FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2126046035> ?p ?o ?g. }

• W2126046035 endingPage "68" @default.
• W2126046035 startingPage "60" @default.
• W2126046035 abstract "Background— Abnormally elevated blood pressure is the most prevalent risk factor for cardiovascular disease. The large-conductance, voltage- and Ca 2+ -dependent K + (BK) channel has been proposed as an important effector in the control of vascular tone by linking membrane depolarization and local increases in cytosolic Ca 2+ to hyperpolarizing K + outward currents. However, the BK channel may also affect blood pressure by regulating salt and fluid homeostasis, particularly by adjusting the renin-angiotensin-aldosterone system. Methods and Results— Here we report that deletion of the pore-forming BK channel α subunit leads to a significant blood pressure elevation resulting from hyperaldosteronism accompanied by decreased serum K + levels as well as increased vascular tone in small arteries. In smooth muscle from small arteries, deletion of the BK channel leads to a depolarized membrane potential, a complete lack of membrane hyperpolarizing spontaneous K + outward currents, and an attenuated cGMP vasorelaxation associated with a reduced suppression of Ca 2+ transients by cGMP. The high level of BK channel expression observed in wild-type adrenal glomerulosa cells, together with unaltered serum renin activities and corticotropin levels in mutant mice, suggests that the hyperaldosteronism results from abnormal adrenal cortical function in BK −/− mice. Conclusions— These results identify previously unknown roles of BK channels in blood pressure regulation and raise the possibility that BK channel dysfunction may underlie specific forms of hyperaldosteronism." @default.
• W2126046035 created "2016-06-24" @default.
• W2126046035 creator A5002685729 @default.
• W2126046035 creator A5006288394 @default.
• W2126046035 creator A5007751883 @default.
• W2126046035 creator A5007948673 @default.
• W2126046035 creator A5013089574 @default.
• W2126046035 creator A5018505044 @default.
• W2126046035 creator A5020528511 @default.
• W2126046035 creator A5027078331 @default.
• W2126046035 creator A5031800219 @default.
• W2126046035 creator A5032918352 @default.
• W2126046035 creator A5038432586 @default.
• W2126046035 creator A5039471192 @default.
• W2126046035 creator A5049411755 @default.
• W2126046035 creator A5050696505 @default.
• W2126046035 creator A5053649940 @default.
• W2126046035 creator A5060809580 @default.
• W2126046035 creator A5063480942 @default.
• W2126046035 creator A5071530070 @default.
• W2126046035 creator A5075355972 @default.
• W2126046035 creator A5079582665 @default.
• W2126046035 creator A5080238797 @default.
• W2126046035 creator A5087533254 @default.
• W2126046035 creator A5091874127 @default.
• W2126046035 date "2005-07-05" @default.
• W2126046035 modified "2023-10-17" @default.
• W2126046035 title "Elevated Blood Pressure Linked to Primary Hyperaldosteronism and Impaired Vasodilation in BK Channel–Deficient Mice" @default.
• W2126046035 cites W1619653867 @default.
• W2126046035 cites W1667367966 @default.
• W2126046035 cites W1884656506 @default.
• W2126046035 cites W1965021019 @default.
• W2126046035 cites W1983532191 @default.
• W2126046035 cites W1989228340 @default.
• W2126046035 cites W1992635534 @default.
• W2126046035 cites W1993608846 @default.
• W2126046035 cites W2015721729 @default.
• W2126046035 cites W2021858120 @default.
• W2126046035 cites W2023033897 @default.
• W2126046035 cites W2027290849 @default.
• W2126046035 cites W2035348154 @default.
• W2126046035 cites W2038721961 @default.
• W2126046035 cites W2065528657 @default.
• W2126046035 cites W2071902495 @default.
• W2126046035 cites W2071969879 @default.
• W2126046035 cites W2091193879 @default.
• W2126046035 cites W2093695309 @default.
• W2126046035 cites W2104933421 @default.
• W2126046035 cites W2110993458 @default.
• W2126046035 cites W2116763228 @default.
• W2126046035 cites W2121486402 @default.
• W2126046035 cites W2122995536 @default.
• W2126046035 cites W2123465466 @default.
• W2126046035 cites W2124663880 @default.
• W2126046035 cites W2125370554 @default.
• W2126046035 cites W2125632358 @default.
• W2126046035 cites W2129827159 @default.
• W2126046035 cites W2140298451 @default.
• W2126046035 cites W2149635665 @default.
• W2126046035 cites W2169117352 @default.
• W2126046035 cites W2187825253 @default.
• W2126046035 cites W2328158010 @default.
• W2126046035 cites W2417371868 @default.
• W2126046035 cites W4244463437 @default.
• W2126046035 doi "https://doi.org/10.1161/01.cir.0000156448.74296.fe" @default.
• W2126046035 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/15867178" @default.
• W2126046035 hasPublicationYear "2005" @default.
• W2126046035 type Work @default.
• W2126046035 sameAs 2126046035 @default.
• W2126046035 citedByCount "216" @default.
• W2126046035 countsByYear W21260460352012 @default.
• W2126046035 countsByYear W21260460352013 @default.
• W2126046035 countsByYear W21260460352014 @default.
• W2126046035 countsByYear W21260460352015 @default.
• W2126046035 countsByYear W21260460352016 @default.
• W2126046035 countsByYear W21260460352017 @default.
• W2126046035 countsByYear W21260460352018 @default.
• W2126046035 countsByYear W21260460352019 @default.
• W2126046035 countsByYear W21260460352020 @default.
• W2126046035 countsByYear W21260460352021 @default.
• W2126046035 countsByYear W21260460352022 @default.
• W2126046035 countsByYear W21260460352023 @default.
• W2126046035 crossrefType "journal-article" @default.
• W2126046035 hasAuthorship W2126046035A5002685729 @default.
• W2126046035 hasAuthorship W2126046035A5006288394 @default.
• W2126046035 hasAuthorship W2126046035A5007751883 @default.
• W2126046035 hasAuthorship W2126046035A5007948673 @default.
• W2126046035 hasAuthorship W2126046035A5013089574 @default.
• W2126046035 hasAuthorship W2126046035A5018505044 @default.
• W2126046035 hasAuthorship W2126046035A5020528511 @default.
• W2126046035 hasAuthorship W2126046035A5027078331 @default.
• W2126046035 hasAuthorship W2126046035A5031800219 @default.
• W2126046035 hasAuthorship W2126046035A5032918352 @default.
• W2126046035 hasAuthorship W2126046035A5038432586 @default.
• W2126046035 hasAuthorship W2126046035A5039471192 @default.
• W2126046035 hasAuthorship W2126046035A5049411755 @default.
• W2126046035 hasAuthorship W2126046035A5050696505 @default.
• W2126046035 hasAuthorship W2126046035A5053649940 @default.

• next