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Renal vascular responses in an experimental model of preeclampsia
Rosa Amalia Bobadilla Lugo1, Víctor M Pérez-Alvarez, Liliana Anguiano Robledo
1Departamento de Fisiología y Farmacología, Escuela Superior de Medicina del IPN, Plan de San Luis y Diáz Mirón, Casco de Santo Tomás, México 11340 D.F. rabobadilla@terra.com.mx
In pregnancy there is an attenuated response to vasoconstrictors and pressor agents, including Angiotensin II (Ang II). This effect is reverted in preeclampsia. We evaluated the renal pressor response induced by Ang II in an experimental model of preeclampsia based on the development of feto-placental ischemia produced by a subrenal aortic coarctation (SRAC). Dose-response curves for Ang II were obtained in an isolated perfused kidney preparation comparing groups of SRAC pregnant and non-pregnant rats in the presence and absence of losartan (AT1 antagonist) or PD123319 (AT2 antagonist). Kidneys from the experimental model of pre-eclampsia showed an enhanced response to AngII. In addition, losartan (10 nM) inhibited the vasopressor effect to Ang II in this model but not in the control group. PD 123319 (1 nM), increased the response in both groups, but the effect was more evident in the pre-eclamptic group. This suggests modifications in the relative participation of renal vascular receptors AT1/AT2 induced by an experimental model of pre-eclampsia, with an increased participation of AT1 and a decreased participation of AT2.
In pregnancy there is an attenuated response to vasoconstrictors and pressor agents, including Angiotensin II (Ang II). This effect is reverted in preeclampsia. We evaluated the renal pressor response induced by Ang II in an experimental model of preeclampsia based on the development of feto-placental ischemia produced by a subrenal aortic coarctation (SRAC). Dose-response curves for Ang II were obtained in an isolated perfused kidney preparation comparing groups of SRAC pregnant and non-pregnant rats in the presence and absence of losartan (AT1 antagonist) or PD123319 (AT2 antagonist). Kidneys from the experimental model of pre-eclampsia showed an enhanced response to AngII. In addition, losartan (10 nM) inhibited the vasopressor effect to Ang II in this model but not in the control group. PD 123319 (1 nM), increased the response in both groups, but the effect was more evident in the pre-eclamptic group. This suggests modifications in the relative participation of renal vascular receptors AT1/AT2 induced by an experimental model of pre-eclampsia, with an increased participation of AT1 and a decreased participation of AT2.
