Vascular compliance and mean circulatory filling pressure in trout: Effects of ACE inhibition

Y. Zhang, E. Jenkinson, Kenneth Olson

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

Mean circulatory filling pressure (MCFP), whole body vascular compliance (C), and unstressed blood volume (USV) are important indexes of cardiovascular function in mammals, but they have not been measured in fish. In the present experiments, dorsal aortic (P(DA)) and sinus venosus (P(SV)) pressures were measured in unanesthetized trout before and during electrical cardiac fibrillation, while blood volume (BV) was manipulated between 50 and 150% of normal. Measurements were repeated after angiotensin-converting enzyme (ACE) inhibition with lisinopril. Cardiac fibrillation (zero-flow condition) rapidly (~5 s) dropped P(DA) and increased P(SV) (equals MCFP). MCFP in normovolemic trout (4.8 ± 0.3 mmHg) varied directly with BV. C determined from in vivo capacitance curves was similar to that obtained gravimetrically, in vitro (3.4 and 3.5 ml · mmHg-1 · kg body wt-1, respectively). USV was 13.3 ml/kg body wt (~45% of BV). ACE inhibition reduced P(DA) in unfibrillated trout at all BV and reduced P(DA) in fibrillated fish at BV ≥ 80%. ACE inhibition did not affect P(SV), MCFP, C, or USV. The systemic arteriovenous pressure gradient at zero flow (ΔPF0) was greatest at 100% BV (8.2 ± 0.5 mmHg) and was reduced by ACE inhibition at 80-120% BV. These results show that key indexes of venous function are readily measured in fish and that the trout venous system is not an effector of angiotensin-mediated regulation of arterial blood pressure. Thus angiotensin acts solely on arterial resistance vessels. Furthermore, the drop in ΔPF0 during ACE inhibition is due to a decrease in arteriolar resistance.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume268
Issue number5 37-5
StatePublished - 1995
Externally publishedYes

Fingerprint

blood volume
enzyme inhibition
Trout
peptidyl-dipeptidase A
Peptidyl-Dipeptidase A
Blood Volume
blood vessels
compliance
trout
Compliance
Blood Vessels
Pressure
sinuses
angiotensins
Fishes
Angiotensins
fish
Lisinopril
Sinus of Valsalva
capacitance

Keywords

  • blood pressure
  • cardiovascular
  • fish
  • renin angiotensin system
  • vein

ASJC Scopus subject areas

  • Physiology
  • Agricultural and Biological Sciences(all)

Cite this

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title = "Vascular compliance and mean circulatory filling pressure in trout: Effects of ACE inhibition",
abstract = "Mean circulatory filling pressure (MCFP), whole body vascular compliance (C), and unstressed blood volume (USV) are important indexes of cardiovascular function in mammals, but they have not been measured in fish. In the present experiments, dorsal aortic (P(DA)) and sinus venosus (P(SV)) pressures were measured in unanesthetized trout before and during electrical cardiac fibrillation, while blood volume (BV) was manipulated between 50 and 150{\%} of normal. Measurements were repeated after angiotensin-converting enzyme (ACE) inhibition with lisinopril. Cardiac fibrillation (zero-flow condition) rapidly (~5 s) dropped P(DA) and increased P(SV) (equals MCFP). MCFP in normovolemic trout (4.8 ± 0.3 mmHg) varied directly with BV. C determined from in vivo capacitance curves was similar to that obtained gravimetrically, in vitro (3.4 and 3.5 ml · mmHg-1 · kg body wt-1, respectively). USV was 13.3 ml/kg body wt (~45{\%} of BV). ACE inhibition reduced P(DA) in unfibrillated trout at all BV and reduced P(DA) in fibrillated fish at BV ≥ 80{\%}. ACE inhibition did not affect P(SV), MCFP, C, or USV. The systemic arteriovenous pressure gradient at zero flow (ΔPF0) was greatest at 100{\%} BV (8.2 ± 0.5 mmHg) and was reduced by ACE inhibition at 80-120{\%} BV. These results show that key indexes of venous function are readily measured in fish and that the trout venous system is not an effector of angiotensin-mediated regulation of arterial blood pressure. Thus angiotensin acts solely on arterial resistance vessels. Furthermore, the drop in ΔPF0 during ACE inhibition is due to a decrease in arteriolar resistance.",
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T2 - Effects of ACE inhibition

AU - Zhang, Y.

AU - Jenkinson, E.

AU - Olson, Kenneth

PY - 1995

Y1 - 1995

N2 - Mean circulatory filling pressure (MCFP), whole body vascular compliance (C), and unstressed blood volume (USV) are important indexes of cardiovascular function in mammals, but they have not been measured in fish. In the present experiments, dorsal aortic (P(DA)) and sinus venosus (P(SV)) pressures were measured in unanesthetized trout before and during electrical cardiac fibrillation, while blood volume (BV) was manipulated between 50 and 150% of normal. Measurements were repeated after angiotensin-converting enzyme (ACE) inhibition with lisinopril. Cardiac fibrillation (zero-flow condition) rapidly (~5 s) dropped P(DA) and increased P(SV) (equals MCFP). MCFP in normovolemic trout (4.8 ± 0.3 mmHg) varied directly with BV. C determined from in vivo capacitance curves was similar to that obtained gravimetrically, in vitro (3.4 and 3.5 ml · mmHg-1 · kg body wt-1, respectively). USV was 13.3 ml/kg body wt (~45% of BV). ACE inhibition reduced P(DA) in unfibrillated trout at all BV and reduced P(DA) in fibrillated fish at BV ≥ 80%. ACE inhibition did not affect P(SV), MCFP, C, or USV. The systemic arteriovenous pressure gradient at zero flow (ΔPF0) was greatest at 100% BV (8.2 ± 0.5 mmHg) and was reduced by ACE inhibition at 80-120% BV. These results show that key indexes of venous function are readily measured in fish and that the trout venous system is not an effector of angiotensin-mediated regulation of arterial blood pressure. Thus angiotensin acts solely on arterial resistance vessels. Furthermore, the drop in ΔPF0 during ACE inhibition is due to a decrease in arteriolar resistance.

AB - Mean circulatory filling pressure (MCFP), whole body vascular compliance (C), and unstressed blood volume (USV) are important indexes of cardiovascular function in mammals, but they have not been measured in fish. In the present experiments, dorsal aortic (P(DA)) and sinus venosus (P(SV)) pressures were measured in unanesthetized trout before and during electrical cardiac fibrillation, while blood volume (BV) was manipulated between 50 and 150% of normal. Measurements were repeated after angiotensin-converting enzyme (ACE) inhibition with lisinopril. Cardiac fibrillation (zero-flow condition) rapidly (~5 s) dropped P(DA) and increased P(SV) (equals MCFP). MCFP in normovolemic trout (4.8 ± 0.3 mmHg) varied directly with BV. C determined from in vivo capacitance curves was similar to that obtained gravimetrically, in vitro (3.4 and 3.5 ml · mmHg-1 · kg body wt-1, respectively). USV was 13.3 ml/kg body wt (~45% of BV). ACE inhibition reduced P(DA) in unfibrillated trout at all BV and reduced P(DA) in fibrillated fish at BV ≥ 80%. ACE inhibition did not affect P(SV), MCFP, C, or USV. The systemic arteriovenous pressure gradient at zero flow (ΔPF0) was greatest at 100% BV (8.2 ± 0.5 mmHg) and was reduced by ACE inhibition at 80-120% BV. These results show that key indexes of venous function are readily measured in fish and that the trout venous system is not an effector of angiotensin-mediated regulation of arterial blood pressure. Thus angiotensin acts solely on arterial resistance vessels. Furthermore, the drop in ΔPF0 during ACE inhibition is due to a decrease in arteriolar resistance.

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