Abstract
IN the isolated, perfused heart, increased activity induced by catecholamines and/or calcium ions is followed by enhanced coronary flow, attributable to some metabolic process in the myocardium. This metabolically induced coronary baso-dilatation (MCD) is inhibited by prostaglandin E1 (ref. 1). The increased MCD response correlates with 3′5′-cyclic AMP levels. Furthermore, when prostaglandins (PGs) are infused, inhibition of MCD correlates with diminished cyclic AMP production2,3. The inhibition of MCD by exogenous administration of PGs suggests that these autacoids may play a role as modulators of the coronary reaction to increased cardiac activity4. If it were possible to demonstrate the participation of PGs produced endogenously, their relevance in this modu-latory mechanism of adaptation of coronary flow would become evident.
This is a preview of subscription content, access via your institution
Access options
Subscribe to this journal
Receive 51 print issues and online access
$199.00 per year
only $3.90 per issue
Buy this article
- Purchase on Springer Link
- Instant access to full article PDF
Prices may be subject to local taxes which are calculated during checkout
Similar content being viewed by others
References
Sunahara, F. A., and Talesnik, J., Proc. Can. Fed. biol. Soc., 14, 100 (1971).
Sunahara, F. A., Talesnik, J., and Sen, A. K., Proc. Fifth Int. Cong. Pharmac., No. 1350, 225 (San Francisco, 1972).
Sen, A. K., Sunahara, F. A., and Talesnik, J., Proc. Fifth Int. Cong. Pharmacol., No. 1244, 208 (San Francisco, 1972).
Sunahara, F. A., Sen, A. K., and Talesnik, J., Can. med. Ass. J., 107, 634 (1972).
Vane, J. R., Nature new Biol., 231, 232 (1971).
Smith, W. L., and Lands, W. E. M., J. biol. Chem., 246, 6700 (1971).
Flower, R., Gryglewski, R., Herbaczynska-Cedro, K., and Vane, J. R., Nature new Biol., 238, 104 (1972).
Feinberg, H., Boyd, E., and Katz, L. N., Am. J. Physiol., 202, 643 (1962).
Zachariah, P., J. Physiol., 158, 59 (1961).
Douglas, R. C., Armengol, V., and Talesnik, J., Acta physiol. latinoam., 10, 205 (1960).
Hinke, J. A. M., Wilson, M. L., and Burnham, S. C., Am. J. Physiol., 206, 211 (1964).
Somlyo, A. P., and Somlyo, A. V., Pharmac. Rev., 20, 197 (1968).
Seidel, C. L., and Bohr, D. F., Circ. Res., Suppl. II, 29, 88 (1971).
Gregg, D. E., and Fisher, L. C., in Handbook of Physiology (edit. by Hamilton, W. H., and Dow, P.), 2, 1517 (Williams and Wilkins, Baltimore, 1963).
Ferreira, S. H., Moncada, S., and Vane, J. R., Nature new Biol., 231, 237 (1971).
Ackenfels, A., and Vane, J. R., Br. J. Pharmac., 45, 451 (1972).
Tomlinson, R. V., Ringold, H. J., Qureshi, M. C., and Forchielli, E., Biochem. biophys. Res. Commun., 46, 552 (1972).
Wennamalm, Å., and Stjärne, L., Life Sci., 10, 471 (1971).
Junstad, M., and Wennmalm, Å., Acta physiol. scand., 85, 573 (1972).
Hedqvist, P., Stjärne, L., and Wennmalm, Å., Acta physiol. scand., 83, 430 (1971).
Samuelsson, B., and Wennmalm, Å., Acta physiol. scand., 83, 163 (1971).
Shio, H., Shaw, J., and Ramwell, P., Ann. NY Acad. Sci., 185, 327 (1971).
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
TALESNIK, J., SUNAHARA, F. Enhancement of Metabolic Coronary Dilatation by Aspirin-like Substances by Suppression of Prostaglandin Feedback Control?. Nature 244, 351–353 (1973). https://doi.org/10.1038/244351a0
Received:
Revised:
Issue Date:
DOI: https://doi.org/10.1038/244351a0
Comments
By submitting a comment you agree to abide by our Terms and Community Guidelines. If you find something abusive or that does not comply with our terms or guidelines please flag it as inappropriate.
