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Pressure induces in...
Pressure induces intracellular calcium changes in juxtaglomerular cells in perfused afferent arterioles
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- Lai, En Yin (författare)
- Uppsala universitet,Integrativ Fysiologi
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Wang, Yibing (författare)
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- Persson, Erik (författare)
- Uppsala universitet,Integrativ Fysiologi
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Manning, Roy Davis, Jr. (författare)
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Liu, Ruisheng (författare)
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(creator_code:org_t)
- 2011-06-02
- 2011
- Engelska.
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Ingår i: Hypertension Research. - : Springer Science and Business Media LLC. - 0916-9636 .- 1348-4214. ; 34:8, s. 942-948
- Relaterad länk:
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https://www.nature.c...
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https://urn.kb.se/re...
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https://doi.org/10.1...
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Abstract
Ämnesord
Stäng
- Calcium (Ca(2+)) has an important role in nearly all types of cellular secretion, with a particularly novel role in the juxtaglomerular (JG) cells in the kidney. In JG cells, Ca(2+) inhibits renin secretion, which is a major regulator of blood pressure and renal hemodynamics. However, whether alterations in afferent arteriolar (Af-Art) pressure change intracellular Ca(2+) concentration ([Ca(2+)](i)) in JG cells and whether [Ca(2+)](i) comes from extracellular or intracellular sources remains unknown. We hypothesize that increases in perfusion pressure in the Af-Art result in elevations in [Ca(2+)](i) in JG cells. We isolated and perfused Af-Art of C57BL6 mice and measured changes in [Ca(2+)](i) in JG cells in response to perfusion pressure changes. The JG cells' [Ca(2+)](i) was 93.3 +/- 2.2 nM at 60 mm Hg perfusion pressure and increased to 111.3 +/- 13.4, 119.6 +/- 7.3, 130.3 +/- 2.9 and 140.8 +/- 12.1 nM at 80, 100, 120 and 140 mm Hg, respectively. At 120 mm Hg, increases in [Ca(2+)](i) were reduced in mice receiving the following treatments: (1) the mechanosensitive cation channel blocker, gadolinium (94.6 +/- 7.5 nM); (2) L-type calcium channel blocker, nifedipine (105.8 +/- 7.5 nM); and (3) calcium-free solution plus ethylene glycol tetraacetic acid (96.0 +/- 5.8 nM). Meanwhile, the phospholipase C inhibitor, inositol triphosphate receptor inhibitor, T-type calcium channel blocker, N-type calcium channel blocker and Ca(2+)-ATPase inhibitor did not influence changes in [Ca(2+)](i) in JG cells. In summary, JG cell [Ca(2+)](i) rise as perfusion pressure increases; furthermore, the calcium comes from extracellular sources, specifically mechanosensitive cation channels and L-type calcium channels.
Nyckelord
- angiotensin
- juxtaglomerular apparatus
- kidney
- myogenic response
- renin
- MEDICINE
- MEDICIN
Publikations- och innehållstyp
- ref (ämneskategori)
- art (ämneskategori)
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