Pressure induces intracellular calcium changes in juxtaglomerular cells in perfused afferent arterioles
2011 (English)In: Hypertension Research, ISSN 0916-9636, Vol. 34, no 8, 942-948 p.Article in journal (Refereed) Published
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.
Place, publisher, year, edition, pages
2011. Vol. 34, no 8, 942-948 p.
angiotensin, juxtaglomerular apparatus, kidney, myogenic response, renin
Medical and Health Sciences
IdentifiersURN: urn:nbn:se:uu:diva-157247DOI: 10.1038/hr.2011.65ISI: 000293576100010OAI: oai:DiVA.org:uu-157247DiVA: diva2:437066