Vasoconstrictor-induced secretion of ANP in fetal sheep

C. R. Rosenfeld, W. K. Samson, T. A. Roy, D. J. Faucher, R. R. Magness

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Fetal secretion of atrial natriuretic peptide (ANP) increases during volume expansion and hypoxia. It is unknown whether this is associated with alterations in right atrial pressure (RAP) or distension and whether increases in ANP secretion reflect effects of specific vasopressors. To address this we studied fetal sheep (n = 13) at 125-140 days gestation, infusing either angiotensin II (ANG II; 0.023-5.73 μg/min) or the α-agonist phenylephrine (Phen; 0.031-7.64 μg/min) while monitoring mean arterial pressure (MAP), RAP, heart rate, and amniotic sac pressure. Arterial blood was obtained before and at 5 min of infusion to measure ANP, blood gases, and pH; umbilical venous blood was collected to determine placental clearance of ANP. ANG II caused dose-dependent increases in MAP and plasma ANP (P < 0.05), whereas Phen caused dose-dependent increases in MAP, but ANP rose only with the highest dose (40 ± 12%). ΔMAP and ΔRAP were highly correlated for Phen (r = 0.74, P = 0.002) and ANG II (r = 0.90, P < 0.001), but for both agents the increase in ΔRAP was proportionately greater than ΔMAP, and increases in plasma ANP were greater per millimeter mercury rise in RAP than that observed with MAP. Increases in ANP were associated with a dose-dependent rise in hematocrit, suggesting decreases in intravascular volume. There was no fetal placental clearance of ANP. As in adults, ANG II- and α-agonist- induced fetal ANP secretion appears to primarily reflect increases in RAP and thus right atrial distension.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Endocrinology and Metabolism
Volume263
Issue number3 26-3
StatePublished - 1992

Fingerprint

Atrial Natriuretic Factor
Vasoconstrictor Agents
Sheep
Atrial Pressure
Arterial Pressure
Blood
Umbilicus
Phenylephrine
Plasmas
Mercury
Hematocrit
Angiotensin II
Heart Rate
Gases
Pressure
Pregnancy

Keywords

  • α-agonist
  • angiotensin II
  • atrial natriuretic peptide
  • phenylephrine
  • placental clearance
  • right atrial pressure

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology
  • Physiology

Cite this

Vasoconstrictor-induced secretion of ANP in fetal sheep. / Rosenfeld, C. R.; Samson, W. K.; Roy, T. A.; Faucher, D. J.; Magness, R. R.

In: American Journal of Physiology - Endocrinology and Metabolism, Vol. 263, No. 3 26-3, 1992.

Research output: Contribution to journalArticle

Rosenfeld, C. R. ; Samson, W. K. ; Roy, T. A. ; Faucher, D. J. ; Magness, R. R. / Vasoconstrictor-induced secretion of ANP in fetal sheep. In: American Journal of Physiology - Endocrinology and Metabolism. 1992 ; Vol. 263, No. 3 26-3.
@article{82d7aa82637b4e37b17ca12365699418,
title = "Vasoconstrictor-induced secretion of ANP in fetal sheep",
abstract = "Fetal secretion of atrial natriuretic peptide (ANP) increases during volume expansion and hypoxia. It is unknown whether this is associated with alterations in right atrial pressure (RAP) or distension and whether increases in ANP secretion reflect effects of specific vasopressors. To address this we studied fetal sheep (n = 13) at 125-140 days gestation, infusing either angiotensin II (ANG II; 0.023-5.73 μg/min) or the α-agonist phenylephrine (Phen; 0.031-7.64 μg/min) while monitoring mean arterial pressure (MAP), RAP, heart rate, and amniotic sac pressure. Arterial blood was obtained before and at 5 min of infusion to measure ANP, blood gases, and pH; umbilical venous blood was collected to determine placental clearance of ANP. ANG II caused dose-dependent increases in MAP and plasma ANP (P < 0.05), whereas Phen caused dose-dependent increases in MAP, but ANP rose only with the highest dose (40 ± 12{\%}). ΔMAP and ΔRAP were highly correlated for Phen (r = 0.74, P = 0.002) and ANG II (r = 0.90, P < 0.001), but for both agents the increase in ΔRAP was proportionately greater than ΔMAP, and increases in plasma ANP were greater per millimeter mercury rise in RAP than that observed with MAP. Increases in ANP were associated with a dose-dependent rise in hematocrit, suggesting decreases in intravascular volume. There was no fetal placental clearance of ANP. As in adults, ANG II- and α-agonist- induced fetal ANP secretion appears to primarily reflect increases in RAP and thus right atrial distension.",
keywords = "α-agonist, angiotensin II, atrial natriuretic peptide, phenylephrine, placental clearance, right atrial pressure",
author = "Rosenfeld, {C. R.} and Samson, {W. K.} and Roy, {T. A.} and Faucher, {D. J.} and Magness, {R. R.}",
year = "1992",
language = "English (US)",
volume = "263",
journal = "American Journal of Physiology - Heart and Circulatory Physiology",
issn = "0363-6135",
publisher = "American Physiological Society",
number = "3 26-3",

}

TY - JOUR

T1 - Vasoconstrictor-induced secretion of ANP in fetal sheep

AU - Rosenfeld, C. R.

AU - Samson, W. K.

AU - Roy, T. A.

AU - Faucher, D. J.

AU - Magness, R. R.

PY - 1992

Y1 - 1992

N2 - Fetal secretion of atrial natriuretic peptide (ANP) increases during volume expansion and hypoxia. It is unknown whether this is associated with alterations in right atrial pressure (RAP) or distension and whether increases in ANP secretion reflect effects of specific vasopressors. To address this we studied fetal sheep (n = 13) at 125-140 days gestation, infusing either angiotensin II (ANG II; 0.023-5.73 μg/min) or the α-agonist phenylephrine (Phen; 0.031-7.64 μg/min) while monitoring mean arterial pressure (MAP), RAP, heart rate, and amniotic sac pressure. Arterial blood was obtained before and at 5 min of infusion to measure ANP, blood gases, and pH; umbilical venous blood was collected to determine placental clearance of ANP. ANG II caused dose-dependent increases in MAP and plasma ANP (P < 0.05), whereas Phen caused dose-dependent increases in MAP, but ANP rose only with the highest dose (40 ± 12%). ΔMAP and ΔRAP were highly correlated for Phen (r = 0.74, P = 0.002) and ANG II (r = 0.90, P < 0.001), but for both agents the increase in ΔRAP was proportionately greater than ΔMAP, and increases in plasma ANP were greater per millimeter mercury rise in RAP than that observed with MAP. Increases in ANP were associated with a dose-dependent rise in hematocrit, suggesting decreases in intravascular volume. There was no fetal placental clearance of ANP. As in adults, ANG II- and α-agonist- induced fetal ANP secretion appears to primarily reflect increases in RAP and thus right atrial distension.

AB - Fetal secretion of atrial natriuretic peptide (ANP) increases during volume expansion and hypoxia. It is unknown whether this is associated with alterations in right atrial pressure (RAP) or distension and whether increases in ANP secretion reflect effects of specific vasopressors. To address this we studied fetal sheep (n = 13) at 125-140 days gestation, infusing either angiotensin II (ANG II; 0.023-5.73 μg/min) or the α-agonist phenylephrine (Phen; 0.031-7.64 μg/min) while monitoring mean arterial pressure (MAP), RAP, heart rate, and amniotic sac pressure. Arterial blood was obtained before and at 5 min of infusion to measure ANP, blood gases, and pH; umbilical venous blood was collected to determine placental clearance of ANP. ANG II caused dose-dependent increases in MAP and plasma ANP (P < 0.05), whereas Phen caused dose-dependent increases in MAP, but ANP rose only with the highest dose (40 ± 12%). ΔMAP and ΔRAP were highly correlated for Phen (r = 0.74, P = 0.002) and ANG II (r = 0.90, P < 0.001), but for both agents the increase in ΔRAP was proportionately greater than ΔMAP, and increases in plasma ANP were greater per millimeter mercury rise in RAP than that observed with MAP. Increases in ANP were associated with a dose-dependent rise in hematocrit, suggesting decreases in intravascular volume. There was no fetal placental clearance of ANP. As in adults, ANG II- and α-agonist- induced fetal ANP secretion appears to primarily reflect increases in RAP and thus right atrial distension.

KW - α-agonist

KW - angiotensin II

KW - atrial natriuretic peptide

KW - phenylephrine

KW - placental clearance

KW - right atrial pressure

UR - http://www.scopus.com/inward/record.url?scp=0026767474&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0026767474&partnerID=8YFLogxK

M3 - Article

VL - 263

JO - American Journal of Physiology - Heart and Circulatory Physiology

JF - American Journal of Physiology - Heart and Circulatory Physiology

SN - 0363-6135

IS - 3 26-3

ER -