ArticleProceedings of the National Academy of Sciences of the United States of America1992
Nitric oxide synthase in macula densa regulates glomerular capillary pressure.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.
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Who cites it
98 citing papers in PubMed, 528 citations in OpenAlex.
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- The Pathophysiological Basis of Diabetic Kidney Protection by Inhibition of SGLT2 and SGLT1.Kidney and dialysis · 2022Article
- Role of the macula densa sodium glucose cotransporter type 1-neuronal nitric oxide synthase-tubuloglomerular feedback pathway in diabetic hyperfiltration.Kidney international · 2022Article
- Knockout of Macula Densa Neuronal Nitric Oxide Synthase Increases Blood Pressure in db/db Mice.Hypertension (Dallas, Tex. : 1979) · 2021Article
- Nitric oxide signalling in kidney regulation and cardiometabolic health.Nature reviews. Nephrology · 2021Review
- Spatial transcriptional mapping of the human nephrogenic program.Developmental cell · 2021Article
- Relationship between Endothelial Dysfunction and Prevalence of Chronic Kidney Disease: The Circulatory Risk in Communities Study (CIRCS).Journal of atherosclerosis and thrombosis · 2021Article
- Cellular and Molecular Processes in Pulmonary Hypertension.Advances in experimental medicine and biology · 2021Article
- A new mechanism for the sex differences in angiotensin II-induced hypertension: the role of macula densa NOS1β-mediated tubuloglomerular feedback.American journal of physiology. Renal physiology · 2020Article
- Glucose transporters in the kidney in health and disease.Pflugers Archiv : European journal of physiology · 2020Review
- The tubular hypothesis of nephron filtration and diabetic kidney disease.Nature reviews. Nephrology · 2020Review
- New Mechanism for the Sex Differences in Salt-Sensitive Hypertension: The Role of Macula Densa NOS1β-Mediated Tubuloglomerular Feedback.Hypertension (Dallas, Tex. : 1979) · 2020Article
- Evolution of the Knowledge of Free Radicals and Other Oxidants.Oxidative medicine and cellular longevity · 2020Review
- High-Protein Diet-Induced Glomerular Hyperfiltration Is Dependent on Neuronal Nitric Oxide Synthase β in the Macula Densa via Tubuloglomerular Feedback Response.Hypertension (Dallas, Tex. : 1979) · 2019Article
- Knockout of NaAmerican journal of physiology. Renal physiology · 2019Article
- Hydrochlorothiazide ameliorates polyuria caused by tolvaptan treatment of polycystic kidney disease in PCK rats.Clinical and experimental nephrology · 2019Article
- Macula Densa SGLT1-NOS1-Tubuloglomerular Feedback Pathway, a New Mechanism for Glomerular Hyperfiltration during Hyperglycemia.Journal of the American Society of Nephrology : JASN · 2019Article
- Personalized intervention to improve stress and sleep patterns for glycemic control and weight management in obese Emirati patients with type 2 diabetes: a randomized controlled clinical trial.Diabetes, metabolic syndrome and obesity : targets and therapy · 2019Article
38 more citing papers are in PubMed but not listed here.
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7 authors at 2 institutions in 1 country.
Funding
Abstract
Tubular-fluid reabsorption by specialized cells of the nephron at the junction of the ascending limb of the loop of Henle and the distal convoluted tubule, termed the macula densa, releases compounds causing vasoconstriction of the adjacent afferent arteriole. Activation of this tubuloglomerular feedback response reduces glomerular capillary pressure of the nephron and, hence, the glomerular filtration rate. The tubuloglomerular feedback response functions in a negative-feedback mode to relate glomerular capillary pressure to tubular-fluid delivery and reabsorption. This system has been implicated in renal autoregulation, renin release, and longterm body fluid and blood-pressure homeostasis. Here we report that arginine-derived nitric oxide, generated in the macula densa, is an additional intercellular signaling molecule that is released during tubular-fluid reabsorption and counters the vasoconstriction of the afferent arteriole. Antibody to rat cerebellar constitutive nitric oxide synthase stained rat macula densa cells specifically. Microperfusion of the macula densa segment of single nephrons with N omega-methyl-L-arginine (an inhibitor of nitric oxide synthase) or with pyocyanin (a lipid-soluble inhibitor of endothelium-derived relaxation factor) showed that generation of nitric oxide can vasodilate the afferent arteriole and increase glomerular capillary pressure; this effect was blocked by drugs that prevent tubular-fluid reabsorption. We conclude that nitric oxide synthase in macula densa cells is activated by tubular-fluid reabsorption and mediates a vasodilating component to the tubuloglomerular feedback response. These findings imply a role for arginine-derived nitric oxide in body fluid-volume and blood-pressure homeostasis, in addition to its established roles in modulation of vascular tone by the endothelium and in neurotransmission.
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