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Journal of Pharmacology And Experimental Therapeutics Fast Forward
First published on October 18, 2007; DOI: 10.1124/jpet.107.132175

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Received for publication September 27, 2007.
Revised October 17, 2007.
Accepted for publication October 17, 2007.

Prenatal Nicotine Exposure Increases Heart Susceptibility to Ischemia/Reperfusion Injury in Adult Offspring

Jennifer Lawrence 1, DaLiao Xiao 1, Qin Xue 1, Maryam Rejali 2, Shumei Yang 2, Lubo Zhang 3*

1 Loma Linda University 2 California State University San Bernardino 3 Loma Linda University

* Address correspondence to: E-mail: lzhang{at}llu.edu

Abstract

The present study tested the hypothesis that prenatal nicotine exposure increases heart susceptibility to ischemia/reperfusion (I/R) injury in adult offspring. Nicotine was administered to pregnant rats via subcutaneous osmotic minipumps throughout gestation. Nicotine treatment resulted in a rapid and transient decrease in food-intake and a moderate decrease in maternal body weight gain. Hearts were isolated from adult male and female offspring and subjected to I/R in a Langendorff preparation. Nicotine significantly attenuated left ventricle (LV) developed pressure, heart rate, and coronary flow rate in female but not male hearts at baseline. Additionally, nicotine significantly increased LV infarct size and attenuated postischemic recovery of LV function in both male and female offspring with more pronounced effects in females. In female but not male hearts, nicotine significantly decreased postischemic coronary flow rate. However, coronary nitric oxide release was decreased in male but not female hearts. Caspase-3, -8, and -9 levels were not significantly changed in either female or male hearts. However, nicotine caused a significant decrease in protein levels of PKC{epsilon} in both male and female hearts and a decrease in PKC{delta} levels in female hearts only. Control studies of maternal food restriction showed that a moderate decrease in maternal body weight gain had no effect on female hearts, but significantly improved postischemic recovery of LV function in male hearts. The results suggest that prenatal nicotine exposure causes in utero programming of PKC isozyme gene expression pattern in the developing heart and increases heart susceptibility to I/R injury in adult offspring.


Key words: caspase, cigarette smoking, fetal programming, maternal food restriction, protein kinase C, rat


This article has been cited by other articles:


Home page
 HypertensionHome page
D. Xiao, Z. Xu, X. Huang, L. D. Longo, S. Yang, and L. Zhang
Prenatal Gender-Related Nicotine Exposure Increases Blood Pressure Response to Angiotensin II in Adult Offspring
Hypertension, April 1, 2008; 51(4): 1239 - 1247.
[Abstract] [Full Text] [PDF]


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