Publish in OALib Journal
ISSN: 2333-9721
APC: Only $99

Paper Submission

Views	Downloads

Relative Articles
Endothelin role in the orthostatic stress Papel da endotelina no estresse ortostático
Ambulatory Pessary Trial Unmasks Occult Stress Urinary Incontinence
The Effects of Stress Tensor Fluctuations upon Focusing
Environmental Influences Cause Stress on the Use of Computer
Expression of endothelin in organ-cultured artery under low shear stress 低切应力作用下体外培养动脉内皮细胞内皮素的表达
Liver sinusoidal endothelial cell modulation upon resection and shear stress in vitro
Pre-Disposition and Epigenetics Govern Variation in Bacterial Survival upon Stress
Aspergillus oryzae AoSO Is a Novel Component of Stress Granules upon Heat Stress in Filamentous Fungi
Influences of Annealing on Residual Stress and Structure of HfO2 Films
More...

International Journal of Hypertension 2012

Differential Impact of Stress Reduction Programs upon Ambulatory Blood Pressure among African American Adolescents: Influences of Endothelin-1 Gene and Chronic Stress Exposure

DOI: 10.1155/2012/510291

Mathew J. Gregoski,Vernon A. Barnes,Martha S. Tingen,Yanbin Dong,Haidong Zhu,Frank A. Treiber

Full-Text Cite this paper Add to My Lib

Abstract:

Stress-activated gene × environment interactions may contribute to individual variability in blood pressure reductions from behavioral interventions. We investigated effects of endothelin-1 (ET-1) LYS198ASN SNP and discriminatory stress exposure upon impact of 12-week behavioral interventions upon ambulatory BP (ABP) among 162 prehypertensive African American adolescents. Following genotyping, completion of questionnaire battery, and 24-hour ABP monitoring, participants were randomized to health education control (HEC), life skills training (LST), or breathing awareness meditation (BAM). Postintervention ABP was obtained. Significant three-way interactions on ABP changes indicated that among ET-1 SNP carriers, the only group to show reductions was BAM from low chronic stress environments. Among ET-1 SNP noncarriers, under low chronic stress exposure, all approaches worked, especially BAM. Among high stress exposure noncarriers, only BAM resulted in reductions. If these preliminary findings are replicated via ancillary analyses of archival databases and then via efficacy trials, selection of behavioral prescriptions for prehypertensives will be edging closer to being guided by individual's underlying genetic and environmental factors incorporating the healthcare model of personalized preventive medicine. 1. Introduction Essential hypertension (EH) is a major risk factor for cardiovascular disease (CVD), and EH incidence among youth is increasing [1]. African Americans (AAs) experience a higher prevalence, earlier onset, and greater severity of EH-related complications than other ethnic groups [2]. From late childhood onward, AAs display increased levels of resting and ambulatory blood pressure (ABP) compared to other ethnic groups [3–5]. BP levels are monotonically associated with future CVD morbidity and mortality [6]. Stage I prehypertensive adults (i.e., SBP/DBP 121–129/81–84？mmHg) have a 40% increased risk and adults with stage II prehypertension (i.e., SBP/DBP 130–139/85–89？mmHg) are twice as likely to develop CVD compared to those with optimal BP (<120/<80？mmHg) [6–8]. BP percentile ranking tracks from late childhood into adulthood [9–11] placing AA adolescents with BP between the 50th and 95th percentiles for age and sex at an increased risk of future EH and CVD development [9]. EH, like other multifactorial chronic diseases, results from a complex interplay between an individual’s genetic underpinnings, lifestyle behaviors, psychosocial factors, and exposures to various environmental toxins. Over time, this dynamic interplay eventuates in adverse

References

[1]	P. Muntner, J. He, J. A. Cutler, R. P. Wildman, and P. K. Whelton, “Trends in blood pressure among children and adolescents,” Journal of the American Medical Association, vol. 291, no. 17, pp. 2107–2113, 2004.
[2]	S. Nesbitt and R. G. Victor, “Pathogenesis of hypertension in African Americans,” Congestive Heart Failure, vol. 10, no. 1, pp. 24–29, 2004.
[3]	G. S. Berenson, “Childhood risk factors predict adult risk associated with subclinical cardiovascular disease: the Bogalusa heart study,” American Journal of Cardiology, vol. 90, no. 10, pp. L3–L7, 2002.
[4]	G. A. Harshfield, F. A. Treiber, M. E. Wilson, G. K. Kapuku, and H. C. Davis, “A longitudinal study of ethnic differences in ambulatory blood pressure patterns in youth,” American Journal of Hypertension, vol. 15, no. 6, pp. 525–530, 2002.
[5]	X. Wang, J. C. Poole, F. A. Treiber, G. A. Harshfield, C. D. Hanevold, and H. Snieder, “Ethnic and gender differences in ambulatory blood pressure trajectories: results from a 15-year longitudinal study in youth and young adults,” Circulation, vol. 114, no. 25, pp. 2780–2787, 2006.
[6]	W. B. Kannel, R. S. Vasan, and D. Levy, “Is the relation of systolic blood pressure to risk of cardiovascular disease continuous and graded, or are there critical values?” Hypertension, vol. 42, no. 4, pp. 453–456, 2003.
[7]	B. M. Egan, S. D. Nesbitt, and S. Julius, “Prehypertension: should we be treating with pharmacologic therapy?” Therapeutic Advances in Cardiovascular Disease, vol. 2, no. 4, pp. 305–314, 2008.
[8]	B. M. Egan, D. T. Lackland, and D. W. Jones, “Prehypertension: an opportunity for a new public health paradigm,” Cardiology Clinics, vol. 28, no. 4, pp. 561–569, 2010.
[9]	A. K. Manatunga, J. J. Jones, and J. H. Pratt, “Longitudinal assessment of blood pressures in black and white children,” Hypertension, vol. 22, no. 1, pp. 84–89, 1993.
[10]	W. Bao, S. A. Threefoot, S. R. Srinivasan, and G. S. Berenson, “Essential hypertension predicted by tracking of elevated blood pressure from childhood to adulthood: the bogalusa heart study,” American Journal of Hypertension, vol. 8, no. 7, pp. 657–665, 1995.
[11]	J. C. Dekkers, H. Snieder, E. J. C. G. van den Oord, and F. A. Treiber, “Moderators of blood pressure development from childhood to adulthood: a 10-year longitudinal study in African- and European American youth,” Journal of Pediatrics, vol. 141, no. 6, pp. 770–779, 2002.
[12]	R. C. Lewontin, The Triple Helix : Gene, Organism, and Environment / Richard Lewontin, Harvard University Press, Cambridge, Mass, USA, 2000.
[13]	L. Kurland, L. Lind, and H. Melhus, “Using genotyping to predict responses to anti-hypertensive treatment,” Trends in Pharmacological Sciences, vol. 26, no. 9, pp. 443–447, 2005.
[14]	R. Clark and P. Gochett, “Interactive effects of perceived racism and coping responses predict a school-based assessment of blood pressure in black youth,” Annals of Behavioral Medicine, vol. 32, no. 1, pp. 1–9, 2006.
[15]	D. R. Williams and C. Collins, “US socioeconomic and racial differences in health: patterns and explanations,” Annual Review of Sociology, vol. 21, no. 1, pp. 349–386, 1995.
[16]	K. A. Matthews, K. Salomon, K. Kenyon, and F. Zhou, “Unfair treatment, discrimination, and ambulatory blood pressure in black and white adolescents,” Health Psychology, vol. 24, no. 3, pp. 258–265, 2005.
[17]	D. L. Beatty and K. A. Matthews, “Unfair treatment and trait anger in relation to nighttime ambulatory blood pressure in African American and white adolescents,” Psychosomatic Medicine, vol. 71, no. 8, pp. 813–820, 2009.
[18]	D. A. Calhoun, “Hypertension in blacks: socioeconomic stress and sympathetic nervous system activity,” American Journal of the Medical Sciences, vol. 304, no. 5, pp. 306–311, 1992.
[19]	B. Falkner, “Differences in blacks and whites with essential hypertension: biochemistry and endocrine. State of the art lecture,” Hypertension, vol. 15, no. 6, pp. 681–686, 1990.
[20]	B. Falkner, “The role of cardiovascular reactivity as a mediator of hypertension in African Americans,” Seminars in Nephrology, vol. 16, no. 2, pp. 117–125, 1996.
[21]	L. F. Soto, D. A. Kikuchi, R. A. Arcilla, D. D. Savage, and G. S. Berenson, “Echocardiographic functions and blood pressure levels in children and young adults from a biracial population: the Bogalusa heart study,” American Journal of the Medical Sciences, vol. 297, no. 5, pp. 271–279, 1989.
[22]	P. G. Saab, M. M. Llabre, B. E. Hurwitz et al., “Myocardial and peripheral vascular responses to behavioral challenges and their stability in black and white Americans,” Psychophysiology, vol. 29, no. 4, pp. 384–397, 1992.
[23]	F. A. Treiber, G. K. Kapuku, H. Davis, J. S. Pollock, and D. M. Pollock, “Plasma endothelin-1 release during acute stress: role of ethnicity and sex,” Psychosomatic Medicine, vol. 64, no. 5, pp. 707–713, 2002.
[24]	F. A. Treiber, P. Barbeau, G. Harshfield et al., “Endothelin-1 gene LYS198ASN polymorphism and blood pressure reactivity,” Hypertension, vol. 42, no. 4, pp. 494–499, 2003.
[25]	K. F. Harris and K. A. Matthews, “Interactions between autonomic nervous system activity and endothelial function: a model for the development of cardiovascular disease,” Psychosomatic Medicine, vol. 66, no. 2, pp. 153–164, 2004.
[26]	F. A. Treiber, R. W. Jackson, H. Davis et al., “Racial differences in endothelin-1 at rest and in response to acute stress in adolescent males,” Hypertension, vol. 35, no. 3, pp. 722–725, 2000.
[27]	S. Ergul, D. C. Parish, D. Puett, and A. Ergul, “Racial differences in plasma endothelin-1 concentrations in individuals with essential hypertension,” Hypertension, vol. 28, no. 4, pp. 652–655, 1996.
[28]	R. R. Evans, B. G. Phillips, G. Singh, J. L. Bauman, and A. Gulati, “Racial and gender differences in endothelin-1,” American Journal of Cardiology, vol. 78, no. 4, pp. 486–487, 1996.
[29]	D. C. Cooper, P. J. Mills, W. A. Bardwell, M. G. Ziegler, and J. E. Dimsdale, “The effects of ethnic discrimination and socioeconomic status on endothelin-1 among blacks and whites,” American Journal of Hypertension, vol. 22, no. 7, pp. 698–704, 2009.
[30]	A. F. Popov, E. G. Schulz, J. Hinz et al., “Impact of endothelin-1 Lys198Asn polymorphism on coronary artery disease and endorgan damage in hypertensives,” Coronary Artery Disease, vol. 19, no. 7, pp. 429–434, 2008.
[31]	L. Tiret, O. Poirier, V. Hallet et al., “The Lys198Asn polymorphism in the endothelin-1 gene is associated with blood pressure in overweight people,” Hypertension, vol. 33, no. 5, pp. 1169–1174, 1999.
[32]	T. Asai, T. Ohkubo, T. Katsuya et al., “Endothelin-1 gene variant associates with blood pressure in obese Japanese subjects: the Ohasama study,” Hypertension, vol. 38, no. 6, pp. 1321–1324, 2001.
[33]	A. Barath, E. Endreffy, C. Bereczki et al., “Endothelin-1 gene and endothelial nitric oxide synthase gene polymorphisms in adolescents with juvenile and obesity-associated hypertension,” Acta Physiologica Hungarica, vol. 94, no. 1-2, pp. 49–66, 2007.
[34]	K. M. Rabineau, F. A. Treiber, J. Poole, and D. Ludwig, “Interactive effects of anger expression and ET-1 Lys198Asn polymorphism on vasoconstriction reactivity to behavioral stress,” Annals of Behavioral Medicine, vol. 30, no. 1, pp. 85–89, 2005.
[35]	R. B. Williams, D. A. Marchuk, I. C. Siegler et al., “Childhood socioeconomic status and serotonin transporter gene polymorphism enhance cardiovascular reactivity to mental stress,” Psychosomatic Medicine, vol. 70, no. 1, pp. 32–39, 2008.
[36]	Y. Dong, X. Wang, H. Zhu, F. A. Treiber, and H. Snieder, “Endothelin-1 gene and progression of blood pressure and left ventricular mass: longitudinal findings in youth,” Hypertension, vol. 44, no. 6, pp. 884–890, 2004.
[37]	Z. Pausova, J. Tremblay, and P. Hamet, “Gene-environment interactions in hypertension,” Current Hypertension Reports, vol. 1, no. 1, pp. 42–50, 1999.
[38]	I. G. Imumorin, Y. Dong, H. Zhu et al., “A gene-environment interaction model of stress-induced hypertension,” Cardiovascular Toxicology, vol. 5, no. 2, pp. 109–132, 2005.
[39]	K. C. Light, “Hypertension and the reactivity hypothesis: the next generation,” Psychosomatic Medicine, vol. 63, no. 5, pp. 744–746, 2001.
[40]	J. W. Anderson, C. Liu, and R. J. Kryscio, “Blood pressure response to transcendental meditation: a meta-analysis,” American Journal of Hypertension, vol. 21, no. 3, pp. 310–316, 2008.
[41]	M. B. Ospina, T. K. Bond, M. Karkhaneh et al., “Meditation practices for health: state of the research,” Evidence Report Technology Assessment, no. 155, pp. 1–263, 2007.
[42]	M. V. Rainforth, R. H. Schneider, S. I. Nidich, C. Gaylord-King, J. W. Salerno, and J. W. Anderson, “Stress reduction programs in patients with elevated blood pressure: a systematic review and meta-analysis,” Current Hypertension Reports, vol. 9, no. 6, pp. 520–528, 2007.
[43]	D. S. Black, J. Milam, and S. Sussman, “Sitting-meditation interventions among youth: a review of treatment efficacy,” Pediatrics, vol. 124, no. 3, pp. e532–e541, 2009.
[44]	M. J. Gregoski, V. A. Barnes, M. S. Tingen, G. A. Harshfield, and F. A. Treiber, “Breathing awareness meditation and lifeskills training programs influence upon ambulatory blood pressure and sodium excretion among African American adolescents,” Journal of Adolescent Health, vol. 48, no. 1, pp. 59–64, 2011.
[45]	R. Weisinger, J. Blair-West, P. Burns, N. Chen, and H. Weisinger, “Neurobiology of sodium appetite,” in Neurobiology of Food and Fluid Intake, E. M. Stricker and S. C. Woods, Eds., vol. 14, pp. 547–587, Springer, New York, NY, USA, 2004.
[46]	D. E. Kohan, N. F. Rossi, E. W. Inscho, and D. M. Pollock, “Regulation of blood pressure and salt homeostasis by endothelin,” Physiological Reviews, vol. 91, no. 1, pp. 1–77, 2011.
[47]	V. A. Barnes, R. A. Pendergrast, G. A. Harshfield, and F. A. Treiber, “Impact of breathing awareness meditation on ambulatory blood pressure and sodium handling in prehypertensive African American adolescents,” Ethnicity and Disease, vol. 18, no. 1, pp. 1–5, 2008.
[48]	S. I. Nidich, M. V. Rainforth, D. A. Haaga et al., “A randomized controlled trial on effects of the transcendental meditation program on blood pressure, psychological distress, and coping in young adults,” American Journal of Hypertension, vol. 22, no. 12, pp. 1326–1331, 2009.
[49]	I. Libo, “Same genetic mutation, different genetic disease phenotype,” Nature Education, vol. 1, no. 1, 2008.
[50]	C. E. Lerman, R. A. Schnoll, and M. R. Munafò, “Genetics and smoking cessation. Improving outcomes in smokers at risk,” American Journal of Preventive Medicine, vol. 33, supplement 6, pp. S398–S405, 2007.
[51]	J. C. Florez, K. A. Jablonski, N. Bayley et al., “TCF7L2 polymorphisms and progression to diabetes in the diabetes prevention program,” New England Journal of Medicine, vol. 355, no. 3, pp. 241–250, 2006.
[52]	E. J. Roccella, “Update on the 1987 task force report on high blood pressure in children and adolescents: a working group report from the national high blood pressure education program. National high blood pressure education program working group on hypertension control in children and adolescents,” Pediatrics, vol. 98, no. 4, pp. 649–658, 1996.
[53]	E. O'Brien, F. Mee, K. O'Malley, and N. Atkins, “Accuracy of the spacelabs 90207 determined by the British hypertension society protocol,” Journal of Hypertension, vol. 9, no. 6, pp. 573–574, 1991.
[54]	V. A. Barnes, M. H. Johnson, J. C. Dekkers, and F. A. Treiber, “Reproducibility of ambulatory blood pressure measures in African-American adolescents,” Ethnicity and Disease, vol. 12, supplement 3, pp. S3-101–S3-106, 2002.
[55]	V. A. Barnes, M. H. Johnson, and F. A. Treiber, “Temporal stability of twenty-four-hour ambulatory hemodynamic bioimpedance measures in African American adolescents,” Blood Pressure Monitoring, vol. 9, no. 4, pp. 173–177, 2004.
[56]	R. Clark, A. P. Coleman, and J. D. Novak, “Brief report: initial psychometric properties of the everyday discrimination scale in black adolescents,” Journal of Adolescence, vol. 27, no. 3, pp. 363–368, 2004.
[57]	D. R. Williams, Y. Yu, J. S. Jackson, and N. B. Anderson, “Racial differences in physical and mental health. Socio-economic status, stress and discrimination,” Journal of Health Psychology, vol. 2, no. 3, pp. 335–351, 1997.
[58]	K. H. Banks, L. P. Kohn-Wood, and M. Spencer, “An examination of the African American experience of everyday discrimination and symptoms of psychological distress,” Community Mental Health Journal, vol. 42, no. 6, pp. 555–570, 2006.
[59]	G. J. Botvin, E. Baker, and N. L. Renick, “A cognitive-behavioral approach to substance abuse prevention,” Addictive Behaviors, vol. 9, no. 2, pp. 137–147, 1984.
[60]	J. Kabat-Zinn and T. N. Hanh, Full Catastrophe Living: Using the Wisdom of your Body and Mind to Face Stress, Pain and Illness. The Program of the Stress Reduction Clinic at the University of Massachusetts Medical Center, Delta, New York, NY, USA, 1990.
[61]	L. Kann, S. A. Kinchen, B. I. Williams et al., “Youth risk behavior surveillance—United States, 1997,” Morbidity and Mortality Weekly Report. CDC Surveillance Summaries, vol. 47, no. 3, pp. 1–89, 1998.
[62]	J. DeCoster, A. M. Iselin, and M. Gallucci, “A conceptual and empirical examination of justifications for dichotomization,” Psychological Methods, vol. 14, no. 4, pp. 349–366, 2009.
[63]	S. Rodriguez, T. R. Gaunt, and I. N. Day, “Hardy-Weinberg equilibrium testing of biological ascertainment for Mendelian randomization studies,” American Journal of Epidemiology, vol. 169, no. 4, pp. 505–514, 2009.
[64]	R. H. Schneider, C. N. Alexander, F. Staggers et al., “Long-term effects of stress reduction on mortality in persons years of age with systemic hypertension,” American Journal of Cardiology, vol. 95, no. 9, pp. 1060–1064, 2005.
[65]	S. di Francescomarino, A. Sciartilli, V. di Valerio, A. D. Baldassarre, and S. Gallina, “The effect of physical exercise on endothelial function,” Sports Medicine, vol. 39, no. 10, pp. 797–812, 2009.
[66]	D. H. Thijssen, G. A. Rongen, P. Smits, and M. T. Hopman, “Physical (in)activity and endothelium-derived constricting factors: overlooked adaptations,” Journal of Physiology, vol. 586, no. 2, pp. 319–324, 2008.
[67]	T. Rankinen, T. Church, T. Rice et al., “Effect of endothelin 1 genotype on blood pressure is dependent on physical activity or fitness levels,” Hypertension, vol. 50, no. 6, pp. 1120–1125, 2007.
[68]	S. Julius, N. Kaciroti, B. M. Egan, S. Nesbitt, and E. L. Michelson, “TROPHY study: outcomes based on the seventh report of the joint national committee on hypertension definition of hypertension,” Journal of the American Society of Hypertension, vol. 2, no. 1, pp. 39–43, 2008.
[69]	S. Lüders, J. Schrader, J. Berger et al., “The PHARAO study: prevention of hypertension with the angiotensin-converting enzyme inhibitor ramipril in patients with high-normal blood pressure: a prospective, randomized, controlled prevention trial of the German hypertension league,” Journal of Hypertension, vol. 26, no. 7, pp. 1487–1496, 2008.
[70]	M. A. Weber, H. Black, G. Bakris et al., “A selective endothelin-receptor antagonist to reduce blood pressure in patients with treatment-resistant hypertension: a randomised, double-blind, placebo-controlled trial,” The Lancet, vol. 374, no. 9699, pp. 1423–1431, 2009.
[71]	C. D. Collins, S. Purohit, R. H. Podolsky et al., “The application of genomic and proteomic technologies in predictive, preventive and personalized medicine,” Vascular Pharmacology, vol. 45, no. 5, pp. 258–267, 2006.

Full-Text