-
Something wrong with this record ?
Broad-range TRP channel inhibitors (2-APB, flufenamic acid, SKF-96365) affect differently contraction of resistance and conduit femoral arteries of rat
M. Bencze, M. Behuliak, A. Vavřínová, J. Zicha,
Language English Country Netherlands
Document type Journal Article, Research Support, Non-U.S. Gov't
- MeSH
- Femoral Artery drug effects physiology MeSH
- Imidazoles pharmacology MeSH
- Transient Receptor Potential Channels antagonists & inhibitors physiology MeSH
- Rats MeSH
- Flufenamic Acid pharmacology MeSH
- Organ Culture Techniques MeSH
- Rats, Wistar MeSH
- Boron Compounds pharmacology MeSH
- Muscle, Smooth, Vascular drug effects physiology MeSH
- Vasoconstriction drug effects physiology MeSH
- Dose-Response Relationship, Drug MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
Transient receptor potential (TRP) channels are proposed to contribute to membrane depolarization and Ca2+ influx into vascular smooth muscle (VSM) cells. Our aim was to study the effects of widely used broad-range TRP channel inhibitors--2-aminoethoxydiphenyl borate (2-APB), flufenamic acid (FFA) and SKF-96365--on the contraction of freshly isolated small and large arteries. Endothelium-denuded resistance (≈250 μm) and conduit (≈1000 μm) femoral arteries were isolated from adult Wistar rats and mounted in wire myograph. The effects of the above mentioned TRP channel inhibitors and voltage-dependent calcium channel inhibitor nifedipine were studied on arterial contractions induced by phenylephrine, U-46619 or K+. Phenylephrine-induced contractions were also studied in the absence of extracellular Na+. mRNA expression of particular canonical and melastatin TRP channel subunits in femoral vascular bed was determined. TRP channel inhibitors attenuated K+-induced contraction less than nifedipine. Phenylephrine-induced contraction was more influenced by 2-APB in resistance arteries, while FFA completely prevented U-46619-induced contraction in both sizes of arteries. The absence of extracellular Na+ prevented the inhibitory effects of 2-APB, but not those of FFA. The observed effects of broad-range TRP channel inhibitors, which were dependent on the size of the artery, confirmed the involvement of TRP channels in agonist-induced contractions. The inhibitory effects of 2-APB (but not those of FFA or SKF-96365) were dependent on the presence of extracellular Na+.
References provided by Crossref.org
- 000
- 00000naa a2200000 a 4500
- 001
- bmc16028201
- 003
- CZ-PrNML
- 005
- 20250618090436.0
- 007
- ta
- 008
- 161005e20150916ne f 000 0|eng||
- 009
- AR
- 024 7_
- $a 10.1016/j.ejphar.2015.09.014 $2 doi
- 024 7_
- $a 10.1016/j.ejphar.2015.09.014 $2 doi
- 035 __
- $a (PubMed)26384458
- 040 __
- $a ABA008 $b cze $d ABA008 $e AACR2
- 041 0_
- $a eng
- 044 __
- $a ne
- 100 1_
- $a Bencze, Michal $u Department of Experimental Hypertension, Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic; Department of Physiology, Faculty of Science, Charles University, Prague, Czech Republic. Electronic address: michalbencze@gmail.com.
- 245 10
- $a Broad-range TRP channel inhibitors (2-APB, flufenamic acid, SKF-96365) affect differently contraction of resistance and conduit femoral arteries of rat / $c M. Bencze, M. Behuliak, A. Vavřínová, J. Zicha,
- 520 9_
- $a Transient receptor potential (TRP) channels are proposed to contribute to membrane depolarization and Ca2+ influx into vascular smooth muscle (VSM) cells. Our aim was to study the effects of widely used broad-range TRP channel inhibitors--2-aminoethoxydiphenyl borate (2-APB), flufenamic acid (FFA) and SKF-96365--on the contraction of freshly isolated small and large arteries. Endothelium-denuded resistance (≈250 μm) and conduit (≈1000 μm) femoral arteries were isolated from adult Wistar rats and mounted in wire myograph. The effects of the above mentioned TRP channel inhibitors and voltage-dependent calcium channel inhibitor nifedipine were studied on arterial contractions induced by phenylephrine, U-46619 or K+. Phenylephrine-induced contractions were also studied in the absence of extracellular Na+. mRNA expression of particular canonical and melastatin TRP channel subunits in femoral vascular bed was determined. TRP channel inhibitors attenuated K+-induced contraction less than nifedipine. Phenylephrine-induced contraction was more influenced by 2-APB in resistance arteries, while FFA completely prevented U-46619-induced contraction in both sizes of arteries. The absence of extracellular Na+ prevented the inhibitory effects of 2-APB, but not those of FFA. The observed effects of broad-range TRP channel inhibitors, which were dependent on the size of the artery, confirmed the involvement of TRP channels in agonist-induced contractions. The inhibitory effects of 2-APB (but not those of FFA or SKF-96365) were dependent on the presence of extracellular Na+.
- 650 _2
- $a zvířata $7 D000818
- 650 _2
- $a sloučeniny boru $x farmakologie $7 D001896
- 650 _2
- $a vztah mezi dávkou a účinkem léčiva $7 D004305
- 650 _2
- $a arteria femoralis $x účinky léků $x fyziologie $7 D005263
- 650 _2
- $a kyselina flufenamová $x farmakologie $7 D005439
- 650 _2
- $a imidazoly $x farmakologie $7 D007093
- 650 _2
- $a mužské pohlaví $7 D008297
- 650 _2
- $a svaly hladké cévní $x účinky léků $x fyziologie $7 D009131
- 650 _2
- $a orgánové kultury - kultivační techniky $7 D009924
- 650 _2
- $a krysa rodu Rattus $7 D051381
- 650 _2
- $a potkani Wistar $7 D017208
- 650 _2
- $a kationtové kanály TRP $x antagonisté a inhibitory $x fyziologie $7 D050051
- 650 _2
- $a vazokonstrikce $x účinky léků $x fyziologie $7 D014661
- 655 _2
- $a časopisecké články $7 D016428
- 655 _2
- $a práce podpořená grantem $7 D013485
- 700 1_
- $a Behuliak, Michal $u Department of Experimental Hypertension, Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic. $7 xx0196023
- 700 1_
- $a Vavřínová, Anna $u Department of Experimental Hypertension, Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic; Department of Physiology, Faculty of Science, Charles University, Prague, Czech Republic.
- 700 1_
- $a Zicha, Josef $u Department of Experimental Hypertension, Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic.
- 773 0_
- $w MED00001641 $t European journal of pharmacology $x 1879-0712 $g Roč. 765 (20150916), s. 533-40
- 856 41
- $u https://pubmed.ncbi.nlm.nih.gov/26384458 $y Pubmed
- 910 __
- $a ABA008 $b sig $c sign $y a $z 0
- 990 __
- $a 20161005 $b ABA008
- 991 __
- $a 20250618090427 $b ABA008
- 999 __
- $a ok $b bmc $g 1166515 $s 952831
- BAS __
- $a 3
- BAS __
- $a PreBMC
- BMC __
- $a 2015 $b 765 $c - $d 533-40 $e 20150916 $i 1879-0712 $m European journal of pharmacology $n Eur J Pharmacol $x MED00001641
- LZP __
- $a Pubmed-20161005
