Wednesday, January 29, 2014

Pregnancy increases baroreflex-independent GABAergic inhibition of the RVLM in rats

Lyudmyla Kvochina, Eileen M. Hasser, and Cheryl M. Heesch Department of Biomedical Sciences and Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri Am J Physiol Regul Integr Comp Physiol 293: R2295–R2305, 2007. First published September 26, 2007; doi:10.1152/ajpregu.00365.2007. During pregnancy there is an increase in blood volume, cardiac output, mild tachycardia along with decreased arterial blood pressure. This study wanted to test if arterial baroreflex-independent GABAergic inhibition is enhanced in near-term pregnancy compared to non-pregnancy. Also because there is an interaction between Ang II and GABA and there is an upregulation of the renin-angiotensin system, they wanted to know if activation of AT1 receptors in RVLM might be different between pregnant and non-pregnant rats. In sinoaortic denervated pregnant rat Ang II was injected before blockade of AT1 receptors. In response to Ang II there was an increase in MAP and renal sympathetic nerve activity. However after blockade of AT1 receptors the response to ANG II was blocked. They also compared PE responses between non pregnant and pregnant rats before and after SAD. They found that before the SAD the change in MAP was greater in the non-pregnant compared to the pregnant. As for RSNA it was similar and HR responses in pregnant were greater than non-pregnant. After SAD the MAP was greater than pre-SAD baseline but in the pregnant animals the MAP pressure went below Pre-SAD level after 90 minutes. In response to Bicuculline, pressor and sympathoexcitation were observed however the responses in pregnant were greater. Bicuculline after AT1 blockade responses lead to attenuated responses compared to just bicuculline alone. These data suggest that baroreflex independent GABAergic inhibition might be responsible for the blunted sympathoexcitation during pregnancy and that AT1 receptors may be playing a greater role in GABAergic inhibition-MD

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