Skip to main content
British Journal of Pharmacology logoLink to British Journal of Pharmacology
. 1985 Jul;85(3):647–653. doi: 10.1111/j.1476-5381.1985.tb10560.x

Conjugated catecholamines and pressor responses to angiotensin, luteinizing hormone-releasing hormone and prazosin in conscious toads.

J X Wilson
PMCID: PMC1916520  PMID: 3928012

Abstract

Synthetic angiotensin II (Ang II), mammalian luteinizing hormone-releasing hormone (LHRH) and salmon LHRH (sLHRH) were injected intravenously into conscious, adult toads (Bufo marinus) to elucidate the cardiovascular actions of the hormones. The maximal increases in pulse pressure elicited by the three peptides did not differ from each other but only Ang II increased cardiac frequency. The maximal increases in mean arterial blood pressure (MAP) caused by LHRH and sLHRH were identical, while Ang II caused a 100% greater maximal effect. The median effective doses (ED50) for both Ang II and LHRH were approximately 0.1 nmol kg-1 whereas the potency of sLHRH was 10 fold less. Pressor responses to LHRH and sLHRH were blocked completely by (D-pGlu1, D-Phe2, D-Trp3,6)-LHRH but this antagonist did not inhibit Ang II. Significant proportions of circulating, endogenous dopamine, noradrenaline (NA) and adrenaline (Ad) were found to be sulphoconjugated. Arterial plasma concentration of free NA increased simultaneously with the rise in blood pressure following Ang II injection. The magnitude of the free NA response increased with increasing Ang II dose but even a high dose failed to augment the plasma level of conjugated NA. Ang II did not alter concentrations of free or conjugated dopamine and Ad. Intraarterial injection of an alpha-adrenoceptor antagonist, prazosin, caused sustained elevation of arterial pressure and free Ad. Subsequently Ang II lowered plasma Ad concentration. Prazosin inhibited the NA response to Ang II yet the pressor effects of the alpha-adrenoceptor antagonist and Ang II were additive. Administration of a beta-adrenoceptor antagonist, propranolol, largely reversed the cardiovascular sequelae of alpha-adrenoceptor blockade. It is concluded, firstly, that the cardiovascular actions of Ang II and LHRH are mediated through different receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Full text

PDF
647

Selected References

These references are in PubMed. This may not be the complete list of references from this article.

  1. Alexander N., Yoneda S., Vlachakis N. D., Maronde R. F. Role of conjugation and red blood cells for inactivation of circulating catecholamines. Am J Physiol. 1984 Jul;247(1 Pt 2):R203–R207. doi: 10.1152/ajpregu.1984.247.1.R203. [DOI] [PubMed] [Google Scholar]
  2. Burnstock G. Evolution of the autonomic innervation of visceral and cardiovascular systems in vertebrates. Pharmacol Rev. 1969 Dec;21(4):247–324. [PubMed] [Google Scholar]
  3. Capponi A. M., Catt K. J. Angiotensin II receptors in adrenal cortex and uterus. Binding and activation properties of angiotensin analogues. J Biol Chem. 1979 Jun 25;254(12):5120–5127. [PubMed] [Google Scholar]
  4. Chang P. Sympathomimetic actions of phenoxybenzamine on rat heart. Eur J Pharmacol. 1968 Oct;4(3):240–245. doi: 10.1016/0014-2999(68)90090-3. [DOI] [PubMed] [Google Scholar]
  5. Davidson L., Vandongen R., Beilin L. J., Arkwright P. D. Free and sulfate-conjugated catecholamines during exercise in man. J Clin Endocrinol Metab. 1984 Mar;58(3):415–418. doi: 10.1210/jcem-58-3-415. [DOI] [PubMed] [Google Scholar]
  6. Eiden L. E., Loumaye E., Sherwood N., Eskay R. L. Two chemically and immunologically distinct forms of luteinizing hormone-releasing hormone are differentially expressed in frog neural tissues. Peptides. 1982 May-Jun;3(3):323–327. doi: 10.1016/0196-9781(82)90094-8. [DOI] [PubMed] [Google Scholar]
  7. Grill G., Granger P., Thurau K. The renin angiotensin system of amphibians. I. Determination of the renin content of amphibian kidneys. Pflugers Arch. 1972;331(1):1–12. doi: 10.1007/BF00587186. [DOI] [PubMed] [Google Scholar]
  8. Hasegawa Y., Watanabe T. X., Sokabe H., Nakajima T. Chemical structure of angiotensin in the bullfrog Rana catesbeiana. Gen Comp Endocrinol. 1983 Apr;50(1):75–80. doi: 10.1016/0016-6480(83)90243-5. [DOI] [PubMed] [Google Scholar]
  9. Johnson G. A., Baker C. A., Smith R. T. Radioenzymatic assay of sulfate conjugates of catecholamines and DOPA in plasma. Life Sci. 1980 May 12;26(19):1591–1598. doi: 10.1016/0024-3205(80)90362-8. [DOI] [PubMed] [Google Scholar]
  10. Kalsner S., Quillan M. A hypothesis to explain the presynaptic effects of adrenoceptor antagonists. Br J Pharmacol. 1984 Jun;82(2):515–522. doi: 10.1111/j.1476-5381.1984.tb10788.x. [DOI] [PMC free article] [PubMed] [Google Scholar]
  11. Kirpekar S. M. Support for a role for feedback regulation of norepinephrine release. Fed Proc. 1984 Apr;43(5):1375–1378. [PubMed] [Google Scholar]
  12. Lumbers E. R., Potter E. K. Inhibition of the vagal component of the baroreceptor-cardioinhibitory reflex by angiotensin III in dogs and sheep. J Physiol. 1983 Mar;336:83–89. doi: 10.1113/jphysiol.1983.sp014568. [DOI] [PMC free article] [PubMed] [Google Scholar]
  13. MacKenzie D. S., Gould D. R., Peter R. E., Rivier J., Vale W. W. Response of superfused goldfish pituitary fragments to mammalian and salmon gonadotropin-releasing hormones. Life Sci. 1984 Nov 12;35(20):2019–2026. doi: 10.1016/0024-3205(84)90558-7. [DOI] [PubMed] [Google Scholar]
  14. Morris J. L., Gibbins I. L., Clevers J. Resistance of adrenergic neurotransmission in the toad heart to adrenoceptor blockade. Naunyn Schmiedebergs Arch Pharmacol. 1981;317(4):331–338. doi: 10.1007/BF00501315. [DOI] [PubMed] [Google Scholar]
  15. Phillis J. W., Kirkpatrick J. R. Actions of various gastrointestinal peptides on the isolated amphibian spinal cord. Can J Physiol Pharmacol. 1979 Aug;57(8):887–899. doi: 10.1139/y79-136. [DOI] [PubMed] [Google Scholar]
  16. Sherwood N., Eiden L., Brownstein M., Spiess J., Rivier J., Vale W. Characterization of a teleost gonadotropin-releasing hormone. Proc Natl Acad Sci U S A. 1983 May;80(9):2794–2798. doi: 10.1073/pnas.80.9.2794. [DOI] [PMC free article] [PubMed] [Google Scholar]
  17. Steele M. K., Gallo R. V., Ganong W. F. A possible role for the brain renin-angiotensin system in the regulation of LH secretion. Am J Physiol. 1983 Dec;245(6):R805–R810. doi: 10.1152/ajpregu.1983.245.6.R805. [DOI] [PubMed] [Google Scholar]
  18. Unger T., Buu N. T., Kuchel O., Schürch W. Conjugated dopamine: peripheral origin, distribution, and response to acute stress in the dog. Can J Physiol Pharmacol. 1980 Jan;58(1):22–27. doi: 10.1139/y80-005. [DOI] [PubMed] [Google Scholar]
  19. Wang P. C., Buu N. T., Kuchel O., Genest J. Conjugation patterns of endogenous plasma catecholamines in human and rat. A new specific method for analysis of glucuronide-conjugated catecholamines. J Lab Clin Med. 1983 Jan;101(1):141–151. [PubMed] [Google Scholar]
  20. Wilson J. X. Conjugated catecholamines in birds. Neurosci Lett. 1984 Oct 26;51(3):337–340. doi: 10.1016/0304-3940(84)90399-9. [DOI] [PubMed] [Google Scholar]
  21. Wilson J. X., Van Vliet B. N., West N. H. Gonadotropin-releasing hormone increases plasma catecholamines and blood pressure in toads. Neuroendocrinology. 1984 Nov;39(5):437–441. doi: 10.1159/000124017. [DOI] [PubMed] [Google Scholar]
  22. Yoneda S., Alexander N., Vlachakis N. D. Enzymatic deconjugation of catecholamines in human and rat plasma and red blood cell lysate. Life Sci. 1983 Sep 5;33(10):935–942. doi: 10.1016/0024-3205(83)90749-x. [DOI] [PubMed] [Google Scholar]

Articles from British Journal of Pharmacology are provided here courtesy of The British Pharmacological Society

RESOURCES