Salt sensitivity of blood pressure in NKCC1-deficient mice
نویسندگان
چکیده
منابع مشابه
Salt sensitivity of blood pressure in NKCC1-deficient mice.
NKCC1 is a widely expressed isoform of the Na-2Cl-K cotransporter that mediates several direct and indirect vascular effects and regulates expression and release of renin. In this study, we used NKCC1-deficient (NKCC1-/-) and wild-type (WT) mice to assess day/night differences of blood pressure (BP), locomotor activity, and renin release and to study the effects of high (8%) or low (0.03%) diet...
متن کاملHsd11b2 haploinsufficiency in mice causes salt sensitivity of blood pressure.
Salt sensitivity of blood pressure is an independent risk factor for cardiovascular morbidity. Mechanistically, abnormal mineralocorticoid action and subclinical renal impairment may blunt the natriuretic response to high sodium intake, causing blood pressure to rise. 11β-Hydroxysteroid dehydrogenase type 2 (11βHSD2) controls ligand access to the mineralocorticoid receptor, and ablation of the ...
متن کاملIntestinal ion transport in NKCC1-deficient mice.
The Na(+)-K(+)-2Cl(-) cotransporter (NKCC1) located on the basolateral membrane of intestinal epithelia has been postulated to be the major basolateral Cl(-) entry pathway. With targeted mutagenesis, mice deficient in the NKCC1 protein were generated. The basal short-circuit current did not differ between normal and NKCC1 -/- jejuna. In the -/- jejuna, the forskolin response (22 microA/cm(2); b...
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When olfactory receptor neurons respond to odors, a depolarizing Cl(-) efflux is a substantial part of the response. This requires that the resting neuron accumulate Cl(-) against an electrochemical gradient. In isolated olfactory receptor neurons, the Na(+)+K(+)+2Cl(-) cotransporter NKCC1 is essential for Cl(-) accumulation. However, in intact epithelium, a robust electrical olfactory response...
متن کاملGenetics Hsd11b2 Haploinsufficiency in Mice Causes Salt Sensitivity of Blood Pressure
Salt sensitivity of blood pressure is an independent risk factor for cardiovascular morbidity. Mechanistically, abnormal mineralocorticoid action and subclinical renal impairment may blunt the natriuretic response to high sodium intake, causing blood pressure to rise. 11 -Hydroxysteroid dehydrogenase type 2 (11 HSD2) controls ligand access to the mineralocorticoid receptor, and ablation of the ...
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ژورنال
عنوان ژورنال: American Journal of Physiology-Renal Physiology
سال: 2008
ISSN: 1931-857X,1522-1466
DOI: 10.1152/ajprenal.90392.2008