FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2149266722> ?p ?o ?g. }

• W2149266722 endingPage "130" @default.
• W2149266722 startingPage "121" @default.
• W2149266722 abstract "Abstract The patch-clamp technique was used to examine the inhibition of delayed rectifier K + channels by agents that release intracellular Ca 2+ . During voltage-clamp experiments on isolated myocytes with 4-aminopyridine (4-AP, 10 mmol/L) and niflumic acid (100 μmol/L) present to inhibit delayed rectifier K + current (I K(dr) ) and Ca 2+ -activated Cl − current (I Cl(Ca) ), angiotensin II (Ang II) and caffeine increased Ca 2+ -activated K + current (I K(Ca) ) between −25 and 80 mV (n=5). Conversely, with charybdotoxin (ChTX, 100 nmol/L) and niflumic acid (100 μmol/L) present to inhibit I K(Ca) and I Cl(Ca) , Ang II and caffeine only caused inhibition of I K(dr) . Block was achieved within 15 seconds of drug application and was reversible upon washout (n=5). The effects of Ang II on I K(Ca) and I K(dr) were inhibited by the specific Ang II receptor antagonist losartan (1 mmol/L, n=3). Intracellular BAPTA (10 mmol/L) also abolished the effects of Ang II and caffeine on both I K(Ca) and I K(dr) . In current-clamp experiments, the application of ChTX (100 nmol/L) and niflumic acid (100 μmol/L) caused little change in resting membrane potential; however, subsequent application of caffeine (10 mmol/L) caused a 26±2.9 mV depolarization from −54±3.1 to −28±1.7 mV (n=6). 4-AP (10 mmol/L) blocked the caffeine-induced depolarization. When isolated cells were loaded with the Ca 2+ indicator indo 1 (100 μmol/L), Ang II, caffeine, and 4-AP increased [Ca 2+ ] i and depolarized the cells. Both Ang II and caffeine caused an increase in [Ca 2+ ] i that preceded membrane depolarization, whereas 4-AP depolarized the cell first and then caused an increase in [Ca 2+ ] i (n=4). In inside-out patches, with 200 nmol/L ChTX in the patch pipette to block large-conductance Ca 2+ -activated K + channels, a 45±7-picosiemen 4-AP–sensitive K + channel was identified that was sensitive to cytoplasmic Ca 2+ (n=6). Increasing intracellular Ca 2+ decreased channel opening probability [N×P(open), where N is the number of functional channels in a patch and P(open) is the opening probability] at all membrane potentials examined. At 0 mV, increasing Ca 2+ from <5 to 200 and 600 nmol/L free Ca 2+ decreased N×P(open) by 52±3% and 73±7%, respectively (n=6). The decrease in opening probability of the delayed rectifier K + channel resulted from a concentration- and voltage-dependent decrease in mean open time. The decrease in mean open time reflected significant decreases and increases in open and closed time constants, respectively. These results suggest that agonist-induced changes in intracellular Ca 2+ can alter vascular smooth muscle membrane potential through regulation of delayed rectifier K + channels." @default.
• W2149266722 created "2016-06-24" @default.
• W2149266722 creator A5041646295 @default.
• W2149266722 creator A5066498895 @default.
• W2149266722 date "1995-07-01" @default.
• W2149266722 modified "2023-10-15" @default.
• W2149266722 title "[Ca ²⁺ ] _i Inhibition of K ⁺ Channels in Canine Renal Artery" @default.
• W2149266722 cites W134363133 @default.
• W2149266722 cites W1970366970 @default.
• W2149266722 cites W1983476683 @default.
• W2149266722 cites W2004403903 @default.
• W2149266722 cites W2006501250 @default.
• W2149266722 cites W2009667219 @default.
• W2149266722 cites W2009935511 @default.
• W2149266722 cites W2014671743 @default.
• W2149266722 cites W2027855010 @default.
• W2149266722 cites W2035460943 @default.
• W2149266722 cites W2040668875 @default.
• W2149266722 cites W2047974033 @default.
• W2149266722 cites W2058744604 @default.
• W2149266722 cites W2061193289 @default.
• W2149266722 cites W2070015190 @default.
• W2149266722 cites W2071969879 @default.
• W2149266722 cites W2084976269 @default.
• W2149266722 cites W2110518868 @default.
• W2149266722 cites W2120003464 @default.
• W2149266722 cites W2128535775 @default.
• W2149266722 cites W2136550767 @default.
• W2149266722 cites W2141207242 @default.
• W2149266722 cites W2162439295 @default.
• W2149266722 cites W2180403979 @default.
• W2149266722 cites W2460403442 @default.
• W2149266722 doi "https://doi.org/10.1161/01.res.77.1.121" @default.
• W2149266722 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/7788870" @default.
• W2149266722 hasPublicationYear "1995" @default.
• W2149266722 type Work @default.
• W2149266722 sameAs 2149266722 @default.
• W2149266722 citedByCount "68" @default.
• W2149266722 countsByYear W21492667222013 @default.
• W2149266722 countsByYear W21492667222014 @default.
• W2149266722 countsByYear W21492667222015 @default.
• W2149266722 countsByYear W21492667222016 @default.
• W2149266722 countsByYear W21492667222017 @default.
• W2149266722 countsByYear W21492667222021 @default.
• W2149266722 crossrefType "journal-article" @default.
• W2149266722 hasAuthorship W2149266722A5041646295 @default.
• W2149266722 hasAuthorship W2149266722A5066498895 @default.
• W2149266722 hasConcept C12554922 @default.
• W2149266722 hasConcept C134018914 @default.
• W2149266722 hasConcept C147944092 @default.
• W2149266722 hasConcept C153461711 @default.
• W2149266722 hasConcept C170493617 @default.
• W2149266722 hasConcept C178790620 @default.
• W2149266722 hasConcept C181911157 @default.
• W2149266722 hasConcept C185592680 @default.
• W2149266722 hasConcept C2778500429 @default.
• W2149266722 hasConcept C2779700409 @default.
• W2149266722 hasConcept C2780019300 @default.
• W2149266722 hasConcept C2780419564 @default.
• W2149266722 hasConcept C2908929049 @default.
• W2149266722 hasConcept C4141045 @default.
• W2149266722 hasConcept C519063684 @default.
• W2149266722 hasConcept C55493867 @default.
• W2149266722 hasConcept C79879829 @default.
• W2149266722 hasConcept C86803240 @default.
• W2149266722 hasConceptScore W2149266722C12554922 @default.
• W2149266722 hasConceptScore W2149266722C134018914 @default.
• W2149266722 hasConceptScore W2149266722C147944092 @default.
• W2149266722 hasConceptScore W2149266722C153461711 @default.
• W2149266722 hasConceptScore W2149266722C170493617 @default.
• W2149266722 hasConceptScore W2149266722C178790620 @default.
• W2149266722 hasConceptScore W2149266722C181911157 @default.
• W2149266722 hasConceptScore W2149266722C185592680 @default.
• W2149266722 hasConceptScore W2149266722C2778500429 @default.
• W2149266722 hasConceptScore W2149266722C2779700409 @default.
• W2149266722 hasConceptScore W2149266722C2780019300 @default.
• W2149266722 hasConceptScore W2149266722C2780419564 @default.
• W2149266722 hasConceptScore W2149266722C2908929049 @default.
• W2149266722 hasConceptScore W2149266722C4141045 @default.
• W2149266722 hasConceptScore W2149266722C519063684 @default.
• W2149266722 hasConceptScore W2149266722C55493867 @default.
• W2149266722 hasConceptScore W2149266722C79879829 @default.
• W2149266722 hasConceptScore W2149266722C86803240 @default.
• W2149266722 hasIssue "1" @default.
• W2149266722 hasLocation W21492667221 @default.
• W2149266722 hasLocation W21492667222 @default.
• W2149266722 hasOpenAccess W2149266722 @default.
• W2149266722 hasPrimaryLocation W21492667221 @default.
• W2149266722 hasRelatedWork W1500192109 @default.
• W2149266722 hasRelatedWork W2018983834 @default.
• W2149266722 hasRelatedWork W2044049206 @default.
• W2149266722 hasRelatedWork W2055997287 @default.
• W2149266722 hasRelatedWork W2083038360 @default.
• W2149266722 hasRelatedWork W2376215649 @default.
• W2149266722 hasRelatedWork W2405958842 @default.
• W2149266722 hasRelatedWork W2417181177 @default.
• W2149266722 hasRelatedWork W2996368309 @default.
• W2149266722 hasRelatedWork W3176896983 @default.

• next