title: Effects of natriuretic peptides and nitroprusside on venous function in trout.
abstract: Active venous regulation of cardiovascular function is well known in mammals but has not been demonstrated in fish. In the present studies, the natriuretic peptides (NP) rat atrial natriuretic peptide (ANP) and trout ventricular natriuretic peptide (VNP), clearance receptor inhibitor SC-46542, and sodium nitroprusside (SNP) were infused into unanesthetized trout fitted with pressure cannulas in the ventral aorta, dorsal aorta, and ductus Cuvier, and a ventral aorta (VA) flow probe was used to measure cardiac output (CO). In another group, in vivo vascular (venous) capacitance curves were obtained during ANP or SNP infusion. The in vitro effects of NP on vessels and the heart were also examined. ANP, VNP, and SC-46542 decreased central venous pressure (PVen), CO, stroke volume (SV), and gill resistance (RG), whereas systemic resistance (RS) and heart rate (HR) increased. Dorsal aortic pressure (PDA) transiently increased and then fell even though RS remained elevated. ANP decreased mean circulatory filling pressure (MCFP), increased vascular compliance at all blood volumes, and increased unstressed volume in hypovolemic fish. ANP had no direct effect on the heart. ANP responses in vivo were not altered in trout made hypotensive by prior treatment with the angiotensin-converting enzyme inhibitor lisinopril. SNP reduced ventral aortic pressure (PVA), PDA, and RS, increased CO and HR, but did not affect PVen, SV, or RG. SNP slightly decreased MCFP but did not affect compliance or unstressed volume. In vitro, large systemic arteries were more responsive than veins to NP, whereas SNP relaxed both. These results show that, in vivo, NP decrease venous compliance, thereby decreasing venous return, CO, and arterial pressure. Conversely, SNP hypotension is due to decreased RS. This is the first evidence for active regulation of venous capacitance in fish, which probably occurs in small veins or venules. The presence of venous baroreceptors is also suggested.
authors.affiliation: Indiana University School of Medicine, South Bend Center for Medical Education, University of Notre Dame 46556, USA.
authors.forename: K R
authors.initials: KR
authors.lastname: Olson
authors.forename: D J
authors.initials: DJ
authors.lastname: Conklin
authors.forename: A P
authors.initials: AP
authors.lastname: Farrell
authors.forename: J E
authors.initials: JE
authors.lastname: Keen
authors.forename: Y
authors.initials: Y
authors.lastname: Takei
authors.forename: L
authors.initials: L
authors.lastname: Weaver
authors.forename: M P
authors.initials: MP
authors.lastname: Smith
authors.forename: Y
authors.initials: Y
authors.lastname: Zhang
mesh_terms: D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology*; D009320:Atrial Natriuretic Factor / Q000494:pharmacology*; D002302:Cardiac Output / Q000187:drug effects; D002319:Cardiovascular System / Q000187:drug effects; D005260:Female; D006339:Heart Rate / Q000187:drug effects; D066298:In Vitro Techniques; D008297:Male; D009599:Nitroprusside / Q000494:pharmacology*; D017686:Oncorhynchus mykiss / Q000502:physiology*; D051381:Rats; D018924:Vascular Capacitance / Q000187:drug effects; D014680:Veins / Q000187:drug effects* / Q000502:physiology*
chemical_list: D000959:Antihypertensive Agents; D009599:Nitroprusside; D009320:Atrial Natriuretic Factor