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10.1038/s41467-019-13033-4 http://scihub22266oqcxt.onion/10.1038/s41467-019-13033-4 31727896!6856192!31727896     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Commun 2019 ; 10 (1): 5155 Nephropedia Template TP {{tp|p=31727896|t=2019. Elevated aldosterone and blood pressure in a mouse model of familial hyperaldosteronism with ClC-2 mutation |pdf=|usr=}}{{31727896}} gab.com Text Elevated aldosterone and blood pressure in a mouse model of familial hyperaldosteronism with ClC-2 mutation JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=31727896 #FOAvip Gain-of-function mutations in the chloride channel ClC-2 were recently described as a cause of familial hyperaldosteronism type II (FH-II). Here, we report the generation of a mouse model carrying a missense mutation homologous to the most common FH-II-associated CLCN2 mutation. In these Clcn2(R180Q/+) mice, adrenal morphology is normal, but Cyp11b2 expression and plasma aldosterone levels are elevated. Male Clcn2(R180Q/+) mice have increased aldosterone:renin ratios as well as elevated blood pressure levels. The counterpart knockout model (Clcn2(-/-)), in contrast, requires elevated renin levels to maintain normal aldosterone levels. Adrenal slices of Clcn2(R180Q/+) mice show increased calcium oscillatory activity. Together, our work provides a knockin mouse model with a mild form of primary aldosteronism, likely due to increased chloride efflux and depolarization. We demonstrate a role of ClC-2 in normal aldosterone production beyond the observed pathophysiology. Twit Text FOAVip Elevated aldosterone and blood pressure in a mouse model of familial hyperaldosteronism with ClC-2 mutation ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=31727896 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=31727896 #FOAvip English Wikipedia <ref>{{Cite pmid|31727896}}</ref> Elevated aldosterone and blood pressure in a mouse model of familial hyperaldosteronism with ClC-2 mutation #MMPMID31727896 Schewe J; Seidel E; Forslund S; Marko L; Peters J; Muller DN; Fahlke C; Stolting G; Scholl U Nat Commun 2019[Nov]; 10 (1): 5155 PMID31727896show ga Gain-of-function mutations in the chloride channel ClC-2 were recently described as a cause of familial hyperaldosteronism type II (FH-II). Here, we report the generation of a mouse model carrying a missense mutation homologous to the most common FH-II-associated CLCN2 mutation. In these Clcn2(R180Q/+) mice, adrenal morphology is normal, but Cyp11b2 expression and plasma aldosterone levels are elevated. Male Clcn2(R180Q/+) mice have increased aldosterone:renin ratios as well as elevated blood pressure levels. The counterpart knockout model (Clcn2(-/-)), in contrast, requires elevated renin levels to maintain normal aldosterone levels. Adrenal slices of Clcn2(R180Q/+) mice show increased calcium oscillatory activity. Together, our work provides a knockin mouse model with a mild form of primary aldosteronism, likely due to increased chloride efflux and depolarization. We demonstrate a role of ClC-2 in normal aldosterone production beyond the observed pathophysiology. |*Blood Pressure[MESH] |Adrenal Glands/pathology[MESH] |Aldosterone/*blood[MESH] |Amino Acid Sequence[MESH] |Animals[MESH] |Base Sequence[MESH] |CLC-2 Chloride Channels[MESH] |Chloride Channels/chemistry/*genetics[MESH] |Chlorides/urine[MESH] |Cytochrome P-450 CYP11B2/metabolism[MESH] |Disease Models, Animal[MESH] |Female[MESH] |Heterozygote[MESH] |Hyperaldosteronism/*blood/*physiopathology/urine[MESH] |Male[MESH] |Mice, Inbred C57BL[MESH] |Mutation/*genetics[MESH] |Phenotype[MESH] |Renin/blood[MESH]Elevated aldosterone and blood pressure in a mouse model of familial (epmc).pdf DeepDyve Pubget Overpricing