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In vivo stimulation of AMP-activated protein kinase enhanced tubuloglomerular feedback but reduced tubular sodium transport during high dietary NaCl intake

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In vivo stimulation of AMP-activated protein kinase enhanced tubuloglomerular feedback but reduced tubular sodium transport during high dietary NaCl intake

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Huang, Dan Yang Gao, Huanhuan Boini, Krishna M. Osswald, Hartmut Nürnberg, Bernd Lang, Florian
Description	Country affiliation: Germany Author Affiliation: Huang DY ( Department of Pharmacology and Experimental Therapy, Institute of Experimental and Clinical Pharmacology and Toxicology, Eberhard-Karls-University Hospitals and Clinics, and Interfaculty Centre of Pharmacogenomics and Pharmaceutical Research, University of Tübingen, Wilhelmstr. 56, 72074, Tübingen, Germany. danyang.huang@uni-tuebingen.de)
Abstract	AMP-activated protein kinase (AMPK) is expressed in the apical membrane of cortical thick ascending limb, distal, and collecting tubules as well as macula densa cells of the kidneys. AMPK is an active modulator of epithelial $Na^{+}$ channels, $Na^{+}–2Cl^{−}–K^{+}$ cotransporter, and the ATP-dependent potassium channel. The present experiments explored whether AMPK participates in the regulation of tubuloglomerular feedback (TGF) and renal tubular sodium handling. To this end, renal clearance and micropuncture experiments were performed in anesthetized rats. Under normal NaCl diet, neither TGF response nor renal fluid and sodium excretion were altered by pharmacological activation of AMPK in vivo. However, under high NaCl diet, the TGF response was significantly enhanced after intravenous or intratubular application of the AMPK activator AICAR. Moreover, AICAR application significantly increased fractional delivery of fluid and sodium to the end of the proximal tubule. High dietary NaCl intake increased the renal transcript levels encoding the AMPK-α1 subunit, while it decreased the expression of AMPK-β1 and AMPK-γ2 subunits. Immunoblots revealed that high dietary NaCl intake reduced renal expression of activated AMPK by about three times compared to normal NaCl diet whereas additional AICAR application increased AMPK activity. Our results suggest that AMPK regulates tubuloglomerular balance as well as tubular transport upon change of renal work load.
File Format	HTM / HTML
ISSN	00316768
Issue Number	1
Volume Number	460
e-ISSN	14322013
Journal	Pflügers Archiv - European Journal of Physiology
Language	English
Publisher	Springer
Publisher Date	2010-06-01
Publisher Place	Germany
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Physiology Amp-activated Protein Kinases Metabolism Kidney Glomerulus Enzymology Kidney Tubules Sodium Chloride, Dietary Sodium Water-electrolyte Balance Genetics Aminoimidazole Carboxamide Administration & Dosage Analogs & Derivatives Animals Enzyme Activation Enzyme Activators Feedback, Physiological Hemodynamics Ion Transport Drug Effects Male Phosphorylation Rna, Messenger Rats Rats, Sprague-dawley Ribonucleotides Urine Urodynamics Journal Article Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Physiology Physiology (medical) Clinical Biochemistry

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In vivo stimulation of AMP-activated protein kinase enhanced tubuloglomerular feedback but reduced tubular sodium transport during high dietary NaCl intake

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In vivo stimulation of AMP-activated protein kinase enhanced tubuloglomerular feedback but reduced tubular sodium transport during high dietary NaCl intake

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In vivo stimulation of AMP-activated protein kinase enhanced tubuloglomerular feedback but reduced tubular sodium transport during high dietary NaCl intake