期刊
CURRENT OPINION IN NEPHROLOGY AND HYPERTENSION
卷 18, 期 5, 页码 412-420出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/MNH.0b013e32832f5775
关键词
hypertension; kidney; proximal tubule; sodium transporter
资金
- National Institutes of Health [HL23081, DK39308, HL074940, HL092196, HL68686]
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL092196, P01HL074940, R37HL023081, R01HL023081, P01HL068686] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK039308] Funding Source: NIH RePORTER
Purpose of review Renal proximal tubular sodium reabsorption is regulated by sodium transporters, including the sodium glucose transporter, sodium amino acid transporter, sodium hydrogen exchanger isoform 3 and sodium phosphate cotransporter type 2 located at the luminal/apical membrane, and sodium bicarbonate cotransporter and Na+/K(+)ATPase located at the basolateral membrane. This review summarizes recent studies on sodium transporters that play a major role in the increase in blood pressure in essential/polygenic hypertension. Recent findings Sodium transporters and Na+/K+ATPase are segregated in membrane lipid and nonlipid raft microdomains that regulate their activities and trafficking via cytoskeletal proteins. The increase in renal proximal tubule ion transport in polygenic hypertension is primarily due to increased activity of NHE3 and Cl/HCO3 exchanger at the luminal/apical membrane and a primary or secondary increase in Na+/K(+)ATPase activity. Summary The increase in renal proximal tubule ion transport in hypertension is due to increased actions by prohypertensive factors that are unopposed by antihypertensive factors.
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