Nature Publishing Group, publisher of Nature, and other science journals and reference works
Nature
my account e-alerts subscribe register
   
Wednesday 28 June 2017
Journal Home
Current Issue
AOP
Archive
Download PDF
References
Export citation
Export references
Send to a friend
More articles like this

Letters to Nature
Nature 313, 54 - 56 (03 January 1985); doi:10.1038/313054a0

Calcitonin gene-related peptide is a potent vasodilator

S. D. Brain*, T. J. Williams*, J. R. Tippins, H. R. Morris & I. MacIntyre

Department of Pharmacology, Institute of Basic Medical Sciences, Royal College of Surgeons of England, Lincoln's Inn Fields, London WC2A3PN, UK
Department of Biochemistry, Imperial College, London SW7 2AZ, UK.
Department of Chemical Pathology, Royal Postgraduate Medical School, DuCane Road, London W12 0HS, UK.
*Present address: Section of Vascular Biology, MRC Clinical Research Centre, Watford Road, Harrow, Middlesex HA1 3UJ, UK.

A novel peptide, calcitonin gene-related peptide (CGRP), has been predicted to result from alternative processing of the primary RNA transcript of the calcitonin gene in the rat1,2. Several lines of evidence suggest that CGRP is a transmitter in the central and peripheral nervous system2–4. Human CGRP has been isolated and characterized5, and shown to have potent effects on the heart6. The observations presented here indicate that human and rat CGRP also have potent effects on blood vessels. Intradermal injection of CGRP in femtomole doses induces microvascular dilatation resulting in increased blood flow, which we have detected in the rabbit by using a 133Xe clearance technique7,8. In human skin, CGRP induces persistent local reddening. Microscopic observation of the hamster cheek pouch9 in vivo revealed that topical application of CGRP induces dilatation of arterioles. Furthermore, CGRP relaxes strips of rat aorta in vitro by an endothelial cell-dependent mechanism. Therefore, we suggest that local extravascular release of CGRP may be involved in the physiological control of blood flow and that circulating CGRP may contribute to hyperaemia in certain pathological conditions.

------------------

References

1. Amara, S. G., Jonas, V., Rosenfeld, M. G., Ong, E. S. & Evans, R. M. Nature 298, 240−244 (1982). | PubMed | ISI | ChemPort |
2. Rosenfeld, M. G. et al. Nature 304, 129−135 (1983). | PubMed | ISI | ChemPort |
3. Fisher, L. A. et al. Nature 305, 534−536 (1983). | PubMed | ISI | ChemPort |
4. Mason, R. T. et al. Nature 308, 653−655 (1984). | PubMed | ISI | ChemPort |
5. Morris, H. R. et al. Nature 308, 746−748 (1984). | PubMed | ISI | ChemPort |
6. Etienne, T. et al. J. Physiol., Lond. 351, 48P (1984).
7. Williams, T. J. J. Physiol., Lond. 254, 4−5P (1976). | ChemPort |
8. Williams, T. J. Br. J. Pharmac. 65, 517−524 (1979). | ISI | ChemPort |
9. Duling, B. R. Microvasc. Res. 5, 423−429 (1973). | Article | PubMed | ISI | ChemPort |
10. Hillyard, C. J. et al. Lancet i, 846−848 (1983). | Article |
11. Williams, T. J. & Peck, M. J. Nature 270, 530−532 (1977). | PubMed | ISI | ChemPort |
12. Williams, T. J. Br. J. Pharmac. 77, 505−509 (1982). | ISI | ChemPort |
13. Furchgott, R. F. & Zawadzki, J. V. Nature 288, 373−376 (1980). | PubMed | ISI | ChemPort |
14. Solomon, L. M., Juhlin, L. & Kirschenbaum, M. B. J. invest. Derm. 51, 280−282 (1968). | PubMed | ISI | ChemPort |
15. Cohen, S. L., MacIntyre, I., Grahame-Smith, D. & Walker, J. G. Lancet II, 1172−1174 ( 1973). | Article |
16. Jancso, G., Kiraly, E. & Jancso-Gabor, A. Nature 270, 741−743 (1977). | PubMed | ISI | ChemPort |
17. Lembeck, F. & Holzer, P. Naunyn-Schmiedebergs Archs Pharmak. 310, 175−183 (1979). | ChemPort |



© 1985 Nature Publishing Group
Privacy Policy