectifying Cells Cultured 030304 developmental biology 0303 health sciences Chemistry Myocardium Electric Conductivity atrial natriuretic factor regulation Rats diazoxide [SDV.BBM.BP]Life Sciences [q-bio]/Biochemistry Molecular Biology/Biophysics Endocrinology tolbutamide Circulatory system [SDV.SP.PHARMA]Life Sciences [q-bio]/Pharmaceutical sciences/Pharmacology Tonicity Sulfonylurea receptor ATP-Binding Cassette Transporters Cardiology and Cardiovascular Medicine atrial natriuretic factor Intracellular hormones hormone substitutes and hormone antagonists medicine.drug |
Zdroj: | AJP-Heart and Circulatory Physiology AJP-Heart and Circulatory Physiology, American Physiological Society, 2000, 278 (6), pp.H2028-H2038. ⟨10.1152/ajpheart.2000.278.6.H2028⟩ |
ISSN: | 0363-6135 1522-1539 |
DOI: | 10.1152/ajpheart.2000.278.6.H2028⟩ |
Popis: | Stretch-induced atrial natriuretic factor (ANF) secretion was studied in cultures of neonate atrial appendage myocytes. Stretch, applied for 40 min by hypotonic swelling, increased the mean area of 44 individually imaged myocytes by 4.8–8.8% ( P < 0.0001) at 6 min and by 2.3–6.2% ( P < 0.05) at 35 min. Stretch increased immunoreactive ANF release by 42% ( P < 0.05) from a baseline of 315 pg/ml. The ATP-sensitive K+(KATP)-channel blocker tolbutamide (100 μmol/l) increased the stretch-stimulated release to 84% ( P < 0.01) over baseline, whereas lower concentrations (1, 10, and 30 μmol/l) had no stimulatory effect. The KATP-channel opener diazoxide (0.1, 1, 10, 30, and 100 μmol/l) inhibited stretch- plus tolbutamide-stimulated ANF release in a concentration-dependent manner, with IC50 = 2.2 μmol/l, although 100 μmol/l diazoxide did not reduce the increase in mean cell area. The stretch-stimulated KATP current, monitored in 82 whole cell recordings with sulfonylurea receptor (SUR) ligands, was inversely correlated with the stretch-induced ANF release ( r 2 = 0.79, P < 0.0001). In the absence of stretch, the KATP current had no relationship with baseline ANF release, and baseline ANF release was not affected by the KATP-channel modulators. The results show that SUR ligands that open KATP channels inhibit stretch-induced ANF release in atrial myocytes, in correlation with the stretch-activated KATP current. The subcellular site of action of the SUR ligands—plasmalemma or intracellular organelles—remains to be determined. |
Databáze: | OpenAIRE |
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