期刊
CURRENT OPINION IN NEPHROLOGY AND HYPERTENSION
卷 21, 期 1, 页码 52-60出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/MNH.0b013e32834db4a0
关键词
ATP; ENaC; hypertension; P2Y(2); sodium transport
资金
- NIH [R01 DK59594, R01 DK087460, R01 DK070571]
- AHA [EIA 0640054N, GRNT344038]
- [R01 HL094728]
- [R01 DK28602]
- [P2 GM066232]
- [P30 DK079337]
- [R01 HL102310]
- [P01 HL088052]
Purpose of review This review summarizes the new evidence for an intrinsic control system in the aldosterone-sensitive distal nephron in which purinergic signaling regulates sodium transport and governs renal sodium excretion. Recent findings Electrophysiological studies identify epithelial Na+ channels (ENaC) as final effectors of purinergic signaling via P2Y(2) receptors in the distal nephron. Inhibition of ENaC by autocrine/paracrine purinergic signaling reduces sodium reabsorption allowing an appropriately graded pressure-natriuresis response when delivery of sodium to the distal nephron is high. Disruption of this intrinsic control mechanism decreases sodium excretion and therefore has a prohypertensive effect. Because purinergic inhibition of ENaC is tonic yet submaximal, its enhancement increases sodium excretion and therefore has an antihypertensive action. Summary Purinergic inhibitory regulation of ENaC is a key component of an intrinsic control system that enables the distal nephron to respond appropriately to the delivered load of sodium. This control system is physiologically important and functions in parallel with extrinsic control by the renin-angiotensin-aldosterone system, enabling sodium excretion to keep pace with sodium intake, especially when intake is high, and thereby maintaining arterial blood pressure. Disruption of intrinsic control of sodium transport by the distal nephron likely contributes to diseases such as arterial hypertension.
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