IGF-I regulation of Na(+)-K(+)-ATPase in rat arterial smooth muscle
| Autor: | Mary F. Walsh, Feng Zhang, Ricardo M. Zayas, Paul R. Standley, James R. Sowers, Ranganath Muniyappa, Edward Cragoe |
|---|---|
| Rok vydání: | 1997 |
| Předmět: |
Male
medicine.medical_specialty Sodium-Hydrogen Exchangers Time Factors Vascular smooth muscle Transcription Genetic Physiology Endocrinology Diabetes and Metabolism medicine.medical_treatment Aorta Thoracic Vasodilation Biology Muscle Smooth Vascular Ouabain Rats Sprague-Dawley Physiology (medical) Internal medicine medicine Animals Enzyme Inhibitors Insulin-Like Growth Factor I Na+/K+-ATPase Cells Cultured Protein Kinase C Protein kinase C Growth factor Cell Membrane Sodium Protein-Tyrosine Kinases Rubidium Rats Isoenzymes Nitric oxide synthase Kinetics Sodium–hydrogen antiporter NG-Nitroarginine Methyl Ester Endocrinology Protein Biosynthesis biology.protein Nitric Oxide Synthase Sodium-Potassium-Exchanging ATPase medicine.drug |
| Zdroj: | American Journal of Physiology-Endocrinology and Metabolism. 273:E113-E121 |
| ISSN: | 1522-1555 0193-1849 |
| DOI: | 10.1152/ajpendo.1997.273.1.e113 |
| Popis: | Insulin-like growth factor I (IGF-I) is vasodilatory and mitogenic for vascular smooth muscle cells (VSMC). Alteration in VSMC Na(+)-K(+)-adenosinetriphosphatase (Na(+)-K(+)-ATPase) activity is hypothesized to underlie abnormal vascular tone and growth in hypertension and diabetes. Therefore, we investigated effects of IGF-I on Na(+)-K(+)-ATPase activity in rat aortic VSMC. IGF-I increases pump activity in a dose- and time-dependent manner: the minimal dose required was 10(-10) M, and the minimal time required was 20 min (at 10(-8) M) to increase activity. Similar effects persisted through 12 h. In Na(+)-loaded cells, IGF-I does not further stimulate activity. Blockade of Na+/H+ exchange attenuates IGF-I-induced increases in activity after 30 min but has no effect after 12 h. Northern blot analyses reveal that expression of the alpha 1- and the alpha 2-subunits of the pump were unaffected by IGF-I. Plasma membrane alpha 1- and alpha 2-protein were also unaffected, suggesting translocation of preformed pools was not responsible for the increases. Inhibitors revealed that neither tyrosine kinase activity, RNA transcription, protein synthesis, nitric oxide synthase activity, or protein kinase C activity mediated this IGF-I effect. Therefore, IGF-I regulates Na pump activity in the short term by an Na+/H+ exchange-dependent but transcription/translocation-independent mechanism. These data suggest that IGF-I, known to be produced by VSMC, may regulate tone and growth responses abnormal in disease states such as hypertension and diabetes. |
| Databáze: | OpenAIRE |
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