2007
DOI: 10.1161/01.hyp.0000255172.84842.d2
|View full text |Cite
|
Sign up to set email alerts
|

Abstract: Abstract-We have shown previously that decreasing intracellular calcium in the juxtaglomerular cells increases both cAMP formation and renin release. We hypothesized that this is because of an interaction between intracellular calcium and the calcium-inhibitable isoform of adenylyl cyclase, type-V. We used primary cultures of juxtaglomerular cells isolated from C-57/B6 mice at 70% to 80% confluence. Western blots were performed on isolated juxtaglomerular cells using antibodies against either of the 2 calcium … Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1

Citation Types

11
86
1

Year Published

2009
2009
2013
2013

Publication Types

Select...
7
1
1

Relationship

2
7

Authors

Journals

citations
Cited by 54 publications
(98 citation statements)
references
References 24 publications
11
86
1
Order By: Relevance
“…16 JG cells have been shown to express these isoforms of AC, and their role in control of AC activity and cAMP formation in cultured cells has been documented by using specific antagonists and smallinterfering RNA approaches. 17,18 However, the presence of calcium-regulated ACs in JG cells may not satisfactorily explain the observations in the study presented here. Because the interaction between calcium and the catalytic subunit of AC is believed to be direct, 19,20 lowering calcium should activate AC5 and/or AC6 regardless of whether or not Gs␣ signaling is intact.…”
Section: Discussioncontrasting
confidence: 58%
“…16 JG cells have been shown to express these isoforms of AC, and their role in control of AC activity and cAMP formation in cultured cells has been documented by using specific antagonists and smallinterfering RNA approaches. 17,18 However, the presence of calcium-regulated ACs in JG cells may not satisfactorily explain the observations in the study presented here. Because the interaction between calcium and the catalytic subunit of AC is believed to be direct, 19,20 lowering calcium should activate AC5 and/or AC6 regardless of whether or not Gs␣ signaling is intact.…”
Section: Discussioncontrasting
confidence: 58%
“…Thus, the regulation of (pro)renin release in HMC-1 cells is identical to that in other renin-producing cells, including renal juxtaglomerular cells and adrenal glomerulosa cells. [22][23][24] However, activation of the adenylyl cyclase-cAMP pathway with the nonselective ␤-adrenoceptor agonist isoproterenol did not affect renin release from HMC-1 cells. This most likely relates to the mast cell-stabilizing action of ␤ 2 -adrenoceptors, 25 which are the predominant ␤-adrenoceptors on mast cells.…”
Section: Discussionmentioning
confidence: 91%
“…We have previously found that CaSRmediated increases in intracellular calcium result in suppression of the calcium-inhibitable isoform-five (45) of adenylyl cyclase (AC-V), and also enhance the calcium-activated isoform of phosphodiesterase, 1C (PDE1C) (43). Thus activation of the JG cell CaSR results in intracellular calcium-mediated suppression of cAMP formation and inhibition of renin release (43,45,46). But what couples the receptor to calcium-mediated events?…”
mentioning
confidence: 99%