NDLI: Use of electrochemical impedance measurements to monitor β-adrenergic stimulation of bovine aortic endothelial cells

Content Provider	Springer Nature Link
Author	Wegener, Joachim Zink, Sigrid Rösen, Peter Galla, H. J.
Copyright Year	1999
Abstract	Due to the high permeability of endothelial cell layers derived from macrovascular vessels, precise determination of their barrier function towards ion movement requires refined experimental techniques. We thus cultured bovine aortic endothelial cells (BAEC) directly on thin gold-film electrodes and measured the electrochemical impedance to study their passive electrical properties in general and during β-adrenergic stimulation. Impedance spectra (10–2·106 Hz) of confluent cell monolayers revealed that the electrical characteristics of the cells can be modelled by a simple resistor-capacitor parallel network. Under control conditions the overall resistance of confluent BAEC monolayers was 3.6±0.6 Ω·cm2 (n=30) and the capacitance was 0.6±0.1 µF/cm2. Both quantities are discussed with respect to morphological characteristics of these cells. Stimulation of BAECs with the synthetic β-adrenoceptor agonist isoproterenol leads to a concentration-dependent, highly specific increase of the cell layer resistance characterized by a concentration for half-maximal response (EC50) of 0.3±0.1 µM. The cell layer capacitance, however, remained unaffected. Using impedance measurements at a single frequency, we analysed the response of BAECs to treatment with isoproterenol in comparison with several chemically unrelated compounds known to stimulate the adenosine 3’,5’-cyclic monophosphate (cAMP)-dependent signal transduction cascade. These studies confirmed that the enhancement of the cell layer resistance after β-adrenergic stimulation is mediated by an increase in intracellular cAMP.
Starting Page	925
Ending Page	934
Page Count	10
File Format	PDF
ISSN	00316768
Journal	Pflügers Archiv
Volume Number	437
Issue Number	6
e-ISSN	14322013
Language	English
Publisher	Springer-Verlag
Publisher Date	1999-04-22
Publisher Place	Berlin, Heidelberg
Access Restriction	One Nation One Subscription (ONOS)
Content Type	Text
Resource Type	Article
Subject	Physiology Physiology (medical) Clinical Biochemistry

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

FCCP depolarizes plasma membrane potential by activating proton and Na+ currents in bovine aortic endothelial cells

Differential lusitropic responsiveness to β-adrenergic stimulation in rat atrial and ventricular cardiac myocytes

Impedance analysis of GPCR-mediated changes in endothelial barrier function: overview and fundamental considerations for stable and reproducible measurements

Ca2+ entry through cardiac L-type Ca2+ channels modulates β-adrenergic stimulation in mouse ventricular myocytes

Co-ordinated changes in cAMP, phosphorylated phospholamban, Ca2+ and contraction following β-adrenergic stimulation of rat heart

Correlation of HSP70 Expression and Cell Viability Following Thermal Stimulation of Bovine Aortic Endothelial Cells

Change of quantal size and parameters of release with stimulation in bovine chromaffin cells

Accentuated antagonism by angiotensin II on guinea-pig cardiac L-type Ca-currents enhanced by β-adrenergic stimulation

The relative relevance of phosphorylation of the Thr17 residue of phospholamban is different at different levels of β-adrenergic stimulation

Use of electrochemical impedance measurements to monitor β-adrenergic stimulation of bovine aortic endothelial cells

Similar Documents

FCCP depolarizes plasma membrane potential by activating proton and Na+ currents in bovine aortic endothelial cells

Differential lusitropic responsiveness to β-adrenergic stimulation in rat atrial and ventricular cardiac myocytes

Impedance analysis of GPCR-mediated changes in endothelial barrier function: overview and fundamental considerations for stable and reproducible measurements

Ca2+ entry through cardiac L-type Ca2+ channels modulates β-adrenergic stimulation in mouse ventricular myocytes

Co-ordinated changes in cAMP, phosphorylated phospholamban, Ca2+ and contraction following β-adrenergic stimulation of rat heart

Correlation of HSP70 Expression and Cell Viability Following Thermal Stimulation of Bovine Aortic Endothelial Cells

Change of quantal size and parameters of release with stimulation in bovine chromaffin cells

Accentuated antagonism by angiotensin II on guinea-pig cardiac L-type Ca-currents enhanced by β-adrenergic stimulation

The relative relevance of phosphorylation of the Thr17 residue of phospholamban is different at different levels of β-adrenergic stimulation

Use of electrochemical impedance measurements to monitor β-adrenergic stimulation of bovine aortic endothelial cells