cardiovascular-agents has been researched along with cesium-chloride* in 2 studies
2 other study(ies) available for cardiovascular-agents and cesium-chloride
Article | Year |
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Hyperpolarization-activated cyclic nucleotide-gated channels in peripheral diaphragmatic lymphatics.
Diaphragmatic lymphatic function is mainly sustained by pressure changes in the tissue and serosal cavities during cardiorespiratory cycles. The most peripheral diaphragmatic lymphatics are equipped with muscle cells (LMCs), which exhibit spontaneous contraction, whose molecular machinery is still undetermined. Hypothesizing that spontaneous contraction might involve hyperpolarization-activated cyclic nucleotide-gated (HCN) channels in lymphatic LMCs, diaphragmatic specimens, including spontaneously contracting lymphatics, were excised from 33 anesthetized rats, moved to a perfusion chamber containing HEPES-Tyrode's solution, and treated with HCN channels inhibitors cesium chloride (CsCl), ivabradine, and ZD-7288. Compared with control, exposure to 10 mM CsCl reduced (-65%, n = 13, P < 0.01) the contraction frequency (F Topics: Animals; Benzazepines; Cardiovascular Agents; Cesium; Chlorides; Diaphragm; Female; Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels; Immunohistochemistry; Ivabradine; Lymphatic Vessels; Male; Muscle, Smooth, Vascular; Myocytes, Smooth Muscle; Potassium Channels; Pyrimidines; Rats; Rats, Wistar; Real-Time Polymerase Chain Reaction; Vasoconstriction | 2016 |
Slow oscillations (=1 Hz) mediated by GABAergic interneuronal networks in rat hippocampus.
Perfusion of rat brain slices with low millimole CsCl elicits slow oscillations of =1 Hz in hippocampal CA1 pyramidal neurons. These oscillations are GABAA receptor-mediated hyperpolarizations that permit a coherent fire-pause pattern in a population of CA1 neurons. They can persist without the activation of ionotropic glutamate receptors but require adenosine-dependent inhibition of glutamate transmission. In response to external Cs+, multiple interneurons in the CA1 region display rhythmic discharges that correlate with the slow oscillations in CA1 pyramidal neurons. The interneuronal discharges arise spontaneously from the resting potential, and their rhythmicity is regulated by periodic, GABAA receptor-mediated hyperpolarizations. In addition, interneurons show periodic partial spikes and neurobiotin coupling, and applications of known gap junctional uncouplers interrupt the Cs+-induced slow rhythm in both CA1 pyramidal neurons and interneurons. We propose that these slow oscillations originate from a GABAergic interneuronal network that interacts through reciprocal inhibition and possibly gap junctional connection. Topics: 2-Amino-5-phosphonovalerate; 6-Cyano-7-nitroquinoxaline-2,3-dione; Adenosine; Age Factors; Animals; Benzoates; Bicuculline; Cardiovascular Agents; Cesium; Chlorides; Excitatory Amino Acid Antagonists; GABA Antagonists; gamma-Aminobutyric Acid; Gap Junctions; Glycine; Hippocampus; Interneurons; Male; Membrane Potentials; Neural Pathways; Organ Culture Techniques; Patch-Clamp Techniques; Periodicity; Pyrimidines; Rats; Rats, Wistar; Receptors, GABA-A; Synapses; Temperature; Xanthines | 1998 |