Macula densa cell signaling

被引:93
作者
Bell, PD [1 ]
Lapointe, JY
Peti-Peterdi, J
机构
[1] Univ Alabama Birmingham, Ctr Nephrol Res & Training, Div Nephrol, Dept Med, Birmingham, AL 35294 USA
[2] Univ Alabama Birmingham, Ctr Nephrol Res & Training, Div Nephrol, Dept Physiol, Birmingham, AL 35294 USA
[3] Univ Montreal, Membrane Transport Res Grp, Montreal, PQ H3C 3J7, Canada
关键词
kidney; tubuloglomerular feedback; renal hemodynamics; cell-to-cell; communication;
D O I
10.1146/annurev.physiol.65.050102.085730
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Macula densa cells are renal sensor elements that detect changes in distal tubular fluid composition and transmit signals to the glomerular vascular elements. This tubuloglomerular feedback mechanism plays an important role in regulating glomerular filtration rate and blood flow. Macula densa cells detect changes in luminal sodium chloride concentration through a complex series of ion transport-related intracellular events. NaCl entry via a Na:K:2Cl cotransporter and Cl exit through a basolateral channel lead to cell depolarization and increases in cytosolic calcium. Na/H exchange (NHE2) results in cell alkalization, whereas intracellular [Na] is regulated by an apically located H(Na)-K ATPase and not by the traditional basolateral Na:K ATPase. Communication from macula densa cells to the glomerular vascular elements involves ATP release across the macula densa basolateral membrane through a maxi-anion channel. The adaptation of multi-photon microscopy is providing new insights into macula densa-glomerular signaling.
引用
收藏
页码:481 / 500
页数:22
相关论文
共 97 条
[1]   EXPRESSION OF NHE-3 IN THE APICAL MEMBRANE OF RAT RENAL PROXIMAL TUBULE AND THICK ASCENDING LIMB [J].
AMEMIYA, M ;
LOFFING, J ;
LOTSCHER, M ;
KAISSLING, B ;
ALPERN, RJ ;
MOE, OW .
KIDNEY INTERNATIONAL, 1995, 48 (04) :1206-1215
[2]  
BARAJAS L, 1979, AM J PHYSIOL-RENAL, V7, pF333
[3]   Characteristics of membrane transport processes of macula densa cells [J].
Bell, PD ;
Lapointe, JY .
CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, 1997, 24 (07) :541-547
[4]  
Bell PD, 1999, J AM SOC NEPHROL, V10, pS225
[5]   DIRECT MEASUREMENT OF BASOLATERAL MEMBRANE-POTENTIALS FROM CELLS OF THE MACULA DENSA [J].
BELL, PD ;
LAPOINTE, JY ;
CARDINAL, J .
AMERICAN JOURNAL OF PHYSIOLOGY, 1989, 257 (03) :F463-F468
[6]   RELATIONSHIP BETWEEN TUBULO-GLOMERULAR FEEDBACK RESPONSES AND PERFUSATE HYPOTONICITY [J].
BELL, PD ;
NAVAR, LG .
KIDNEY INTERNATIONAL, 1982, 22 (03) :234-239
[7]  
BELL PD, 2002, UNPUB P NATL ACAD SC
[8]   IMMUNOCYTOCHEMICAL CHARACTERIZATION OF NA+-H+ EXCHANGER ISOFORM NHE-1 IN RABBIT KIDNEY [J].
BIEMESDERFER, D ;
REILLY, RF ;
EXNER, M ;
IGARASHI, P ;
ARONSON, PS .
AMERICAN JOURNAL OF PHYSIOLOGY, 1992, 263 (05) :F833-F840
[9]  
BRIGGS JP, 1987, ANNU REV PHYSIOL, V49, P251
[10]   Abolished tubuloglomerular feedback and increased plasma renin in adenosine A1 receptor-deficient mice [J].
Brown, R ;
Ollerstam, A ;
Johansson, B ;
Skott, O ;
Gebre-Medhin, S ;
Fredholm, B ;
Persson, AEG .
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY, 2001, 281 (05) :R1362-R1367