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http://dx.doi.org/10.1016/0002-8703(84)90717-8 | DOI Listing |
eNeurologicalSci
March 2025
Department of Neurology, Nagoya City University Graduate School of Medical Sciences, Aichi, Japan.
L-type calcium channel antagonists are uncommon causes of myoclonus, and the underlying mechanism remains unclear. Here, we report a case of parkinsonian syndrome with deterioration of preexisting myoclonus after nifedipine use. A 96-year-old woman was administered a single dose of sustained-release nifedipine for chest pain.
View Article and Find Full Text PDFAntibiotics (Basel)
August 2019
Department of Dental and Maxillofacial Sciences, "Sapienza" University of Rome, 00100 Rome, Italy.
Hypertens Res
February 2019
Department. of Experimental Hypertension, Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic.
Basal calcium sensitization is decreased in spontaneously hypertensive rats, although their blood pressure (BP) response to acute Rho-kinase inhibition is enhanced. Using fasudil (Rho-kinase inhibitor) or nifedipine (L-VDCC blocker), we evaluated the contribution of calcium sensitization and calcium entry to BP maintenance in hypertensive transgenic Ren-2 rats (TGR) focusing on the influence of major vasoactive systems and/or baroreflex efficiency on BP responses to these two drugs. Homozygous TGR and normotensive Hannover Sprague-Dawley (HanSD) control rats aged 5, 11, or 22 weeks were used.
View Article and Find Full Text PDFCalcium (Ca) signaling is critical for successful fertilization. In spermatozoa, capacitation, hyperactivation of motility and the acrosome reaction are all mediated by increases in intracellular Ca through CatSper (sperm-specific cation channel). The CatSper channel complex contains four pore-forming α subunits (CatSper1-4) and five accessory subunits called β, δ, ε, γ and ζ.
View Article and Find Full Text PDFJ Hypertens
December 2015
aInstitute of Physiology, Czech Academy of Sciences bDepartment of Physiology, Faculty of Sciences, Charles University, Prague, Czech Republic.
Background: Altered calcium sensitization (mediated by RhoA/Rho-kinase pathway) and enhanced calcium entry through L-type voltage-dependent calcium channels (L-VDCCs) participate in blood pressure (BP) maintenance of adult spontaneously hypertensive rats (SHRs). This study aimed to evaluate ontogenetic changes of these two pathways in BP control of SHR and Wistar-Kyoto (WKY) aged 3, 5, 7, 13, 26 and 42 weeks.
Methods: BP response to acute administration of Rho-kinase inhibitor fasudil or L-VDCC blocker nifedipine and the expression of particular components of RhoA/Rho-kinase pathway were determined in young and adult animals.
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