Characterization of the effects of vasoactive substances on the bulbus arteriosus of the eel, Anguilla rostrata.
The fish bulbus arteriosus (BA) smooths cardiac output by expanding during cardiac systole and rebounding during diastole, thereby providing constant perfusion of the gills downstream. Published data have demonstrated innervation of the teleost BA and shown that the tension and compliance of the BA responded to vasoactive agonists, such as epinephrine and acetylcholine, suggesting that the BA was more than a mere "windkessel." To examine vasoactivity in the BA more directly, we measured the responses of isolated tissue rings from the BA of the eel, Anguilla rostrata to a suite of putative vasoactive agonists, which had been shown to affect vascular smooth muscle in a variety of teleosts. The BA of the eel was insensitive to acetylcholine but constricted when endothelin (ET-1) was applied. Nitric oxide, sodium nitroprusside (SNP; NO donor), natriuretic peptides (NP), and prostaglandin E1 (but not the prostacyclin agonist carbaprostacyclin) produced significant dilation in the BA. Since both ET-1 and sarafotoxin S6c produced concentration-dependent constriction, it appears that endothelin receptor B-type (ETB) receptors (and possibly ETA receptors) are present. The dilation produced by SNP was also concentration dependent, as were the dilations produced by porcine C-type natriuretic peptide, eel atrial natriuretic peptide (NP receptor agonists), Sulprostone and Butaprost (PGE receptor agonists). Our data demonstrate that the BA of eel is responsive to a variety of vasoactive agonists, suggesting that the BA is under neurohumoral control. The role of agonist-induced changes in BA tension in fish cardiovascular physiology remains to be determined, as do the specific receptor types involved.
Evans
David H
DH
Mt. Desert Island Biological Laboratory, Salsbury Cove, Maine 04672, USA. devans@zoo.ufl.edu
Harrie
Ann C
AC
Kozlowski
Matthew S
MS
D000811:Anguilla / Q000033:anatomy & histology / Q000502:physiology*; D000818:Animals; D002319:Cardiovascular System / Q000187:drug effects*; D014662:Vasoconstrictor Agents / Q000494:pharmacology*; D014665:Vasodilator Agents / Q000494:pharmacology*
D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents