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The Hypertension and Vascular Disease Center (L.A.A.N., A.F.W., D.B.A., C.M.F., K.B.B.), and Public Health Sciences (M.P.W.), Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157-1932
Address all correspondence and requests for reprints to: K. Bridget Brosnihan, Ph.D., The Hypertension and Vascular Disease Center, Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, North Carolina 27157-1032. E-mail: bbrosnih{at}wfubmc.edu.
The vasoactive effect of angiotensin (Ang)-(17) in mesenteric resistance arteries together with its plasma and kidney concentration and urinary excretion was assessed in pregnant and virgin rats. Mesenteric arteries (230290 µm) were mounted in a pressurized myograph system and Ang-(17) concentration-dependent response curves (10-1010-5 M) were determined in arteries preconstricted with endothelin-1 (10-7 M). The Ang-(17) response was investigated in vessels with and without pretreatment with the Ang-(17) antagonist [D-[Ala7]-Ang-(17)] (10-7 M). Ang-(17) caused a significantly enhanced, concentration-dependent dilation of mesenteric vessels (EC50 = 2.7 nM) from pregnant compared with virgin female rats. D-[Ala7]-Ang-(17) eliminated the vasodilator effect of Ang-(17). There was no significant change in plasma concentration of Ang-(17) in pregnant animals. On the other hand, 24 h urinary excretion and kidney concentration of Ang-(17) were significantly higher in pregnant animals. The increased mesenteric dilation to Ang-(17) with enhanced kidney concentration and 24 h urinary excretion rate of Ang-(17) suggests an important role for this peptide in cardiovascular regulation during pregnancy.
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