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

@entity1 @entity1169 @entity101 @entity935 @entity2178 @entity1425 @entity3159 @entity2661 @entity1063
Synthetic @entity2178 ( @entity2178 ), @entity1 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 @entity2178 increased cardiac frequency. The maximal @entity101 (MAP) caused by LHRH and sLHRH were identical, while @entity2178 caused a 100% greater maximal effect. The median effective doses (ED50) for both @entity2178 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 @entity2178 . Significant proportions of circulating, endogenous @entity935 , @entity1063 (NA) and @entity1425 (Ad) were found to be sulphoconjugated. Arterial plasma concentration of free NA increased simultaneously with the rise in blood pressure following @entity2178 injection. The magnitude of the free NA response increased with increasing @entity2178 dose but even a high dose failed to augment the plasma level of conjugated NA. @entity2178 did not alter concentrations of free or conjugated @entity935 and Ad. Intraarterial injection of an alpha-adrenoceptor antagonist, @entity3159 , caused sustained elevation of arterial pressure and free Ad. Subsequently @entity2178 lowered plasma Ad concentration. @entity3159 inhibited the NA response to @entity2178 yet the pressor effects of the alpha-adrenoceptor antagonist and @entity2178 were additive. Administration of a beta-adrenoceptor antagonist, @entity1169 , largely reversed the cardiovascular sequelae of alpha-adrenoceptor blockade. It is concluded, firstly, that the cardiovascular actions of @entity2178 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 @entity2661 cannot account for the pressor response to @entity2178 . Thirdly, both free and conjugated @entity2661 circulate in toads; however the extent of conjugation can be dissociated from the changes in free NA and Ad induced by @entity2178 and prazosin.
