AJP - Heart and Circulatory Physiology, Vol 259, Issue 1 197-H203, Copyright © 1990 by American Physiological Society

ARTICLES

Differential responses of uterine and umbilical vasculatures to angiotensin II and norepinephrine

K. E. Clark, G. L. Irion and C. E. Mack
A.E. Seeds Perinatal Research Center, Department of Obstetrics and Gynecology, University of Cincinnati College of Medicine, Ohio 45267-0526.

Although the uterine vascular responses to endogenous vasoactive substances have been extensively investigated in pregnant sheep, the fetal umbilical responses to angiotensin II (ANG II) and norepinephrine (NE) have not been well characterized. Twenty-five pregnant ewes between 105 and 115 days of gestation were anesthetized and instrumented for hemodynamic measurements, systemic fetal and maternal intravenous infusions, and local maternal uterine arterial infusions of ANG II and NE. Fetal and maternal arterial pressure and heart rate, maternal uterine blood flow (total of left and right middle uterine arteries), and fetoplacental blood flow (common umbilical artery) were measured during continuous infusions of ANG II or NE. Fetal infusions of ANG II (0.03-1.0 micrograms.min-1.kg estimated fetal body wt-1) increased fetal arterial blood pressure by as much as 44% over base-line values, decreased umbilical blood flow by as much as 63%, and increased umbilical vascular resistance by up to 345%. Fetal infusions of NE (0.1-3 micrograms.min-1.kg-1) increased fetal arterial pressure 42% and increased umbilical vascular resistance by up to 38% but did not significantly alter fetoplacental blood flow. No significant maternal changes were observed during fetal infusions. Maternal infusion of ANG II increased maternal arterial pressure by as much as 59% and significantly increased uterine vascular resistance at the two highest doses but significantly decreased uterine blood flow only at the highest dose (17%; P less than 0.05). Maternal infusions of NE increased arterial pressure by as much as 113%, decreased uterine blood flow by as much as 76%, and increased uterine vascular resistance 3- to 10-fold over the base-line value.(ABSTRACT TRUNCATED AT 250 WORDS)

This article has been cited by other articles:

				B. E. Cox, T. A. Roy, and C. R. Rosenfeld Angiotensin II mediates uterine vasoconstriction through {alpha}-stimulation Am J Physiol Heart Circ Physiol, July 1, 2004; 287(1): H126 - H134. [Abstract] [Full Text] [PDF]

				Z. Xu, L. Shi, and J. Yao Central angiotensin II-induced pressor responses and neural activity in utero and hypothalamic angiotensin receptors in preterm ovine fetus Am J Physiol Heart Circ Physiol, April 1, 2004; 286(4): H1507 - H1514. [Abstract] [Full Text] [PDF]

				C. R. Rosenfeld Mechanisms regulating angiotensin II responsiveness by the uteroplacental circulation Am J Physiol Regulatory Integrative Comp Physiol, October 1, 2001; 281(4): R1025 - R1040. [Abstract] [Full Text] [PDF]

				B. E. Cox, C. E. Williams, and C. R. Rosenfeld Angiotensin II indirectly vasoconstricts the ovine uterine circulation Am J Physiol Regulatory Integrative Comp Physiol, February 1, 2000; 278(2): R337 - R344. [Abstract] [Full Text] [PDF]

				D. S. Lambers, S. G. Greenberg, and K. E. Clark Functional role of angiotensin II type 1 and 2 receptors in regulation of uterine blood flow in nonpregnant sheep Am J Physiol Heart Circ Physiol, February 1, 2000; 278(2): H353 - H359. [Abstract] [Full Text] [PDF]

				J. R. Kaiser, B. E. Cox, T. A. Roy, and C. R. Rosenfeld Differential development of umbilical and systemic arteries. I. ANG II receptor subtype expression Am J Physiol Regulatory Integrative Comp Physiol, March 1, 1998; 274(3): R797 - R807. [Abstract] [Full Text] [PDF]