HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 287/1/H126    most recent 00046.2003v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (4) Citing Articles via Google Scholar Google Scholar Articles by Cox, B. E. Articles by Rosenfeld, C. R. Search for Related Content PubMed PubMed Citation Articles by Cox, B. E. Articles by Rosenfeld, C. R.

Angiotensin II mediates uterine vasoconstriction through -stimulation

Department of Pediatrics, The University of Texas Southwestern Medical Center at Dallas, Dallas, Texas 75390

Submitted 17 January 2003 ; accepted in final form 17 February 2004

Intravenous angiotensin II (ANG II) increases uterine vascular resistance (UVR), whereas uterine intra-arterial infusions do not. Type 2 ANG II (AT₂) receptors predominate in uterine vascular smooth muscle; this may reflect involvement of systemic type 1 ANG II (AT₁) receptor-mediated -adrenergic activation. To examine this, we compared systemic pressor and UVR responses to intravenous phenylephrine and ANG II without and with systemic or uterine -receptor blockade and in the absence or presence of AT₁ receptor blockade in pregnant and nonpregnant ewes. Systemic -receptor blockade inhibited phenylephrine-mediated increases in mean arterial pressure (MAP) and UVR, whereas uterine -receptor blockade alone did not alter pressor responses and resulted in proportionate increases in UVR and MAP. Although neither systemic nor uterine -receptor blockade affected ANG II-mediated pressor responses, UVR responses decreased >65% and also were proportionate to increases in MAP. Systemic AT₁ receptor blockade inhibited all responses to intravenous ANG II. In contrast, uterine AT₁ receptor blockade + systemic -receptor blockade resulted in persistent proportionate increases in MAP and UVR. Uterine AT₂ receptor 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 receptor-mediated release of an -agonist and uterine autoregulatory responses.

angiotensin receptors; autoregulation; pregnancy; uterine blood flow; blood pressure

This article has been cited by other articles:

				C. R. Rosenfeld, X.-t. Liu, and K. DeSpain Pregnancy modifies the large conductance Ca2+-activated K+ channel and cGMP-dependent signaling pathway in uterine vascular smooth muscle Am J Physiol Heart Circ Physiol, June 1, 2009; 296(6): H1878 - H1887. [Abstract] [Full Text] [PDF]

				C. R. Rosenfeld, R. A. Word, K. DeSpain, and X.-t. Liu Large Conductance Ca2+--Activated K+ Channels Contribute to Vascular Function in Nonpregnant Human Uterine Arteries Reproductive Sciences, September 1, 2008; 15(7): 651 - 660. [Abstract] [PDF]

				H. Zhang and L. Zhang Role of Protein Kinase C Isozymes in the Regulation of alpha1-Adrenergic Receptor-Mediated Contractions in Ovine Uterine Arteries Biol Reprod, January 1, 2008; 78(1): 35 - 42. [Abstract] [Full Text] [PDF]

				H. Zhang, D. Xiao, L. D. Longo, and L. Zhang Regulation of {alpha}1-adrenoceptor-mediated contractions of uterine arteries by PKC: effect of pregnancy Am J Physiol Heart Circ Physiol, November 1, 2006; 291(5): H2282 - H2289. [Abstract] [Full Text] [PDF]

				C. R. Rosenfeld, T. Roy, K. DeSpain, and B. E. Cox Large-Conductance Ca2+-Dependent K+ Channels Regulate Basal Uteroplacental Blood Flow in Ovine Pregnancy Reproductive Sciences, September 1, 2005; 12(6): 402 - 408. [Abstract] [PDF]