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

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. Secondly, although it had been shown that alpha- and beta-adrenoceptor mechanisms mediate the pressor effect of LHRH, the present experiments showed that mobilization of catecholamines cannot account for the pressor response to Ang II. Thirdly, both free and conjugated catecholamines circulate in toads; however the extent of conjugation can be dissociated from the changes in free NA and Ad induced by Ang II and prazosin.