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Enhanced Release of Prostaglandins Contributes to Flow-Induced Arteriolar Dilation in eNOS Knockout Mice
Abstract
Abstract—Nitric oxide and prostaglandins were shown to contribute to the endothelial mediation of flow-induced dilation of skeletal muscle arterioles of rats. Thus, we hypothesized that flow-induced dilation and its mediation are altered in gracilis muscle arterioles of mice deficient in the gene for endothelial nitric oxide synthase (eNOS-KO) compared with control wild-type (WT) mice. Gracilis muscle arterioles (≈80 μm) of male mice were isolated, then cannulated and pressurized in a vessel chamber. The increases in diameter elicited by increases in perfusate flow from 0 to 10 μL/min were similar in arterioles from eNOS-KO (n=28) and WT (n=22) mice (≈20 μm at 10 μL/min flow). Removal of the endothelium eliminated flow-induced dilations in vessels of both strains of mice.Nω-nitro-l-arginine (L-NNA, 10−4 mol/L) significantly inhibited flow-induced dilation in arterioles of WT mice by ≈51% but had no effect on responses of arterioles from eNOS-KO mice. Indomethacin (INDO, 10−5 mol/L) inhibited flow-induced dilation of WT mice by ≈49%, whereas it completely abolished this response in arterioles of eNOS-KO mice. Simultaneous administration of INDO and L-NNA eliminated flow-induced responses in arterioles of WT mice. Dilations to carbaprostacyclin were similar at concentrations of 10−8 and 3×10−8 mol/L but decreased significantly at 10−7 mol/L in arterioles of eNOS-KO compared with those of WT mice. These findings demonstrate that, despite the lack of nitric oxide mediation, flow-induced dilation is close to normal in arterioles of eNOS-KO mice because of an enhanced release of endothelial dilator prostaglandins and suggest that this vascular adaptation may contribute to the regulation of peripheral resistance in eNOS-KO mice.
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“Although activation of AMP kinase can lead to mitochondrial biogenesis and increased mitochondrial number, this pathway can also directly be stimulated by mitochondrial hydrogen peroxide-dependent activation of the MAP kinase Akt (911, 919).”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [911]
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Furchgott, R. F., & Zawadzki, J. V. (1980) · Nature · doi:10.1038/288373a0 · Cited by 12,064
Nitric oxide release accounts for the biological activity of endothelium-derived relaxing factor
Palmer, R. M. J., Ferrige, A. G., & Moncada, S. (1987) · Nature · doi:10.1038/327524a0 · Cited by 10,704
Hypertension in mice lacking the gene for endothelial nitric oxide synthase
Huang, P. L., Huang, Z., Mashimo, H., Bloch, K. D., Moskowitz, M. A., Bevan, J. A., & Fishman, M. C. (1995) · Nature · doi:10.1038/377239a0 · Cited by 2,070
Role of endothelium-derived nitric oxide in the regulation of blood pressure.
Rees, D. D., Palmer, R. M. J., & Moncada, S. (1989) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.86.9.3375 · Cited by 1,827
Sessa, W. C., Pritchard, K., Seyedi, N., Wang, J., & Hintze, T. H. (1994) · Circulation Research · doi:10.1161/01.res.74.2.349 · Cited by 934
Elevated blood pressures in mice lacking endothelial nitric oxide synthase
Shesely, E. G., Maeda, N., Kim, H.-S., Desai, K. M., Krege, J. H., Laubach, V. E., Sherman, P. A., Sessa, W. C., & Smithies, O. (1996) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.93.23.13176 · Cited by 908
Self-citationDirect evidence for the importance of endothelium-derived nitric oxide in vascular remodeling.
Rudic, R. D., Shesely, E. G., Maeda, N., Smithies, O., Segal, S. S., & Sessa, W. C. (1998) · Journal of Clinical Investigation · doi:10.1172/jci1699 · Cited by 821
Self-citationNitric Oxide Attenuates the Release of Endothelium-Derived Hyperpolarizing Factor
Bauersachs, J. K., Popp, R., Hecker, M., Sauer, E., Fleming, I., & Busse, R. (1996) · Circulation · doi:10.1161/01.cir.94.12.3341 · Cited by 430
Interaction of pressure- and flow-induced responses in porcine coronary resistance vessels
Kuo, L., Chilian, W. M., & Davis, M. J. (1991) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.1991.261.6.h1706 · Cited by 392
Moroi, M., Zhang, L., Yasuda, T., Virmani, R., Gold, H., Fishman, M. C., & Huang, P. L. (1998) · Journal of Clinical Investigation · doi:10.1172/jci1293 · Cited by 337
Research works printed but not linked: 12
- 10.1161/res.74.3.8118950 · DOI
- 10.1161/res.70.3.1537085 · DOI
- 10.1161/res.76.4.544 · DOI
- 10.1161/res.74.2.7507417 · DOI
- 10.1161/res.81.1.34 · DOI
- 10.1161/res.79.2.343 · DOI
- 10.1161/res.79.6.1161 · DOI
- 10.1161/res.82.2.186 · DOI
- 10.1161/res.82.12.1323 · DOI
- Lamping K, Nuno D, Shesely EG, Maeda N, Faraci F. Preserved responses to acetylcholine in coronary arteries from endothelial nitric oxide synthase deficient mice. FASEB J. 1998;12:A978. Abstract.
- 10.1161/circ.94.12.3341 · DOI
- Huang A, Sun D, Smith CJ, Stackpole C, Shesely EG, Koller A, Kaley G. Attenuated acetylcholine (ACh)-induced dilation in arterioles of eNOS knockout mice. FASEB J. 1999;13:A1066. Abstract 796.5.
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Corretti, M. C., Anderson, T. J., Benjamin, E. J., Celermajer, D. S., Charbonneau, F., Creager, M. A., Deanfield, J. E., Drexler, H., Gerhard‐Herman, M. D., Herrington, D. M., et al. (2002) · Journal of the American College of Cardiology · doi:10.1016/s0735-1097(01)01746-6 · Cited by 4,606
Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation
Tejero, J., Shiva, S., & Gladwin, M. T. (2019) · Physiological Reviews · doi:10.1152/physrev.00036.2017 · Cited by 541
Vascular Endothelial Dysfunction and Mortality Risk in Patients With Chronic Heart Failure
Katz, S. D., Hryniewicz, K. M., Hriljac, I., Balidemaj, K., Dimayuga, C. A., Hudaihed, A., & Yasskiy, A. (2005) · Circulation · doi:10.1161/01.cir.0000153349.77489.cf · Cited by 413
Nitric Oxide and the Vascular Endothelium
Moncada, S., & Higgs, E. A. (2006) · Springer eBooks · doi:10.1007/3-540-32967-6_7 · Cited by 419
Endothelium‐mediated control of vascular tone: COX‐1 and COX‐2 products
Félétou, M., Huang, Y., & Vanhoutte, P. M. (2011) · British Journal of Pharmacology · doi:10.1111/j.1476-5381.2011.01276.x · Cited by 372
Metadata
- Authors
- Sun, D., Huang, A., Smith, C. J., Stackpole, C. J., Connetta, J. A., Shesely, E. G., Koller, A., & Kaley, G.
- Affiliations
- Henry Ford Health (US)
- From the Departments of Physiology (D.S., A.H., A.K., G.K.) and Pathology (C.J. Smith, C.J. Stackpole, J.A.C.), New York Medical College, Valhalla, NY; Division of Hypertension and Vascular Research (E.G.S.), Henry Ford Hospital, Detroit, Mich.
- Venue
- Circulation Research
- Published
- 1999-08-06
- Volume
- 85
- Issue
- 3
- Pages
- 288-293
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- OpenAlex
- W2120622445
- Cited by
- 186
- References
- 36
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 2 · 2022: 1 · 2021: 2 · 2020: 1 · 2019: 1 · 2018: 6 · 2017: 2 · 2016: 9 · 2015: 7 · 2014: 5 · 2013: 4 · 2012: 8
- FWCI
- 4.72
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Circulation Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Heart Association
- National Institutes of Health (HL‐46813, HL-43023)
- National Heart, Lung, and Blood Institute (P01HL043023, HL-46813, HL 43023)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Eicosanoids and Hypertension Pharmacology
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Health and Disease Prevention
- Keywords
- flow-mediated dilation, prostaglandins, endothelial nitric oxide synthase, eNOS knockout mice, nitric oxide, skeletal muscle arterioles, gracilis muscle, indomethacin, L-NNA, endothelium-dependent vasodilation, systemic vascular resistance
- MeSH terms
- Animals, Arterioles, Blood Circulation, Enzyme Inhibitors, Indomethacin, Male, Prostaglandins, Epoprostenol, Vasodilation, Cyclooxygenase Inhibitors, Mice, Knockout, Nitric Oxide Synthase, Nitroarginine, Mice, Nitric Oxide Synthase Type II, Nitric Oxide Synthase Type III, In Vitro Techniques
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