Adenosine A1 receptor-operated calcium entry in renal afferent arterioles is dependent on postnatal maturation of TRPC3 channels.
Adenosine A1 receptor-operated calcium entry in renal afferent arterioles is dependent on postnatal maturation of TRPC3 channels.
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腺苷 A1 受体操纵的钙进入肾传入小动脉依赖于出生后 TRPC3 通道的成熟。
DOI:
10.1152/ajprenal.00335.2017
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发表时间:
2017
期刊:
影响因子:
--
通讯作者:
Adebiyi,Adebowale
中科院分区:
文献类型:
--
作者:
Soni,Hitesh;Peixoto-Neves,Dieniffer;Buddington,RandalK;Adebiyi,Adebowale
Adenosine, a regulator of cardiovascular development and renal function, constricts renal afferent arterioles by inducing intracellular Ca2+concentration ([Ca2+]i) elevation in smooth muscle cells (SMCs) via activation of its cognate A1receptors (A1Rs). Mechanisms that underlie A1R-dependent [Ca2+]ielevation in renal vascular SMCs are not fully resolved. Whether A1R expression and function in preglomerular microvessels are dependent on postnatal kidney maturation is also unclear. In this study, we show that selective activation of A1Rs by 2-chloro-N6-cyclopentyladenosine (CCPA) does not stimulate store-operated Ca2+entry in afferent arterioles isolated from neonatal pigs. However, CCPA-induced [Ca2+]ielevation is dependent on phospholipase C and transient receptor potential cation channel, subfamily C, member 3 (TRPC3). Basal [Ca2+]iwas unchanged in afferent arterioles isolated from newborn (0-day-old) pigs compared with their 20-day-old counterparts. By contrast, CCPA treatment resulted in significantly larger [Ca2+]iin afferent arterioles from 20-day-old pigs. A1R protein expression levels in the kidneys and afferent arterioles were unaltered in 0- vs. 20-day-old pigs. However, the TRPC3 channel protein expression level was ~92 and 78% higher in 20-day-old pig kidneys and afferent arterioles, respectively. These data suggest that activation of A1Rs elicits receptor-operated Ca2+entry in porcine afferent arterioles, the level of which is dependent on postnatal maturation of TRPC3 channels. We propose that TRPC3 channels may contribute to the physiology and pathophysiology of A1Rs.
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DOI:
10.1007/bf00175797
发表时间:
1988
期刊:
Naunyn-Schmiedeberg's Archives of Pharmacology
影响因子:
--
作者:
M. Lohse;K. Klotz;U. Schwabe;G. Cristalli;S. Vittori;M. Grifantini
通讯作者:
M. Grifantini
DOI:
10.1152/ajprenal.00338.2003
发表时间:
2004-03-01
影响因子:
4.2
作者:
Facemire, CS;Mohler, PJ;Arendshorst, WJ
通讯作者:
Arendshorst, WJ
影响因子:
3.6
作者:
FREISSMUTH, M;HAUSLEITHNER, V;SCHUTZ, W
通讯作者:
SCHUTZ, W
DOI:
10.1152/ajpcell.2001.280.5.c1184
发表时间:
2001-05-01
影响因子:
5.5
作者:
Walker, RL;Hume, JR;Horowitz, B
通讯作者:
Horowitz, B
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