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Am J Physiol Heart Circ Physiol (February 19, 2004). doi:10.1152/ajpheart.00046.2003
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Submitted on January 17, 2003
Accepted on February 17, 2004

Angiotensin II Mediates Uterine Vasoconstriction Through {alpha}-Stimulation

Blair E. Cox1*, Timothy A. Roy1, and Charles R. Rosenfeld1

1 Department of Pediatrics, The University of Texas Southwestern Medical Center at Dallas, Dallas, Texas, USA

* To whom correspondence should be addressed. E-mail: Blair.Cox{at}utsouthwestern.edu.

Intravenous angiotensin II (ANG II) increases uterine vascular resistance (UVR), whereas uterine intraarterial infusions do not. Type 2 ANG II receptors (AT2) predominate in uterine vascular smooth muscle; therefore, this may reflect involvement of systemic AT1-mediated {alpha}-adrenergic activation. To examine this, we compared systemic pressor and UVR responses to intravenous phenylephrine and ANG II without and with systemic or uterine {alpha}-receptor blockade and in the absence or presence of AT1 blockade in pregnant and nonpregnant ewes. Systemic {alpha}-blockade inhibited phenylephrinemediated increases in arterial pressure (MAP) and UVR, whereas uterine {alpha}-blockade alone did not alter pressor responses and resulted in proportionate increases in UVR and MAP. Although neither systemic nor uterine {alpha}-blockade affected ANG II-mediated pressor responses, UVR responses decreased >65% and also were proportionate to increases in MAP. Systemic AT1 -blockade inhibited all responses to intravenous ANG II. In contrast, uterine AT1 lockade plus systemic {alpha}-receptor blockade resulted in persistent proportionate increases in MAP and UVR. Uterine AT2 blockade had no effects. We have shown that ANG II-mediated pressor responses reflect activation of systemic vascular AT1 receptors, whereas increases in UVR reflect AT1 -mediated release of an {alpha}-agonist plus uterine autoregulatory responses.




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