scholarly journals Angiotensin II rapidly stimulates the short‐circuit current in opossum kidney cells expressing rat Na,K‐ATPase

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Douglas R. Yingst ◽  
Xia Hou ◽  
Quanwen Li ◽  
Raymond R. Mattingly ◽  
Fei Sun
Keyword(s):  
Angiotensin Ii ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Kidney Cells ◽  
Opossum Kidney ◽  
Opossum Kidney Cells

scholarly journals Ouabain-insensitive acidification by dopamine in renal OK cells: primary control of the Na+/H+exchanger

2001 ◽  
Vol 281 (1) ◽  
pp. R10-R18 ◽  
Author(s):  
Pedro Gomes ◽  
M. A. Vieira-Coelho ◽  
P. Soares-da-Silva
Keyword(s):  
Adenylyl Cyclase ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Kidney Cells ◽  
Primary Control ◽  
Intracellular Acidification ◽  
Opossum Kidney ◽  
Opossum Kidney Cells ◽  
Stimulation Of

The present study was aimed at evaluating the role of D1- and D2-like receptors and investigating whether inhibition of Na+ transepithelial flux by dopamine is primarily dependent on inhibition of the apical Na+/H+ exchanger, inhibition of the basolateral Na+-K+-ATPase, or both. The data presented here show that opossum kidney cells are endowed with D1- and D2-like receptors, the activation of the former, but not the latter, accompanied by stimulation of adenylyl cyclase (EC50 = 220 ± 2 nM), marked intracellular acidification (IC50 = 58 ± 2 nM), and attenuation of amphotericin B-induced decreases in short-circuit current (28.6 ± 4.5% reduction) without affecting intracellular pH recovery after CO2 removal. These results agree with the view that dopamine, through the activation of D1- but not D2-like receptors, inhibits both the Na+/H+ exchanger (0.001933 ± 0.000121 vs. 0.000887 ± 0.000073 pH unit/s) and Na+-K+-ATPase without interfering with the Na+-independent HCO[Formula: see text] transporter. It is concluded that dopamine, through the action of D1-like receptors, inhibits both the Na+/H+ exchanger and Na+-K+-ATPase, but its marked acidifying effects result from inhibition of the Na+/H+exchanger only, without interfering with the Na+-independent HCO[Formula: see text] transporter and Na+-K+-ATPase.

scholarly journals Sequential activation of MAP kinase cascade by angiotensin II in opossum kidney cells

1995 ◽  
Vol 48 (6) ◽  
pp. 1801-1809 ◽  
Author(s):  
Yoshio Terada ◽  
Kimio Tomita ◽  
Miwako K. Homma ◽  
Hiroshi Nonoguchi ◽  
Tianxin Yang ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Map Kinase ◽  
Kidney Cells ◽  
Opossum Kidney ◽  
Map Kinase Cascade ◽  
Opossum Kidney Cells ◽  
Kinase Cascade ◽  
Sequential Activation

Regulation of Sodium-Dependent Phosphate Transport by Parathyroid Hormone in Opossum Kidney Cells: Adenosine 3 ′,5 ′-Monophosphate-Dependent and -Independent Mechanisms*

Endocrinology ◽  
1988 ◽  
Vol 122 (6) ◽  
pp. 2981-2989 ◽  
Author(s):  
JUDITH A. COLE ◽  
LEONARD R. FORTE ◽  
SAMMY EBER ◽  
PAMELA K. THORNE ◽  
RICHARD E. POELLING
Keyword(s):  
Parathyroid Hormone ◽  
Phosphate Transport ◽  
Kidney Cells ◽  
Opossum Kidney ◽  
Opossum Kidney Cells ◽  
Sodium Dependent

Evidence for interference of vitamin D with PTH/PTHrP receptor expression in opossum kidney cells

1998 ◽  
Vol 436 (2) ◽  
pp. 289-294 ◽  
Author(s):  
H. Wald ◽  
Michal Dranitzki-Elhalel ◽  
R. Backenroth ◽  
Mordecai M. Popovtzer
Keyword(s):  
Vitamin D ◽  
Receptor Expression ◽  
Kidney Cells ◽  
Opossum Kidney ◽  
Opossum Kidney Cells ◽  
Pthrp Receptor

scholarly journals Site-1 Protease-Derived Soluble (Pro)Renin Receptor Contributes to Angiotensin II–Induced Hypertension in Mice

Hypertension ◽  
2020 ◽  
Author(s):  
Ye Feng ◽  
Kexin Peng ◽  
Renfei Luo ◽  
Fei Wang ◽  
Tianxin Yang
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Collecting Duct ◽  
Short Circuit ◽  
Ussing Chamber ◽  
Short Circuit Current ◽  
Duct Cell ◽  
Ang Ii ◽  
Cortical Collecting Duct ◽  
Induced Hypertension

Activation of PRR ([pro]renin receptor) contributes to enhancement of intrarenal RAS and renal medullary α-ENaC and thus elevated blood pressure during Ang II (angiotensin II) infusion. The goal of the present study was to test whether such action of PRR was mediated by sPRR (soluble PRR), generated by S1P (site-1 protease), a newly identified PRR cleavage protease. F1 B6129SF1/J mice were infused for 6 days with control or Ang II at 300 ng/kg per day alone or in combination with S1P inhibitor PF-429242 (PF), and blood pressure was monitored by radiotelemetry. S1P inhibition significantly attenuated Ang II–induced hypertension accompanied with suppressed urinary and renal medullary renin levels and expression of renal medullary but not renal cortical α-ENaC expression. The effects of S1P inhibition were all reversed by supplement with histidine-tagged sPRR termed as sPRR-His. Ussing chamber technique was performed to determine amiloride-sensitive short-circuit current, an index of ENaC activity in confluent mouse cortical collecting duct cell line cells exposed for 24 hours to Ang II, Ang II + PF, or Ang II + PF + sPRR-His. Ang II–induced ENaC activity was blocked by PF, which was reversed by sPRR-His. Together, these results support that S1P-derived sPRR mediates Ang II–induced hypertension through enhancement of intrarenal renin level and activation of ENaC.

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