Effects of natriuretic peptides and nitroprusside on venous function in trout

Kenneth Olson, Daniel J. Conklin, Anthony P. Farrell, John E. Keen, Yoshio Takei, Leroy Weaver, M. P. Smith, Yutong Zhang

Research output: Contribution to journalArticle

71 Citations (Scopus)

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 vive 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 (P(Ven)), CO, stroke volume (SV), and gill resistance (R(G)), whereas systemic resistance (R(S)) and heart rate (HR) increased. Dorsal aortic pressure (P(DA)) 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 (P(VA)), P(DA), and R(S), increased CO and HR, but did not affect P(Ven), SV, or R(G). 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 R(S). 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.

Original languageEnglish
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume273
Issue number2 42-2
StatePublished - 1997

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Natriuretic Peptides
Trout
Nitroprusside
Atrial Natriuretic Factor
Cardiac Output
Aorta
Compliance
Arterial Pressure
Fishes
Pressure
Stroke Volume
Veins
Vascular Capacitance
Heart Rate
Lisinopril
Pressoreceptors
Hypovolemia
Central Venous Pressure
Peptide Receptors
Venules

Keywords

  • Cardiovascular
  • Fish
  • Mean circulatory filling pressure
  • Unstressed volume
  • Vascular capacitance

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

Effects of natriuretic peptides and nitroprusside on venous function in trout. / Olson, Kenneth; Conklin, Daniel J.; Farrell, Anthony P.; Keen, John E.; Takei, Yoshio; Weaver, Leroy; Smith, M. P.; Zhang, Yutong.

In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology, Vol. 273, No. 2 42-2, 1997.

Research output: Contribution to journalArticle

Olson, K, Conklin, DJ, Farrell, AP, Keen, JE, Takei, Y, Weaver, L, Smith, MP & Zhang, Y 1997, 'Effects of natriuretic peptides and nitroprusside on venous function in trout', American Journal of Physiology - Regulatory Integrative and Comparative Physiology, vol. 273, no. 2 42-2.
Olson, Kenneth ; Conklin, Daniel J. ; Farrell, Anthony P. ; Keen, John E. ; Takei, Yoshio ; Weaver, Leroy ; Smith, M. P. ; Zhang, Yutong. / Effects of natriuretic peptides and nitroprusside on venous function in trout. In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology. 1997 ; Vol. 273, No. 2 42-2.
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AU - Olson, Kenneth

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AU - Takei, Yoshio

AU - Weaver, Leroy

AU - Smith, M. P.

AU - Zhang, Yutong

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N2 - 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 vive 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 (P(Ven)), CO, stroke volume (SV), and gill resistance (R(G)), whereas systemic resistance (R(S)) and heart rate (HR) increased. Dorsal aortic pressure (P(DA)) 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 (P(VA)), P(DA), and R(S), increased CO and HR, but did not affect P(Ven), SV, or R(G). 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 R(S). 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.

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