کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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1944745 | 1053239 | 2010 | 7 صفحه PDF | دانلود رایگان |
Clinical and experimental data show an increase in sodium reabsorption on the proximal tubule (PT) in essential hypertension. It is well known that there is a link between essential hypertension and renal angiotensin II (Ang II). The present study was designed to examine ouabain-insensitive Na+-ATPase activity and its regulation by Ang II in spontaneously hypertensive rats (SHR). We observed that Na+-ATPase activity was enhanced in 14-week-old but not in 6-week-old SHR. The addition of Ang II from 10− 12 to 10− 6 mol/L decreased the enzyme activity in SHR to a level similar to that obtained in WKY. The Ang II inhibitory effect was completely reversed by a specific antagonist of AT2 receptor, PD123319 (10− 8 mol/L) indicating that a system leading to activation of the enzyme in SHR is inhibited by AT2-mediated Ang II. Treatment of SHR with losartan for 10 weeks (weeks 4–14) prevents the increase in Na+-ATPase activity observed in 14-week-old SHR. These results indicate a correlation between AT1 receptor activation in SHR and increased ouabain-insensitive Na+-ATPase activity. Our results open new possibilities towards our understanding of the pathophysiological mechanisms involved in the increased sodium reabsorption in PT found in essential hypertension.
Journal: Biochimica et Biophysica Acta (BBA) - Biomembranes - Volume 1798, Issue 3, March 2010, Pages 360–366