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Cited by 186Nitric Oxide and Endothelin EffectsEicosanoids and Hypertension PharmacologyCardiovascular Health and Disease Prevention

The DOI matches its Crossref record; 35 of the 36 references it cites were found in a registry or an index.

Enhanced Release of Prostaglandins Contributes to Flow-Induced Arteriolar Dilation in eNOS Knockout Mice

Sun, Dong, Huang, An, Smith, Carolyn J., Stackpole, Christopher J., Connetta, Joseph A., Shesely, Edward G., Koller, Akos, Kaley, Gabor·1999·Circulation Research
DOI 10.1161/01.res.85.3.288
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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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Research works printed but not linked: 12

  1. 10.1161/res.74.3.8118950 · DOI
  2. 10.1161/res.70.3.1537085 · DOI
  3. 10.1161/res.76.4.544 · DOI
  4. 10.1161/res.74.2.7507417 · DOI
  5. 10.1161/res.81.1.34 · DOI
  6. 10.1161/res.79.2.343 · DOI
  7. 10.1161/res.79.6.1161 · DOI
  8. 10.1161/res.82.2.186 · DOI
  9. 10.1161/res.82.12.1323 · DOI
  10. 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.
  11. 10.1161/circ.94.12.3341 · DOI
  12. 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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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.
ORCID
Venue
Circulation Research
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
1999-08-06
Volume
85
Issue
3
Pages
288-293
ISSN
  • 0009-7330 (ISSN-L)
  • 1524-4571
DOI
10.1161/01.res.85.3.288
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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