ArticleAmerican journal of physiology. Renal physiology2008
Intracellular pH regulates superoxide production by the macula densa.
Article in American journal of physiology. Renal physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- NaHCOHypertension (Dallas, Tex. : 1979) · 2019Article
- Effects of reactive oxygen species on renal tubular transport.American journal of physiology. Renal physiology · 2019Review
- Tubule-vascular feedback in renal autoregulation.American journal of physiology. Renal physiology · 2019Review
- Thick Ascending Limb Sodium Transport in the Pathogenesis of Hypertension.Physiological reviews · 2019Review
- Interleukin-13 increases pendrin abundance to the cell surface in bronchial NCI-H292 cells via Rho/actin signaling.Pflugers Archiv : European journal of physiology · 2017Article
- Effects of Reactive Oxygen Species on Tubular Transport along the Nephron.Antioxidants (Basel, Switzerland) · 2017Review
- Macula Densa Nitric Oxide Synthase 1β Protects against Salt-Sensitive Hypertension.Journal of the American Society of Nephrology : JASN · 2016Article
- Inhibition of Nitric Oxide Synthase 1 Induces Salt-Sensitive Hypertension in Nitric Oxide Synthase 1α Knockout and Wild-Type Mice.Hypertension (Dallas, Tex. : 1979) · 2016Article
- Shear stress blunts tubuloglomerular feedback partially mediated by primary cilia and nitric oxide at the macula densa.American journal of physiology. Regulatory, integrative and comparative physiology · 2015Article
- Oxidative status in the macula densa modulates tubuloglomerular feedback responsiveness in angiotensin II-induced hypertension.Acta physiologica (Oxford, England) · 2015Article
- Iodinated contrast media cause direct tubular cell damage, leading to oxidative stress, low nitric oxide, and impairment of tubuloglomerular feedback.American journal of physiology. Renal physiology · 2014Article
- Enhanced expression and activity of Nox2 and Nox4 in the macula densa in ANG II-induced hypertensive mice.American journal of physiology. Renal physiology · 2014Article
- NADPH oxidases, reactive oxygen species, and the kidney: friend and foe.Journal of the American Society of Nephrology : JASN · 2013Review
- Interaction between nitric oxide and superoxide in the macula densa in aldosterone-induced alterations of tubuloglomerular feedback.American journal of physiology. Renal physiology · 2013Article
- Aldosterone stimulates superoxide production in macula densa cells.American journal of physiology. Renal physiology · 2011Article
- Luminal flow regulates NO and O2(-) along the nephron.American journal of physiology. Renal physiology · 2011Review
- Salt-sensitive splice variant of nNOS expressed in the macula densa cells.American journal of physiology. Renal physiology · 2010Article
- GTPase-Rac enhances depolarization-induced superoxide production by the macula densa during tubuloglomerular feedback.American journal of physiology. Regulatory, integrative and comparative physiology · 2010Article
- Isoforms and functions of NAD(P)H oxidase at the macula densa.Hypertension (Dallas, Tex. : 1979) · 2009Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
We hypothesized that elevated macula densa intracellular pH (pH(i)) during tubuloglomerular feedback enhances O(2)(-) production from NAD(P)H oxidase. Microdissected thick ascending limbs from rabbits with intact macula densa were cannulated and perfused with physiological saline. When luminal NaCl was switched from 10 to 80 mM, O(2)(-) production increased from 0.53 +/- 0.09 to 2.62 +/- 0.54 U/min (P < 0.01). To determine whether inhibiting the Na/H exchanger blocks O(2)(-) production, we used dimethyl amiloride (DMA) to block Na/H exchange. In the presence of DMA, O(2)(-) production induced by NaCl was blunted by 40%. To study the effect of pH(i) on O(2)(-) in intact macula densa cells, we measured O(2)(-) while pH(i) was changed by adjusting luminal pH. When the macula densa was perfused with 80 mM NaCl and the pH of the perfusate was switched to 6.8, 7.4, and 8.0, O(2)(-) production was significantly enhanced, but not at 10 mM NaCl. To ascertain the source of O(2)(-), we used the NAD(P)H oxidase inhibitor apocynin. In the presence of apocynin (10(-5) M), O(2)(-) production induced by elevating pH(i) was blocked. Finally, we measured the optimum pH for O(2)(-) production by the macula densa and found optimum extracellular pH is at 7.7 and optimum pH(i) is approximately 8 for O(2)(-) production. We found that elevated pH(i) enhances O(2)(-) production from NAD(P)H oxidase induced by increasing luminal NaCl when the lumen is perfused with 80 mM NaCl, not 10 mM, and O(2)(-) production is pH sensitive, with an optimum pH(i) of 8.
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Registered trials
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