Does nitric oxide contribute to the basal vasodilation of pregnancy in conscious rabbits?

Virginia Brooks, K. A. Clow, L. S. Welch, George Giraud

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11 Citations (Scopus)

Abstract

Pregnancy produces marked systemic vasodilation, but the mechanism is unknown. Experiments were performed in conscious rabbits to test the hypotheses that increased nitric oxide (NO) production contributes to the increased vascular conductance, but that the contribution varies among vascular beds. Rabbits were instrumented with aortic and vena caval catheters and ultrasonic flow probes implanted around the ascending aorta, superior mesenteric artery, terminal aorta, and/or a femoral artery. Hemodynamic responses to intravenous injection of Nω-nitro-L-arginine (L-NA; 20 mg/kg or increasing doses of 2, 5, 10, 15, and 20 mg/kg) were determined in rabbits first before pregnancy (NP) and then at the end of gestation (P). L-NA produced similar increases in arterial pressure between groups, but the following responses were larger (P <0.05) when the rabbits were pregnant: 1) decreases in total peripheral conductance [-3.7 ± 0.3 (NP), -5.0 ± 0.5 (P) ml·min-1·mmHg-1], 2) decreases in mesenteric conductance [-0.47 ± 0.05 (NP), -0.63 ± 0.07 (P) ml·min-1·mmHg-1], 3) decreases in terminal aortic conductance [-0.43 ± 0.05 (NP), -0.95 ± 0,19 ml·min-1·mmHg-1 (P)], and 4) decreases in heart rate [-41 ± 4 (NP), -62 ± 5 beats/min (P)]. Nevertheless, total peripheral and terminal aortic conductances remained elevated in the pregnant rabbits (P <0.05) after L-NA. Furthermore, decreases in cardiac output and femoral conductance were not different between the reproductive states. We conclude that the contribution of NO to vascular tone increases during pregnancy, but only in some vascular beds. Moreover, the data support a role for NO in the pregnancy-induced increase in basal heart rate. Finally, unknown factors in addition to NO must also underlie the basal vasodilation observed during pregnancy.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume281
Issue number5 50-5
StatePublished - 2001

Fingerprint

Vasodilation
Nitric Oxide
Rabbits
Pregnancy
Blood Vessels
Aorta
Heart Rate
Venae Cavae
Superior Mesenteric Artery
Femoral Artery
Thigh
Ultrasonics
Intravenous Injections
Cardiac Output
Arginine
Arterial Pressure
Catheters
Hemodynamics

Keywords

  • Arterial pressure
  • Cardiac output
  • Conductance
  • Femoral flow
  • Heart rate
  • Mesenteric flow
  • Terminal aortic flow
  • Total peripheral resistance

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

@article{639e3a5d17b54fa1b2200bf083b85618,
title = "Does nitric oxide contribute to the basal vasodilation of pregnancy in conscious rabbits?",
abstract = "Pregnancy produces marked systemic vasodilation, but the mechanism is unknown. Experiments were performed in conscious rabbits to test the hypotheses that increased nitric oxide (NO) production contributes to the increased vascular conductance, but that the contribution varies among vascular beds. Rabbits were instrumented with aortic and vena caval catheters and ultrasonic flow probes implanted around the ascending aorta, superior mesenteric artery, terminal aorta, and/or a femoral artery. Hemodynamic responses to intravenous injection of Nω-nitro-L-arginine (L-NA; 20 mg/kg or increasing doses of 2, 5, 10, 15, and 20 mg/kg) were determined in rabbits first before pregnancy (NP) and then at the end of gestation (P). L-NA produced similar increases in arterial pressure between groups, but the following responses were larger (P <0.05) when the rabbits were pregnant: 1) decreases in total peripheral conductance [-3.7 ± 0.3 (NP), -5.0 ± 0.5 (P) ml·min-1·mmHg-1], 2) decreases in mesenteric conductance [-0.47 ± 0.05 (NP), -0.63 ± 0.07 (P) ml·min-1·mmHg-1], 3) decreases in terminal aortic conductance [-0.43 ± 0.05 (NP), -0.95 ± 0,19 ml·min-1·mmHg-1 (P)], and 4) decreases in heart rate [-41 ± 4 (NP), -62 ± 5 beats/min (P)]. Nevertheless, total peripheral and terminal aortic conductances remained elevated in the pregnant rabbits (P <0.05) after L-NA. Furthermore, decreases in cardiac output and femoral conductance were not different between the reproductive states. We conclude that the contribution of NO to vascular tone increases during pregnancy, but only in some vascular beds. Moreover, the data support a role for NO in the pregnancy-induced increase in basal heart rate. Finally, unknown factors in addition to NO must also underlie the basal vasodilation observed during pregnancy.",
keywords = "Arterial pressure, Cardiac output, Conductance, Femoral flow, Heart rate, Mesenteric flow, Terminal aortic flow, Total peripheral resistance",
author = "Virginia Brooks and Clow, {K. A.} and Welch, {L. S.} and George Giraud",
year = "2001",
language = "English (US)",
volume = "281",
journal = "American Journal of Physiology - Renal Fluid and Electrolyte Physiology",
issn = "1931-857X",
publisher = "American Physiological Society",
number = "5 50-5",

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T1 - Does nitric oxide contribute to the basal vasodilation of pregnancy in conscious rabbits?

AU - Brooks, Virginia

AU - Clow, K. A.

AU - Welch, L. S.

AU - Giraud, George

PY - 2001

Y1 - 2001

N2 - Pregnancy produces marked systemic vasodilation, but the mechanism is unknown. Experiments were performed in conscious rabbits to test the hypotheses that increased nitric oxide (NO) production contributes to the increased vascular conductance, but that the contribution varies among vascular beds. Rabbits were instrumented with aortic and vena caval catheters and ultrasonic flow probes implanted around the ascending aorta, superior mesenteric artery, terminal aorta, and/or a femoral artery. Hemodynamic responses to intravenous injection of Nω-nitro-L-arginine (L-NA; 20 mg/kg or increasing doses of 2, 5, 10, 15, and 20 mg/kg) were determined in rabbits first before pregnancy (NP) and then at the end of gestation (P). L-NA produced similar increases in arterial pressure between groups, but the following responses were larger (P <0.05) when the rabbits were pregnant: 1) decreases in total peripheral conductance [-3.7 ± 0.3 (NP), -5.0 ± 0.5 (P) ml·min-1·mmHg-1], 2) decreases in mesenteric conductance [-0.47 ± 0.05 (NP), -0.63 ± 0.07 (P) ml·min-1·mmHg-1], 3) decreases in terminal aortic conductance [-0.43 ± 0.05 (NP), -0.95 ± 0,19 ml·min-1·mmHg-1 (P)], and 4) decreases in heart rate [-41 ± 4 (NP), -62 ± 5 beats/min (P)]. Nevertheless, total peripheral and terminal aortic conductances remained elevated in the pregnant rabbits (P <0.05) after L-NA. Furthermore, decreases in cardiac output and femoral conductance were not different between the reproductive states. We conclude that the contribution of NO to vascular tone increases during pregnancy, but only in some vascular beds. Moreover, the data support a role for NO in the pregnancy-induced increase in basal heart rate. Finally, unknown factors in addition to NO must also underlie the basal vasodilation observed during pregnancy.

AB - Pregnancy produces marked systemic vasodilation, but the mechanism is unknown. Experiments were performed in conscious rabbits to test the hypotheses that increased nitric oxide (NO) production contributes to the increased vascular conductance, but that the contribution varies among vascular beds. Rabbits were instrumented with aortic and vena caval catheters and ultrasonic flow probes implanted around the ascending aorta, superior mesenteric artery, terminal aorta, and/or a femoral artery. Hemodynamic responses to intravenous injection of Nω-nitro-L-arginine (L-NA; 20 mg/kg or increasing doses of 2, 5, 10, 15, and 20 mg/kg) were determined in rabbits first before pregnancy (NP) and then at the end of gestation (P). L-NA produced similar increases in arterial pressure between groups, but the following responses were larger (P <0.05) when the rabbits were pregnant: 1) decreases in total peripheral conductance [-3.7 ± 0.3 (NP), -5.0 ± 0.5 (P) ml·min-1·mmHg-1], 2) decreases in mesenteric conductance [-0.47 ± 0.05 (NP), -0.63 ± 0.07 (P) ml·min-1·mmHg-1], 3) decreases in terminal aortic conductance [-0.43 ± 0.05 (NP), -0.95 ± 0,19 ml·min-1·mmHg-1 (P)], and 4) decreases in heart rate [-41 ± 4 (NP), -62 ± 5 beats/min (P)]. Nevertheless, total peripheral and terminal aortic conductances remained elevated in the pregnant rabbits (P <0.05) after L-NA. Furthermore, decreases in cardiac output and femoral conductance were not different between the reproductive states. We conclude that the contribution of NO to vascular tone increases during pregnancy, but only in some vascular beds. Moreover, the data support a role for NO in the pregnancy-induced increase in basal heart rate. Finally, unknown factors in addition to NO must also underlie the basal vasodilation observed during pregnancy.

KW - Arterial pressure

KW - Cardiac output

KW - Conductance

KW - Femoral flow

KW - Heart rate

KW - Mesenteric flow

KW - Terminal aortic flow

KW - Total peripheral resistance

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