Different Mechanisms of Renal Na-K-ATPase Regulation by Dopamine in the Proximal and Distal Nephron
| Autor: | Masayuki Ominato, Adrian I. Katz, Takeo Satoh |
|---|---|
| Rok vydání: | 1995 |
| Předmět: |
medicine.medical_specialty
Physiology Dopamine Nephron Fenoldopam In Vitro Techniques Kidney Kidney Tubules Proximal Phospholipase A2 Internal medicine Internal Medicine medicine Animals Staurosporine Na+/K+-ATPase Kidney Tubules Distal Protein kinase A Protein Kinase C Protein kinase C Kidney Medulla biology Receptors Dopamine D1 Cyclic AMP-Dependent Protein Kinases Rats Endocrinology Convoluted tubule medicine.anatomical_structure Dopamine Agonists biology.protein Sodium-Potassium-Exchanging ATPase Cardiology and Cardiovascular Medicine Signal Transduction medicine.drug |
| Zdroj: | Hypertension Research. 18:S137-S140 |
| ISSN: | 1348-4214 0916-9636 |
| DOI: | 10.1291/hypres.18.supplementi_s137 |
| Popis: | We reported a novel intracellular mechanism of renal Na-K-ATPase regulation by dopamine (DA) in the rat cortical collecting duct (CCD), which involves stimulation of protein kinase A (PKA) and phospholipase A2 (PLA2). In the present experiments we determined whether this mechanism also operates in other nephron segments. In the medullary thick ascending limbs (MTAL), DA and other cAMP agonists inhibited Na-K-ATPase activity, an effect that was abolished by PKA inhibitor IP20, but various protein kinase C (PKC) activators did not, analogous to our previous findings in CCD. In sharp contrast, DA inhibition on Na-K-ATPase in the proximal convoluted tubule (PCT) was reproduced by PKC agonists. These effects was blocked by PKC inhibitor staurosporine, but not by IP20. Mepacrine, a PLA2 inhibitor, reversed the pump effect of all agents, and arachidonic acid (AA) produced a dose-dependent pump inhibition, in all three nephron segments.We conclude that the intercellular mechanisms of Na-K-ATPase regulation by dopamine differ in the proximal and distal nephron, as they involve stimulation of PKA in MTAL and CCD, and of PKC in PCT. These two pathways probably share a common mechanism in stimulating PLA2 and AA release in both regions of the nephron. (Hypertens Res 1995; 18 Suppl. I: S137-S140) |
| Databáze: | OpenAIRE |
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