ArticleNaunyn-Schmiedeberg's archives of pharmacology2007
Effects of flavoxate hydrochloride on voltage-dependent Ba2+ currents in human detrusor myocytes at different experimental temperatures.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- Article
- Natural and synthetic flavonoids, novel blockers of the volume-regulated anion channels, inhibit endothelial cell proliferation.Pflugers Archiv : European journal of physiology · 2018Article
- Flavoxate in urogynecology: an old drug revisited.International urogynecology journal · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The inhibitory effects of flavoxate hydrochloride (piperidinoethyl-3-methylflavone-8-carboxylate; hereafter referred as flavoxate) on voltage-dependent nifedipine-sensitive inward Ba2+ currents (I Ba) in human detrusor myocytes were investigated at different temperatures using conventional whole-cell patch-clamp techniques. When the bath-solution temperature was increased from 22 degrees C to 30 degrees C, I Ba peak amplitude was enhanced by approximately twice at several test potentials. Neither the I Ba threshold nor the membrane potentials for the I Ba maximum peak amplitude was affected by the temperature change. The concentration-response curves of flavoxate at both 30 degrees C (Ki = 5.1 microM) and 37 degrees C (Ki = 4.6 microM) were slightly shifted to the left in comparison with that at 22 degrees C (Ki = 10.3 microM). Similar results were also obtained in the presence of nifedipine (Ki = 14 nM at 22 degrees C vs. Ki = 2.5 nM at 30 degrees C and Ki = 2.1 nM at 37 degrees C). Altering the bath-solution temperature from 22 degrees C to 30 degrees C shifted the steady-state inactivation curve of I Ba at -90 mV to the left. At 30 degrees C, the steady-state inactivation curve of I Ba in the presence of flavoxate was also shifted to the left in comparison with that in the absence of flavoxate. Either 3-isobutyl-1-methylxanthine (IBMX) or theophylline, a phosphodiesterase inhibitor, caused little effects on I Ba, although cyclic nucleotides (dibutyryl cAMP and 8-Br-cGMP) inhibited I Ba. These results suggest that the inhibitory actions of flavoxate on I Ba in human detrusor myocytes were slightly changed at different experimental temperatures and that flavoxate directly blocked voltage-dependent L-type Ca2+ channels, not through the inhibition of phosphodiesterase activity pathway.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.