The DOI matches its Crossref record; 23 of the 23 references it cites were found in a registry or an index.
Development and mechanism of a specific supersensitivity to nitrovasodilators after inhibition of vascular nitric oxide synthesis in vivo.
Open accessAbstract
The mechanism of the increased sensitivity to nitrovasodilators after removal of endothelial nitric oxide (NO) was investigated in vitro and in vivo. The vasoconstrictor potency of phenylephrine and the force of contraction of rat isolated aortic rings were significantly enhanced after endothelium removal or treatment with inhibitors of endothelial NO synthase. Furthermore, these procedures led to a significant decrease in the basal levels of cGMP in the vascular rings. Moreover, the potency of glyceryl trinitrate (n3Gro) and sodium nitroprusside (SNP) as relaxing agents and the ability of SNP to induce increases in cGMP in aortic rings were significantly enhanced in those rings denuded of endothelium or treated with the inhibitors. These procedures did not affect the vasodilator actions of isoprenaline or 8-bromo-cGMP. In the anesthetized rat, treatment with the inhibitors enhanced significantly the hypotensive responses to n3Gro without affecting those to isoprenaline. These data indicate that the removal of the basal NO-mediated vasodilator tone in the cardiovascular system leads, at the level of the soluble guanylate cyclase, to a specific supersensitivity to nitrovasodilators in vivo. The existence of such a phenomenon has important implications for understanding the local physiological control of blood flow, its pathological disturbances, and the mechanism of action of nitrovasodilators.
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Cites
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
Self-citationVascular endothelial cells synthesize nitric oxide from L-arginine
Palmer, R. M. J., Ashton, D. S., & Moncada, S. (1988) · Nature · doi:10.1038/333664a0 · Cited by 4,769
Self-citationCharacterization of three inhibitors of endothelial nitric oxide synthase in vitro and in vivo
Rees, D. D., Palmer, R. M. J., Schulz, R., Hodson, H. F., & Moncada, S. (1990) · British Journal of Pharmacology · doi:10.1111/j.1476-5381.1990.tb14151.x · Cited by 1,856
Self-citationRole of endothelium-derived nitric oxide in the regulation of blood pressure.
Rees, D. D., Palmer, R. M., & Moncada, S. (1989) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.86.9.3375 · Cited by 1,826
Self-citationEffects of endothelium-derived nitric oxide on peripheral arteriolar tone in man
Vallance, P., Collier, J., & Moncada, S. (1989) · The Lancet · doi:10.1016/s0140-6736(89)91013-1 · Cited by 1,590
Self-citationFlow-induced release of endothelium-derived relaxing factor
Rubanyi, G. M., Romero, J. C., & Vanhoutte, P. M. (1986) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.1986.250.6.h1145 · Cited by 1,366
Palmer, R. M. J., Rees, D. D., Ashton, D. S., & Moncada, S. (1988) · Biochemical and Biophysical Research Communications · doi:10.1016/s0006-291x(88)81362-7 · Cited by 1,349
Self-citationAgonist-induced endothelium-dependent relaxation in rat thoracic aorta may be mediated through cGMP
Rapoport, R. M., & Murad, F. (1983) · Circulation Research · doi:10.1161/01.res.52.3.352 · Cited by 928
Rees, D. D., Palmer, R. M. J., Hodson, H. F., & Moncada, S. (1989) · British Journal of Pharmacology · doi:10.1111/j.1476-5381.1989.tb11833.x · Cited by 850
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Cited by
Endogenous nitric oxide: physiology, pathology and clinical relevance
MONCADA, S., & HIGGS, E. A. (1991) · European Journal of Clinical Investigation · doi:10.1111/j.1365-2362.1991.tb01383.x · Cited by 759
Self-citationRegulation of Nitric Oxide-Sensitive Guanylyl Cyclase
Friebe, A., & Koesling, D. (2003) · Circulation Research · doi:10.1161/01.res.0000082524.34487.31 · Cited by 508
What is the real physiological NO concentration in vivo?
Hall, C. N., & Garthwaite, J. (2009) · Nitric Oxide · doi:10.1016/j.niox.2009.07.002 · Cited by 378
Traylor, T. G., & Sharma, V. S. (1992) · Biochemistry · doi:10.1021/bi00126a001 · Cited by 353
Ohashi, Y., Kawashima, S., Hirata, K. I., Yamashita, T., Ishida, T., Inoue, N., Sakoda, T., Kurihara, H., Yazaki, Y., & Yokoyama, M. (1998) · Journal of Clinical Investigation · doi:10.1172/jci4394 · Cited by 277
Metadata
- Authors
- Moncada, S., Rees, D. D., Schulz, R., & Palmer, R. M.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 1991-03-15
- Volume
- 88
- Issue
- 6
- Pages
- 2166-2170
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W1993783817
- Cited by
- 489
- References
- 23
- FWCI
- 16.85
- Type
- journal article
- Language
- en
- Open access
- green
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- Moncada, S., Rees, D. D., Schulz, R., & Palmer, R. M. (1991). Development and mechanism of a specific supersensitivity to nitrovasodilators after inhibition of vascular nitric oxide synthesis in vivo. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.88.6.2166
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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