Jessica Marksteiner
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Jessica Marksteiner has a total of 12 co-authors. Here are the top co-authors by number of shared publications:
- Benjamin Hackl
Med Univ Vienna, Ctr Physiol & Pharmacol, Dept Neurophysiol & Neuropharmacol, Waehringerstr 13a, A-1190 Vienna, Austria
2 shared publications - Elena Lilliu
Department of Neurophysiology and Neuropharmacology, Center for Physiology and Pharmacology, Medical University of Vienna, 1090 Vienna, Austria
2 shared publications - Hannes Todt
Medical University of Vienna
2 shared publications - Karlheinz Hilber
Medical University of Vienna
2 shared publications - Xaver Koenig
Department of Neurophysiology and Neuropharmacology, Center for Physiology and Pharmacology, Medical University of Vienna, 1090 Vienna, Austria
2 shared publications - Helmut Kubista
Center of Physiology and Pharmacology, Department of Neurophysiology and Neuropharmacology, Medical University of Vienna, Waehringerstrasse 13a, 1090, Vienna, Austria
1 shared publication
Latest Publications
- Open Access
- 5 January 2023
- Published by Elsevier in European Journal of Pharmacology
- Vol. 941, 175495
Modulation of cardiac ventricular conduction: Impact on QRS duration, amplitude and dispersion
- 5 January 2023
- Published by Elsevier in European Journal of Pharmacology
- Vol. 941, 175495
Open AccessModulation of cardiac ventricular conduction: Impact on QRS duration, amplitude and dispersion
- Open Access
Evidence for a Physiological Role of T-Type Ca Channels in Ventricular Cardiomyocytes of Adult Mice
T-type Ca channels are strongly expressed and important in the developing heart. In the adult heart, these channels play a significant role in pacemaker tissues, but there is uncertainty about their presence and physiological relevance in the working myocardium. Here, we show that the T-type Ca channel isoforms Cav3.1 and Cav3.2 are expressed at a protein level in ventricular cardiomyocytes from healthy adult C57/BL6 mice. Myocytes isolated from adult wild-type and Cav3.2 KO mice showed considerable whole cell T-type Ca currents under beta-adrenergic stimulation with isoprenaline. We further show that the detectability of basal T-type Ca currents in murine wild-type cardiomyocytes depends on the applied experimental conditions. Together, these findings reveal the presence of functional T-type Ca channels in the membrane of ventricular myocytes. In addition, electrically evoked Ca release from the sarcoplasmic reticulum was significantly impaired in Cav3.2 KO compared to wild-type cardiomyocytes. Our work implies a physiological role of T-type Ca channels in the healthy adult murine ventricular working myocardium.
Open AccessEvidence for a Physiological Role of T-Type Ca Channels in Ventricular Cardiomyocytes of Adult Mice
T-type Ca channels are strongly expressed and important in the developing heart. In the adult heart, these channels play a significant role in pacemaker tissues, but there is uncertainty about their presence and physiological relevance in the working myocardium. Here, we show that the T-type Ca channel isoforms Cav3.1 and Cav3.2 are expressed at a protein level in ventricular cardiomyocytes from healthy adult C57/BL6 mice. Myocytes isolated from adult wild-type and Cav3.2 KO mice showed considerable whole cell T-type Ca currents under beta-adrenergic stimulation with isoprenaline. We further show that the detectability of basal T-type Ca currents in murine wild-type cardiomyocytes depends on the applied experimental conditions. Together, these findings reveal the presence of functional T-type Ca channels in the membrane of ventricular myocytes. In addition, electrically evoked Ca release from the sarcoplasmic reticulum was significantly impaired in Cav3.2 KO compared to wild-type cardiomyocytes. Our work implies a physiological role of T-type Ca channels in the healthy adult murine ventricular working myocardium.