TY - JOUR
T1 - Does nitric oxide contribute to the basal vasodilation of pregnancy in conscious rabbits?
AU - Brooks, V. L.
AU - Clow, K. A.
AU - Welch, L. S.
AU - Giraud, G. D.
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
UR - http://www.scopus.com/inward/record.url?scp=0035199023&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0035199023&partnerID=8YFLogxK
U2 - 10.1152/ajpregu.2001.281.5.r1624
DO - 10.1152/ajpregu.2001.281.5.r1624
M3 - Article
C2 - 11641135
AN - SCOPUS:0035199023
SN - 0363-6119
VL - 281
SP - R1624-R1632
JO - American Journal of Physiology - Regulatory Integrative and Comparative Physiology
JF - American Journal of Physiology - Regulatory Integrative and Comparative Physiology
IS - 5 50-5
ER -