Macula Densa Sensing and Signaling Mechanisms of Renin Release

被引:126
|
作者
Peti-Peterdi, Janos [1 ,2 ]
Harris, Raymond C. [3 ]
机构
[1] Univ So Calif, Dept Physiol & Biophys, Zilkha Neurogenet Inst, Los Angeles, CA 90089 USA
[2] Univ So Calif, Dept Med, Zilkha Neurogenet Inst, Los Angeles, CA USA
[3] Vanderbilt Univ, Sch Med, Dept Med, Div Nephrol, Nashville, TN 37232 USA
来源
JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY | 2010年 / 21卷 / 07期
关键词
SUCCINATE RECEPTOR GPR91; NITRIC-OXIDE SYNTHASE; CYCLOOXYGENASE-2; EXPRESSION; PROSTAGLANDIN E-2; INHIBITION; KIDNEY; STIMULATION; SYSTEM; ADENOSINE; CELLS;
D O I
10.1681/ASN.2009070759
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
Macula densa cells in the distal nephron, according to the classic paradigm, are salt sensors that generate paracrine chemical signals in the juxtaglomerular apparatus to control vital kidney functions, including renal blood flow, glomerular filtration, and renin release. Renin is the rate-limiting step in the activation of the renin-angiotensin system, a key modulator of body fluid homeostasis. Here, we discuss recent advances in understanding macula densa sensing and suggest these cells, in addition to salt, also sense various chemical and metabolic signals in the tubular environment that directly trigger renin release.
引用
收藏
页码:1093 / 1096
页数:4
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