Abstract-Several clinical and animal studies indicate that essential hypertension is inherited as a multifactorial trait with a significant genetic and environmental component. In the stroke-prone spontaneously hypertensive rat model, investigators have found evidence for linkage to blood pressure regulatory genes (quantitative trait loci) on rat chromosomes 2, 10, and X. In 1 human study of French and UK sib pairs, evidence for linkage has been reported to human chromosome 17q, the syntenic region of the rat chromosome 10 quantitative trait loci (QTL). Our study confirms this linkage (Pϭ0.0005) and refines the location of the blood pressure QTL. (Hypertension. 1999;34:4-7.)Key Words: hypertension, essential Ⅲ linkage Ⅲ chromosome 17 Ⅲ blood pressure Ⅲ obesity E ssential hypertension is one of the most common cardiovascular diseases, affecting 15% to 20% of the population. It is an important risk factor for heart and kidney failure, myocardial ischemia, and stroke. 1 Essential hypertension is considered a complex disease with significant genetic and environmental components that interact to play a role in blood pressure variation. 2 Many candidate genes have been reported to contribute to the susceptibility to hypertension in clinical studies. [3][4][5] The stroke-prone spontaneously hypertensive rat and the Dahl salt-sensitive hypertensive rat have proved to be useful tools in identifying quantitative trait loci (QTL) that contribute to blood pressure variations. 6 -11 Evidence of a blood pressure QTL was found on rat chromosomes 2, 10 10, 6 -11 and X. 7 The rat chromosome 10 QTL is located near the angiotensin-converting enzyme (ACE) locus. The ACE locus is an attractive candidate gene because of its role in the renin-angiotensin system and the association between several polymorphisms in the ACE locus with blood pressure levels in some studies, 12-14 although other studies failed to confirm this finding. [15][16][17] Human chromosome 17 is syntenic with rat chromosome 10, and evidence for linkage between this blood pressure QTL has been reported in French/UK hypertensive sib pairs. 18 These markers are 18 cM proximal to the ACE locus. In addition, linkage of pseudohypoaldosteronism type IIB (hypertension, hyperkalemia, and normal renal glomerular filtration) to this region has been reported in several families. 19 In this study, we tested a series of microsatellite markers near this chromosome 17 blood pressure QTL in a collection of white and black sib pairs from the United States. Evidence of linkage was found in our collection of white sib pairs. MethodsProbands were identified from hypertension clinics in Massachusetts and Texas. Extensive family histories, including medical history, risk factor information, ethnic background, and demographics, were taken. Boston Medical Center Institutional Review Board for Human Subjects approved this study, and all subjects gave informed consent. Blood samples were collected from 74 white patients and 97 of their affected sibs (125 sib pairs) and from 45 black patients...
Objective African-Americans have been shown to have low prevalence of hypothyroidism. Brazil has a high ethnic admixture allowing further exploration into whether environmental factors can explain the ethnic differences. Design A survey, representative of the population of Rio de Janeiro, a large metropolitan city in Brazil. Factors studied included race, parity, income, schooling, and smoking. Population The survey was carried out in Rio de Janeiro whereby households (1500) were selected using three-stage probability sampling. A total of 1298 (86.5%) women participated in the survey (non-response: 13.5%). Measurements TSH from blood drawn at the households. Anti-thyroperoxidase (anti-TPO) antibodies and free T4 were also measured. Results Overall prevalence of hypothyroidism (TSH > 4 mUI/ml or taking medication) was 12.3%. Prevalence was 6.9% in black people, 8.8% in Mulatto people, and 16.7% among white people. The mean serum TSH of the population was 2.65 (95% confidence interval 2.33-2.97). The TSH distribution of black and Mulatto people was shifted to the left compared to white people. After adjustment for age, income, smoking and presence of anti-TPO, Black and Mulatto people were still protected from hypothyroidism. The adjusted odds ratio for black compared to white people was 0.45 (95% CI 0.30-0.68) and for Mulatto people was 0.34 (95% CI 0.18-0.63). Serum TSH levels were significantly lower in smokers than in non-smokers, but there was no association between number of cigarettes smoked and serum TSH level. Conclusions This is the first time it has been demonstrated that Mulatto people have a prevalence of hypothyroidism which lies between that of white and black people, independent of the prevalence of anti-TPO and smoking.
Essential hypertension, a clinically significant elevation in blood pressure with no recognizable cause, is believed to be attributable to the collective effect of genetic predisposing factors in combination with specific environmental factors, such as diet and stress. Of the genetic causes, genes coding for proteins involved in blood pressure regulation, such as the alpha- and beta-adrenergic receptors, are obvious candidates. The alpha2-adrenergic receptor plays a key role in the sympathetic nervous system by mediating the effects of epinephrine and norepinephrine. To evaluate the potential role between the alpha2B receptor and essential hypertension, we scanned the alpha2B-receptor gene for genetic variation in 108 affected sibling pairs. The screening revealed two major forms of the receptor. They differ by the presence of either 9 or 12 glutamic acid residues in the acidic domain of the third cytoplasmic loop of the protein. Investigation of the pattern of this variation in hypertensive sibling pairs suggests that the alpha2B receptor locus does not contribute substantially to genetic susceptibility for essential hypertension.
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