Abstract
Essential hypertension is a major risk factor for several cardiovascular diseases, the etiology of which is not yet completely understood. The problem is that blood pressure (BP) is a typical quantitative trait with multifactorial determination. The interactions of multiple genetic and environmental factors as well as gene–gene interactions cause modifications of various systems that adjust blood pressure to actual living conditions. Numerous environmental factors surrounding the organism could modify its development not only by the influence on the expression of genetic information but mainly by epigenetic mechanisms. However, despite considerable research effort, it is still difficult to identify all genes and/or other genetic determinants leading to essential hypertension and other cardiovascular diseases. This is mainly because these diseases usually become a medical problem in adulthood, although their roots might be traced back to earlier stages of ontogeny. The link between distinct developmental periods (e.g., birth and adulthood) should involve the changes in gene expression involving epigenetic phenomena. The purpose of the present paper is to bring some light on gene–environmental interactions potentially implicated in the pathogenesis of hypertension, with special attention to epigenetic inheritance.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
References
Reid CM, Thrift AG. Hypertension 2020: confronting tomorrow’s problem today. Clin Exp Pharmacol Physiol. 2005;32:374–6.
Nugent R. Chronic diseases in developing countries: health and economic burdens. Ann NY Acad Sci. 2008;1136:70–9.
Taylor JY, Maddox R, Wu CY. Genetic and environmental risks for high blood pressure among African American mothers and daughters. Biol Res Nurs. 2009;11:53–65.
Kuneš J, Zicha J. Developmental windows and environment as important factors in the expression of genetic information: a cardiovascular physiologist‘s view. Clin Sci Lond. 2006;111:295–305.
Kuneš J, Zicha J. The interaction of genetic and environmental factors in the etiology of hypertension. Physiol Res. 2009;58(Suppl 2):S33–41.
Gibson G. Epistasis and pleiotropy as natural properties of transcriptional regulation. Theor Popul Biol. 1196;49:58–89.
Greenland S, Rothman KJ. Concepts of interaction. In: Rothman KJ, Greenland S, editors. Modern epidemiology. Philadelphia, PA: Lippincott-Raven; 1998. p. 329–42.
Zicha J, Kuneš J. Ontogenetic aspects of hypertension development: analysis in the rat. Physiol Rev. 1999;79:1227–82.
Weder AB, Schork NJ. Adaptation, allometry, and hypertension. Hypertension. 1994;24:145–56.
Wilson TW, Grim CE. Biohistory of slavery and blood pressure differences in blacks today. A hypothesis. Hypertension. 1991;17(1 Suppl):I122–8.
Neel JV, Weder AB, Julius S. Type II diabetes, essential hypertension, and obesity as “syndromes of impaired genetic homeostasis”: the “thrifty genotype” hypothesis enters the 21st century. Perspect Biol Med. 1998;42:44–74.
Rapp JP. Genetic analysis of inherited hypertension in the rat. Physiol Rev. 2000;8:135–72.
Cicila GT. Strategy for uncovering complex determinants of hypertension using animal models. Curr Hypertens Rep. 2000;2:1–10.
Glazier AM, Nadeu JH, Aitman TJ. Finding genes that underlie complex traits. Science. 2002;298:2345–9.
Svenson KL, Bogue MA, Peters LL. Identifying new mouse models of cardiovascular disease: a review of high-throughput screens of mutagenized and inbred strains. J Appl Physiol. 2003;94:1650–9.
Trippodo NC, Frohlich ED. Similarities of genetic (spontaneous) hypertension. Man and rat. Circ Res. 1981;48:309–19.
McGiff JC, Quilley CP. The rat with spontaneous genetic hypertension is not suitable model of human essential hypertension. Circ Res. 1981;48:455–63.
Rettig R, Folberth C, Stauss H, et al. Role of the kidney in primary hypertension: a renal transplantation study in rats. Am J Physiol. 1990;258:F606–11.
Campbell DJ, Duncan AM, Kladis A, et al. Converting enzyme inhibition and its withdrawal in spontaneously hypertensive rats. J Cardiovasc Pharmacol. 1995;26:426–36.
de Souza Bomfim A, Mandarim-de-Lacerda CA. Effects of ACE inhibition during fetal development on cardiac microvasculature in adult spontaneously hypertensive rats. Int J Cardiol. 2005;101:237–42.
Iyer SN, Lu D, Katovich MJ, et al. Chronic control of high blood pressure in the spontaneously hypertensive rat by delivery of angiotensin type 1 receptor antisense. Proc Natl Acad Sci USA. 1996;93:9960–5.
Pachori AS, Huentelman MJ, Francis SC, et al. The future of hypertension therapy: sense, antisense, or nonsense? Hypertension. 2001;37:357–64.
Pinto YM, Paul M, Ganten D. Lessons from rat models of hypertension: from Goldblatt to genetic engineering. Cardiovasc Res. 1998;39:77–88.
Yamori Y. Implication of hypertensive rat models for primordial nutritional prevention of cardiovascular diseases. Clin Exp Pharmacol Physiol. 1999;26:568–72.
Barker DJP, Osmond C, Golding J, et al. Growth in utero, blood pressure in childhood and adult life, and mortality from cardiovascular disease. Br Med J. 1989;298:564–7.
Huxley RR, Shiel AW, Law CM. The role of size at birth and postnatal catch-up growth in determining systolic blood pressure: a systemic review of the literature. J Hypertens. 2000;18:815–31.
De Boo HA, Harding JE. The developmental origins of adult disease (Barker) hypothesis. Aust N Z J Obstet Gynaecol. 2006;46:4–14.
Eriksson JG, Forsón TJ, Kajantie E, et al. Childhood growth and hypertension in later life. Hypertension. 2007;49:1414–21.
Falkner B, Hulman S, Kushner H. Effect of birth weight on blood pressure and body size in early adolescence. Hypertension. 2004;43:203–7.
Zandi-Nejad K, Luyckx VA, Brenner BM. Adult hypertensuion and kidney disease. The role of fetal programming. Hypertension. 2006;47:502–8.
Bo S, Cavallo-Perin P, Scaglione L, et al. Low birthweight and metabolic abnormalities in twins with increased susceptibility to Type 2 diabetes mellitus. Diabet Med. 2000;17:365–70.
Iliadou A, Cnattingius S, Lichtenstein P. Low birthweight and Type 2 diabetes: a study on 11 162 Swedish twins. Int J Epidemiol. 2004;33:948–53.
Cheung YF, Taylor MJ, Fisk NM, et al. Fetal origins of reduced arterial distensibility in the donor twin in twin-twin transfusion syndrome. Lancet. 2000;355:1157–8.
Gärtner K. A third component causing random variability beside environment and genotype. A reason for the limited success of a 30 year long effort to standardize laboratory animals? Lab Anim. 1990;24:71–7.
Waterland RA, Jirtle RL. Early nutrition, epigenetic changes at transposons and imprinted genes, and enhanced susceptibility to adult chronic diseases. Nutrition. 2004;20:63–8.
Reik W, Dean W, Walter J. Epigenetic reprogramming in mammalian development. Science. 2001;293:1089–93.
Nafee TM, Farrell WE, Carroll WD, et al. Epigenetic control of fetal gene expression. BJOG. 2008;115:158–68.
Surani MA. Reprogramming of genome function through epigenetic inheritance. Nature. 2001;414:122–8.
Wolff GL, Kodell RL, Moore SR, et al. Maternal epigenetics and methyl supplements affect agouti gene expression in Avy/a mice. FASEB J. 1998;12:949–57.
Morgan HD, Sutherland HG, Martin DI, et al. Epigenetic inheritance at the agouti locus in the mouse. Nat Genet. 1999;23:314–8.
Waterland RA, Jirtle RL. Transposable elements: targets for early nutritional effects on epigenetic gene regulation. Mol Cell Biol. 2003;23:5293–300.
Heijmans BT, Tobi EW, Stein AD, et al. Persistent epigenetic differences associated with prenatal exposure to famine in humans. Proc Natl Acad Sci USA. 2008;105:17046–9.
Tobi EW, Lumey LH, Talens RP, et al. DNA methylation differences after exposure to prenatal famine are common and timing- and sex-specific. Hum Mol Genet. 2009;18:4046–53.
Heijmans BT, Kremer D, Tobi EW, et al. Heritable rather than age-related environmental and stochastic factors dominate variation in DNA methylation of the human IGF2/H19 locus. Hum Mol Genet. 2007;16:547–54.
Fraga MF, Ballestar E, Paz MF, et al. Epigenetic differences arise during the lifetime of monozygotic twins. Proc Natl Acad Sci USA. 2005;102:10604–9.
Kadlecová M, Dobešová Z, Zicha J, et al. Abnormal Igf2 gene in Prague hereditary hypertriglyceridemic rats: its relation to blood pressure and plasma lipids. Mol Cell Biochem. 2008;314:37–43.
Martens JR, Reaves PY, Lu D, et al. Prevention of renovascular and cardiac pathophysiological changes in hypertension by angiotensin II type 1 receptor antisense gene therapy. Proc Natl Acad Sci USA. 1998;95:2664–9.
Katovich MJ, Gelband CH, Reaves P, et al. Reversal of hypertension by angiotensin II type 1 receptor antisense gene therapy in the adult SHR. Am J Physiol Heart Circ Physiol. 1999;277:H1260–4.
Author information
Authors and Affiliations
Corresponding author
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 2011 Springer Science+Business Media, LLC
About this chapter
Cite this chapter
Kunes, J., Kadlecova, M., Zicha, J. (2011). Gene–Environment Interactions: Their Role in Hypertension Development. In: Ostadal, B., Nagano, M., Dhalla, N. (eds) Genes and Cardiovascular Function. Springer, Boston, MA. https://doi.org/10.1007/978-1-4419-7207-1_17
Download citation
DOI: https://doi.org/10.1007/978-1-4419-7207-1_17
Published:
Publisher Name: Springer, Boston, MA
Print ISBN: 978-1-4419-7206-4
Online ISBN: 978-1-4419-7207-1
eBook Packages: MedicineMedicine (R0)