title: Dogmas and controversies in the handling of nitrogenous wastes: 5-HT2-like receptors are involved in triggering pulsatile urea excretion in the gulf toadfish, Opsanus beta.
abstract: When injected arterially, serotonin (5-hydroxytryptamine; 5-HT) has been shown to elicit naturally sized urea pulse events in the gulf toadfish, Opsanus beta. The goal of the present study was to determine which 5-HT receptor(s) was involved in mediating this serotonergic stimulation of the pulsatile excretion mechanism. Toadfish were surgically implanted with caudal arterial catheters and intraperitoneal catheters and injected with either 8-OH-DPAT (1 micro mol kg(-1)), a selective 5-HT(1A) receptor agonist, alpha-methyl-5-HT (1 micro mol kg(-1)), a 5-HT(2) receptor agonist, or ketanserin, a 5-HT(2) receptor antagonist (0.01, 0.1, 1 and 10 micro mol kg(-1)) plus alpha-methyl-5-HT. 8-OH-DPAT injection did not mediate an increase in urea excretion, ruling out the involvement of 5-HT(1A) receptors in pulsatile excretion. However, within 5 min, alpha-methyl-5-HT injection caused an increase in the excretion of urea in >95% (N=27) of the fish injected, with an average pulse size of 652+/-102 micro mol N kg(-1) (N=26). With alpha-methyl-5-HT injection there was no corresponding increase in ammonia or [(3)H]PEG 4000 permeability. Urea pulses elicited by alpha-methyl-5-HT were inhibited in a dose-dependent fashion by the 5-HT(2) receptor antagonist ketanserin, which at low doses caused a significant inhibition of pulse size and at higher doses significantly inhibited the occurrence of pulsatile excretion altogether. However, neither 8-OH-DPAT nor alpha-methyl 5-HT injection had an effect on plasma cortisol or plasma urea concentrations. These findings suggest the involvement of a 5-HT(2)-like receptor in the regulation of pulsatile urea excretion.
authors.affiliation: Division of Marine Biology and Fisheries, NIEHS Marine and Freshwater Biomedical Science Center, Rosenstiel School of Marine and Atmospheric Science, University of Miami, Miami, Florida 33149-1098, USA. dmcdonald@rsmas.miami.edu
authors.forename: M Danielle
authors.initials: MD
authors.lastname: McDonald
authors.forename: Patrick J
authors.initials: PJ
authors.lastname: Walsh
mesh_terms: D017371:8-Hydroxy-2-(di-n-propylamino)tetralin / Q000378:metabolism / Q000494:pharmacology; D000704:Analysis of Variance; D000818:Animals; D024541:Batrachoidiformes / Q000378:metabolism*; D001692:Biological Transport / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D006854:Hydrocortisone / Q000097:blood; D007650:Ketanserin / Q000378:metabolism / Q000494:pharmacology; D011092:Polyethylene Glycols / Q000378:metabolism; D044348:Receptors, Serotonin, 5-HT2 / Q000378:metabolism*; D012701:Serotonin / Q000031:analogs & derivatives / Q000378:metabolism / Q000494:pharmacology; D058826:Serotonin 5-HT2 Receptor Agonists; D013997:Time Factors; D014316:Tritium; D014508:Urea / Q000097:blood / Q000378:metabolism*
chemical_list: D044348:Receptors, Serotonin, 5-HT2; D058826:Serotonin 5-HT2 Receptor Agonists; D014316:Tritium; C042390:alpha-methylserotonin; D012701:Serotonin; D011092:Polyethylene Glycols; D017371:8-Hydroxy-2-(di-n-propylamino)tetralin; D014508:Urea; D007650:Ketanserin; D006854:Hydrocortisone