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Cited by 14Renin-Angiotensin System StudiesRegulation of Appetite and ObesityCardiovascular, Neuropeptides, and Oxidative Stress Research

TIME‐DEPENDENT TRANSITION FROM H2O2–EXTRACELLULAR SIGNAL‐REGULATED KINASE‐ TO O2−–NITRIC OXIDE‐DEPENDENT MECHANISMS IN THE STIMULATORY EFFECT OF LEPTIN ON RENAL Na+/K+‐ATPase IN THE RAT

Marciniak, Andrzej, Borkowska, Ewelina, Kȩdra, Anna, Rychlik, Monika, Beltowski, Jerzy·2006·Clinical and Experimental Pharmacology and Physiology
DOI 10.1111/j.1440-1681.2006.04513.x
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Abstract

1. Recent studies suggest that leptin, a peptide hormone secreted by white adipose tissue, is involved in the pathogenesis of arterial hypertension, in part by regulating renal sodium handling. Previously, we have demonstrated that in normal rats leptin has a time-dependent effect on renal Na(+)/K(+)-ATPase that drives tubular sodium reabsorption. Short-term leptin infusion results in a transient decrease in Na(+)/K(+)-ATPase activity, whereas prolonged administration stimulates the enzyme. 2. In the present study, we investigated whether these acute effects of leptin are preserved in rats with experimentally induced chronic hyperleptinaemia. 3. Hyperleptinaemia was induced by administration of exogenous leptin (0.25 mg/kg twice daily, s.c., for 7 days). Acute effects of leptin in anaesthetized control (normoleptinaemic) and hyperleptinaemic animals was investigated. Leptin was infused into the abdominal aorta proximally to the renal arteries for 0.5, 1, 2 or 3 h. 4. Leptin (1 microg/min per kg) had a time-dependent effect on renal Na(+)/K(+)-ATPase in both the control and hyperleptinaemic groups. The inhibitory effect observed after 0.5 h infusion was impaired in the hyperleptinaemic group. However, in both groups this effect was abolished by the Janus kinase inhibitor tyrphostin AG490 (100 nmol/min per kg), as well as by the phosphatidylinositol 3-kinase inhibitors wortmannin (10 nmol/min per kg) and LY294002 (1 micromol/min per kg). 5. The stimulatory effect of leptin on Na(+)/K(+)-ATPase activity was observed after 3 h of infusion and was of similar magnitude in control and hyperleptinaemic groups. In the control group, the stimulatory effect of leptin was abolished by the NADPH oxidase inhibitor apocynin (1 micromol/min per kg), the H(2)O(2) scavenger catalase (1 mg/min per kg) and the extracellular signal-regulated kinase (ERK) inhibitor PD98059 (100 nmol/min per kg). In contrast, in the hyperleptinaemic group, the stimulatory effect of leptin was abolished by the cGMP analogue 8-bromo-cGMP (100 nmol/min per kg) and by the superoxide dismutase mimetic tempol (100 micromol/min per kg) but was not affected by catalase or PD98059. 6. Leptin increased urinary H(2)O(2) excretion and ERK phosphorylation in the renal tissue only in the control group. 7. The results suggest that the acute stimulatory effect of leptin on renal Na(+)/K(+)-ATPase is mediated by divergent mechanisms depending on the chronic leptin level (i.e. by H(2)O(2)-dependent stimulation of ERK in normoleptinaemic animals and by superoxide-dependent impairment of the nitric oxide-cGMP pathway in hyperleptinaemic rats).

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Authors
Marciniak, A., Borkowska, E., Kȩdra, A., Rychlik, M., & Beltowski, J.
Affiliations
Medical University of Lublin (PL)
ORCID
Rychlik, Monika
Venue
Clinical and Experimental Pharmacology and Physiology
Publisher
Wiley
Published
2006-12
Volume
33
Issue
12
Pages
1216-1224
ISSN
  • 0305-1870 (ISSN-L)
  • 1440-1681
DOI
10.1111/j.1440-1681.2006.04513.x
OpenAlex
W1975758672
Cited by
14
References
52
Citations by year
2022: 1
FWCI
2.36
Type
journal article
Language
en
Open access
closed
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor, 19 d)
Locations
  • Clinical and Experimental Pharmacology and Physiology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
  • Health Sciences › Medicine › Surgery › Cardiovascular, Neuropeptides, and Oxidative Stress Research
Keywords
leptin, renal Na+/K+-ATPase, hyperleptinemia, NADPH oxidase, nitric oxide, superoxide, renal sodium reabsorption, hypertension, Janus kinase inhibition, PI3K inhibition, apocynin
MeSH terms
Phosphoinositide-3 Kinase Inhibitors, Acetophenones, Sodium-Potassium-Exchanging ATPase, Animals, Cyclic N-Oxides, Enzyme Inhibitors, Hydrogen Peroxide, Indicators and Reagents, Kidney, Male, Nitric Oxide, Phosphorylation, Spin Labels, Stimulation, Chemical, Superoxides, Superoxide Dismutase, Free Radical Scavengers, Oxidants, Rats, Wistar, Phosphatidylinositol 3-Kinases, Leptin, Extracellular Signal-Regulated MAP Kinases, Rats, Janus Kinases

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