The Davidge laboratory studies cardiovascular physiology with a specific interest in the area of women’s, maternal and perinatal cardiovascular health. We investigate potential mediators for vascular endothelial cell dysfunction in both aging and estrogen deficiency as well as in the pregnancy complication, preeclampsia. Moreover, we combine our expertise in aging and pregnancy complications to study the long term cardiovascular effects for offspring born from an adverse intrauterine environment (also known as developmental origins of disease).
Studies include understanding mechanisms for normal cardiovascular adaptations of pregnancy as well as mechanisms for impaired vascular responses in women with preeclampsia, a pregnancy disorder characterized by hypertension and proteinuria. This work addresses the regulation of vascular tone by factors such as nitric oxide and matrix metalloproteinase. Moreover, we study the effect of oxidative stress on endothelial cell function as a potential mechanism for vascular dysfunction in women with preeclampsia.
Another area of research for this laboratory is studying the impact of aging on the vasculature with a specific interest for the action of sex steroids on vascular function. Moreover, the age at which women deliver their first child has increased steadily. In Canada, births occurring among women aged 35 years and older account for over 18% of total live births. Childbirth at an advanced maternal age (≥35 years) has a myriad of clinical ramifications, including increased risk of preeclampsia and intrauterine growth restriction. Children born from a suboptimal intrauterine environment are at a greater risk of cardiovascular morbidities later in life. Our laboratory is studying the consequences of maternal aging on vascular function with interests in both maternal and offspring health.
Complications in pregnancy may also influence cardiovascular health in the offspring. Numerous epidemiological studies have determined an association between a poor uterine environment (usually reflected by low birth weight) and the occurrence of cardiovascular diseases later in life. It is likely that adaptive responses to fetal/neonatal environmental stresses lead to permanent changes that negatively influence metabolic and cardiovascular health in adult life. However, the mechanisms underlying these changes are not known. Our laboratory assesses mechanisms for altered cardiovascular responses in pregnancies from an adverse maternal environment as well as assessing the offspring from these pregnancies in various life stages (fetal, neonatal, young and aged adults).
The Davidge laboratory is committed to the training of undergraduate and graduate students as well as post-doctoral fellows with an average of 8-10 trainees in the laboratory.
This research is supported by the Canadian Institutes of Health Research, the Heart and Stroke Foundation of Canada, Alberta Innovates – Health Solutions and the Women and Children’s Health Research Institute, through the generous support of the Stollery Children's Hospital Foundation and the Royal Alexandra Hospital Foundation.
• Vascular function studies using myography are conducted on isolated small arteries from our various animal models.
• Analysis of the expression of various enzymes and receptors using Western blot and Immunohistochemistry techniques.
• Cell cultures of endothelial and smooth muscle cells to assess cellular mechanisms.
Selected Refereed Publications (First author is a trainee, last two years, trainees are underlined)
Shah A, Quon A, Morton JS, DAVIDGE ST. Postnatal resveratrol supplementation improves cardiovascular function in male and female intrauterine growth restricted offspring. Physiological Reports, In Press, 2017
Aljunaidy MM, Morton JS, Cooke CL, DAVIDGE ST. Maternal vascular responses to hypoxia in a rat model of intrauterine growth restriction. Am J PhysiolRegul Integr Comp Physiol, 311(6):R1068-R1075, 2016
Brennan L, Morton JS, Quon A, DAVIDGE ST. Postpartum vascular dysfunction in the Reduced Uteroplacental Perfusion model of preeclampsia. PLOS ONE, 11(9):e0162487, 2016
Care AS, Sung M, Panahi S, Gragasin FS, Dyck JRB, DAVIDGE ST, Bourque SL. Perinatal resverartrol supplementation to spontaneously hypertensive rat dams mitigates the development of hypertension in adult offspring. Hypertension, 67(5):1038-44, 2016
Kao CK, Morton JS, Quon AL, Reyes L, Lopez-Jaramillo P, DAVIDGE ST. Mechanisms of vascular dysfunction due to circulating factors in women with preeclampsia. Clinical Science, 130: 539-549, 2016
Shah A, Reyes LM, Morton JS, Fung D, Schneider J, DAVIDGE ST. Effect of resveratrol on metabolic and cardiovascular function in male and female adult offspring exposed to prenatal hypoxia. J Physiol, 594:1465-1482, 2016
Reyes LM, Kirschenman R, Quon A, Morton JS, Shah A, DAVIDGE ST. Aerobic exercise training reduces cardiac function in adult male offspring exposed to prenatal hypoxia. Am J Physiol, Regul Integr Comp Physiol, 309(5):R489-498, 2015
Care AS, Bourque SL, Morton JS, Hjartarson EP, DAVIDGE ST. Effect of advanced maternal age on pregnancy outcomes and vascular function in the rat. Hypertension, 65(6):1324-1330, 2015
Reyes LM, Morton JS, Kirchenman R, DeLorey DS, DAVIDGE ST. Vascular effects of aerobic exercise training in rat adult offspring exposed to hypoxia-induced intrauterine growth restriction. J Physiology, 593(8): 1913–1929, 2015
Refereed Book Chapters / Invited Reviews (Trainees are underlined, last two years)
Morton JS, Care AS, DAVIDGE ST. Mechanisms for uterine artery dysfunction in pregnancy complications, Invited Review for Journal of Cardiovascular Pharmacology, In Press, 2017
Morton JS, Cooke CL, DAVIDGE ST. In Utero Origins of Hypertension: Mechanisms and Targets for Therapy, Invited Review for Physiological Reviews, 96:549-603, 2016
Chakrabarti S, DAVIDGE ST. Analysis of G-protein Coupled Receptor 30 (GPR30) on Endothelial Inflammation. Chapter 39 in Methods in Molecular Biology. 1366:503-16, 2016
Goulopoulou S, DAVIDGE ST. Molecular mechanisms of maternal vascular dysfunction in preeclampsia. Trends in Molecular Medicine, 21:88-97, 2015