ArticleJournal of the American Society of Nephrology : JASN2009
Hypotonicity-induced Renin exocytosis from juxtaglomerular cells requires aquaporin-1 and cyclooxygenase-2.
Article in Journal of the American Society of Nephrology : JASN, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 23 citations in OpenAlex.
- Increased COX-2 after ureter obstruction attenuates fibrosis and is associated with EPActa physiologica (Oxford, England) · 2022Article
- Connexin Hemichannels Contribute to the Activation of cAMP Signaling Pathway and Renin Production.International journal of molecular sciences · 2020Article
- Experimental Evaluation of the Transport Mechanisms of PoIFN-α in Caco-2 Cells.Frontiers in pharmacology · 2017Article
- Disruption of cyclooxygenase type 2 exacerbates apoptosis and renal damage during obstructive nephropathy.American journal of physiology. Renal physiology · 2015Article
- Genetic Variants of C-5312T REN Increased Renin Levels and Diastolic Blood Pressure Response to Angiotensin Receptor Blockers.International journal of hypertension · 2015Article
- Article
- Regulation of renin secretion by renal juxtaglomerular cells.Pflugers Archiv : European journal of physiology · 2013Review
- Synthesis and secretion of renin in mice with induced genetic mutations.Kidney international · 2012Review
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9 authors at 1 institution in 1 country.
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Abstract
The mechanism by which extracellular hypotonicity stimulates release of renin from juxtaglomerular (JG) cells is unknown. We hypothesized that osmotically induced renin release depends on water movement through aquaporin-1 (AQP1) water channels and subsequent prostanoid formation. We recorded membrane capacitance (C(m)) by whole-cell patch clamp in single JG cells as an index of exocytosis. Hypotonicity increased C(m) significantly and enhanced outward current. Indomethacin, PLA(2) inhibition, and an antagonist of prostaglandin transport impaired the C(m) and current responses to hypotonicity. Hypotonicity also increased exocytosis as determined by a decrease in single JG cell quinacrine fluorescence in an indomethacin-sensitive manner. In single JG cells from COX-2(-/ -) and AQP1(-/ -) mice, hypotonicity increased neither C(m) nor outward current, but 0.1-muM PGE(2) increased both in these cells. A reduction in osmolality enhanced cAMP accumulation in JG cells but not in renin-producing As4.1 cells; only the former had detectable AQP1 expression. Inhibition of protein kinase A blocked the hypotonicity-induced C(m) and current response in JG cells. Taken together, our results show that a 5 to 7% decrease in extracellular tonicity leads to AQP1-mediated water influx in JG cells, PLA(2)/COX-2-mediated prostaglandin-dependent formation of cAMP, and activation of PKA, which promotes exocytosis of renin.
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