Vitamin D stimulation of calcium-dependent adenosine triphosphatase in chick intestinal brush borders

Biochemistry ◽  
1970 ◽  
Vol 9 (8) ◽  
pp. 1658-1664 ◽  
Author(s):  
Mark J. Melancon ◽  
Hector F. De Luca
Keyword(s):  
Vitamin D ◽  
Adenosine Triphosphatase ◽  
Calcium Dependent ◽  
Brush Borders ◽  
Stimulation Of

scholarly journals Environmental CO2 Stimulation of Mitochondrial Adenosine Triphosphatase Activity

1963 ◽  
Vol 238 (2) ◽  
pp. 836-842
Author(s):  
D.D. Fanestil ◽  
A Baird Hastings ◽  
Theodore A. Mahowald
Keyword(s):  
Adenosine Triphosphatase ◽  
Adenosine Triphosphatase Activity ◽  
Stimulation Of

scholarly journals Cholinergic stimulation of the Na+/K+ adenosine triphosphatase as revealed by microphysiometry

1993 ◽  
Vol 64 (3) ◽  
pp. 813-823 ◽  
Author(s):  
D.L. Miller ◽  
J.C. Olson ◽  
J.W. Parce ◽  
J.C. Owicki
Keyword(s):  
Adenosine Triphosphatase ◽  
Cholinergic Stimulation ◽  
Stimulation Of

scholarly journals Calcium-dependent phosphodiesterase 1C inhibits renin release from isolated juxtaglomerular cells

2009 ◽  
Vol 297 (5) ◽  
pp. R1469-R1476 ◽  
Author(s):  
M. Cecilia Ortiz-Capisano ◽  
Tang-Dong Liao ◽  
Pablo A. Ortiz ◽  
William H. Beierwaltes
Keyword(s):  
Western Blot ◽  
Blot Analysis ◽  
Western Blot Analysis ◽  
Renin Release ◽  
Calcium Sensing Receptor ◽  
Calcium Dependent ◽  
Calcium Sensing ◽  
Inhibitory Modulation ◽  
Camp Formation ◽  
Stimulation Of

Renin release from the juxtaglomerular (JG) cell is stimulated by the second messenger cAMP and inhibited by calcium. We previously showed JG cells contain a calcium sensing receptor (CaSR), which, when stimulated, decreases cAMP formation and inhibits renin release. We hypothesize CaSR activation decreases cAMP and renin release, in part, by stimulating a calcium calmodulin-activated phosphodiesterase 1 (PDE1). We incubated our primary culture of JG cells with two selective PDE1 inhibitors [8-methoxymethil-IBMX (8-MM-IBMX; 20 μM) and vinpocetine (40 μM)] and the calmodulin inhibitor W-7 (10 μM) and measured cAMP and renin release. Stimulation of the JG cell CaSR with the calcimimetic cinacalcet (1 μM) resulted in decreased cAMP from a basal of 1.13 ± 0.14 to 0.69 ± 0.08 pM/mg protein ( P < 0.001) and in renin release from 0.89 ± 0.16 to 0.38 ± 0.08 μg ANG I/ml·h−1·mg protein−1 ( P < 0.001). However, the addition of 8-MM-IBMX with cinacalcet returned both cAMP (1.10 ± 0.19 pM/mg protein) and renin (0.57 ± 0.16 μg ANG I/ml·h−1·mg protein−1) to basal levels. Similar results were obtained with vinpocetine, and also with W-7. Combining 8-MM-IBMX and W-7 had no additive effect. To determine which PDE1 isoform is involved, we performed Western blot analysis for PDE1A, B, and C. Only Western blot analysis for PDE1C showed a characteristic band apparent at 80 kDa. Immunofluorescence showed cytoplasmic distribution of PDE1C and renin in the JG cells. In conclusion, PDE1C is expressed in isolated JG cells, and contributes to calcium's inhibitory modulation of renin release from JG cells.

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