The occupancy of atrial natriuretic peptide (ANP) receptors of the ANPA type in human neuroblastoma NB-OK-1 cells elevates cGMP. In this study, ANP concentrations of 10 nM or more increased total K+ uptake. Data obtained in the presence of bumetanide and/or ouabain demonstrated that 1 microM ANP induced a primary stimulation (by 82%) of Na-K-Cl cotransport and a subsequent indirect stimulation (by 15%) of Na,K-ATPase. ANP also inhibited Na/H exchange through an amiloride-sensitive mechanism, as shown by intracellular pH measurement in cells challenged or not by an acid or alkaline load. (Bu)2cGMP mimicked all ANP effects, suggesting that ANP acted through a cGMP-dependent mechanism.
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http://dx.doi.org/10.1210/endo.133.1.8391430 | DOI Listing |
Exp Anim
January 2025
Department of Neurosciences, School of Medical Sciences, Universiti Sains Malaysia.
Status epilepticus is linked to cognitive decline due to damage to the hippocampus, a key structure involved in cognition. The hippocampus's high vulnerability to epilepsy-related damage is the main reason for this impairment. Convulsive seizures, such as those observed in status epilepticus, can cause various hippocampal pathologies, including inflammation, abnormal neurogenesis, and neuronal death.
View Article and Find Full Text PDFAm J Physiol Gastrointest Liver Physiol
December 2024
Department of Physiology and APC Microbiome Ireland, University College Cork, Cork, Ireland.
Arch Toxicol
December 2024
Department of Nephrology and Hypertension, Dokkyo Medical University, Tochigi, Japan.
Sci Transl Med
September 2024
Department of Neurobiology, University of Texas Medical Branch, Galveston, TX 77555, USA.
Spinal cord injury (SCI) results in acute damage and triggers secondary injury responses with sustained neuronal loss and dysfunction. However, the underlying mechanisms for these delayed neuronal pathologies are not entirely understood. SCI results in the swelling of spinal neurons, but the contribution of cell swelling to neuronal loss and functional deficits after SCI has not been systematically characterized.
View Article and Find Full Text PDFCNS Neurosci Ther
September 2024
School of Rehabilitation Medicine, Capital Medical University, Beijing, China.
Aim: We aimed to explore whether the combination of CLP290 and bumetanide maximally improves neuropathic pain following spinal cord injury (SCI) and its possible molecular mechanism.
Methods: Rats were randomly divided into five groups: Sham, SCI + vehicle, SCI + CLP290, SCI + bumetanide, and SCI + combination (CLP290 + bumetanide). Drug administration commenced on the 7th day post-injury (7 dpi) and continued for 14 days.
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