Up-regulation of Apical Sodium Chloride Cotransporter and Basolateral Chloride Channels Are Responsible for the Maintenance of Salt Sensitive Hypertension

نویسندگان

  • Giovambattista Capasso
  • Maria Rizzo
  • Maria Lisa Garavaglia
  • Francesco Trepiccione
  • Miriam Zacchia
  • Alessandra Mugione
  • Patrizia Ferrari
  • Markus Paulmichl
  • Florian Lang
  • Johannes Loffing
  • Monique Carrel
  • Sara Damiano
  • Carsten A. Wagner
  • Giuseppe Bianchi
چکیده

Department of Internal Medicine, Chair of Nephrology, Faculty of Medicine, Second University of Napoli (Italy), Prassis Research Institute, Sigma Tau, Milan (Italy), Department of Physiology, University of Tuebingen (Germany), Institute of Anatomy and Physiology, University of Zurich (Switzerland), Chair of Nephrology, Ateneo Vita e Salute, S. Raffaele Hospital, Milan (Italy),**Department of Pharmacology, Paracelsius Medical University, Salzburg (Austria), *Department of Biomolecular Sciences and Biotechnology, Free University of Milan (Italy).

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Upregulation of apical sodium-chloride cotransporter and basolateral chloride channels is responsible for the maintenance of salt-sensitive hypertension.

We investigated which of the NaCl transporters are involved in the maintenance of salt-sensitive hypertension. Milan hypertensive (MHS) rats were studied 3 mo after birth. In MHS, compared with normotensive strain (MNS), mRNA abundance, quantified by competitive PCR on isolated tubules, was unchanged, both for Na+/H+ isoform 3 (NHE3) and Na+-K+-2Cl- (NKCC2), but higher (119%, n = 5, P < 0.005) ...

متن کامل

Renal sodium transport in renin-deficient Dahl salt-sensitive rats

OBJECTIVE The Dahl salt-sensitive rat is a well-established model of salt-sensitive hypertension. The goal of this study was to assess the expression and activity of renal sodium channels and transporters in the renin-deficient salt-sensitive rat. METHODS Renin knockout (Ren(-/-)) rats created on the salt-sensitive rat background were used to investigate the role of renin in the regulation of...

متن کامل

Role of WNK kinases in regulating tubular salt and potassium transport and in the development of hypertension.

A recently discovered family of protein kinases is responsible for an autosomal-dominant disease known as Gordon's syndrome or pseudohypoaldosteronism type II (PHA-II) that features hyperkalemia and hyperchloremic metabolic acidosis, accompanied by hypertension and hypercalciuria. Four genes have been described in this kinase family, which has been named WNK, due to the absence of a key lysine ...

متن کامل

CALL FOR PAPERS Central Control of Fluid and Electrolyte Homeostasis Norepinephrine-evoked salt-sensitive hypertension requires impaired renal sodium chloride cotransporter activity in Sprague-Dawley rats

Walsh KR, Kuwabara JT, Shim JW, Wainford RD. Norepinephrine-evoked salt-sensitive hypertension requires impaired renal sodium chloride cotransporter activity in Sprague-Dawley rats. Am J Physiol Regul Integr Comp Physiol 310: R115–R124, 2016. First published November 25, 2015; doi:10.1152/ajpregu.00514.2014.— Recent studies have implicated a role of norepinephrine (NE) in the activation of the ...

متن کامل

Invited Review Role of WNK kinases in regulating tubular salt and potassium transport and in the development of hypertension

Gamba, Gerardo. Role of WNK kinases in regulating tubular salt and potassium transport and in the development of hypertension. Am J Physiol Renal Physiol 288: F245–F252, 2005; doi:10.1152/ajprenal.00311.2004.—A recently discovered family of protein kinases is responsible for an autosomal-dominant disease known as Gordon’s syndrome or pseudohypoaldosteronism type II (PHA-II) that features hyperk...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره   شماره 

صفحات  -

تاریخ انتشار 2008