Essential hypertension

Abstract

Hypertension is a frequent, chronic, age-related disorder, which often entails debilitating cardiovascular and renal complications. Blood pressure is usually noted in combination with other cardiovascular risk factors. Diagnosis of hypertension increasingly relies on automated techniques of blood pressure measurement. The pathophysiology of essential hypertension depends on the primary or secondary inability of the kidney to excrete sodium at a normal blood pressure. The central nervous system, endocrine factors, the large arteries, and the microcirculation also have roles in the disorder. Although monogenic forms of blood pressure dysregulation exist, hypertension mostly arises as a complex quantitative trait that is affected by varying combinations of genetic and environmental factors. Non-pharmacological strategies can reduce blood pressure. Antihypertensive drug treatment diminishes the complications of hypertension. The concept that a few major genes will provide the final clue to the pathogenesis of essential hypertension is an oversimplification that contradicts the heterogeneous nature of this disorder. Further integration of genetic, molecular, clinical, and epidemiological research could disclose subsets of patients in whom specific combinations of genetic and environmental factors raise blood pressure, and might lead to more individualised treatment.

Twenty-four hour ambulatory blood pressure for the management of antihypertensive treatment: a randomized controlled trial

“…We based our decision on a classification proposed at the Eighth International Consensus Conference on Ambulatory Blood Pressure Measurement in 2001. 32 It has been shown recently that a 24-h blood pressure and antihypertensive treatment D Conen et al population-based outcome-driven threshold for hypertension exactly corresponds to the one chosen in this study, 33 confirming the validity of this threshold. This study should be evaluated in the context of its limitations.…”

Antihypertensive therapy, the α-adducin polymorphism, and cardiovascular disease in high-risk hypertensive persons: the Genetics of Hypertension-Associated Treatment Study

“…12 Indeed, the pathogenesis of high BP is complex, involves multiple genes, and lifestyle and environmental factors. 38 There is precedent for gene-by-sex interactions for both BP levels and the response to BP-lowering medication. Yamagishi et al 39 showed that the a-adducin TrpTrp genotype was associated with higher systolic BP among men with a higher sodium intake, whereas there was no such association in women.…”

Arterial properties in relation to genetic variation in α-adducin and the renin–angiotensin system in a White population

“…In smokers, median tobacco use was 14 cigarettes per day (interquartile range, [8][9][10][11][12][13][14][15][16][17][18][19][20]. In drinkers, the median alcohol consumption was 10 g day À1 (interquartile range, [4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20]. Table 2 lists the arterial properties by generation and vascular territory.…”

“…3 Variation in the Na þ ,K þ -ATPase activity and in the intracellular Na þ concentration might influence the sodium-dependent transmembranous Ca þ 2 transport in vascular smooth muscle cells. 4 We have earlier demonstrated that interaction between the ADD1 Gly460Trp and the angiotensinconverting enzyme ACE I/D polymorphisms modulates femoral artery properties. Indeed, in the presence of the ADD1 460Trp allele, femoral intimamedia thickness was higher in ACE D carriers than in II homozygotes.…”

“…7 Experimental studies in fibroblasts from 51 subjects and in transfected cell models showed higher membrane-bound ACE activity in cells carrying the ADD1 Trp allele. 7 In view of the aforementioned evidence, [1][2][3][4][5][6][7] we hypothesized that arterial properties might be related not only to interactions of ADD1 with ACE, but also to interactions of ADD1 with other genes encoding various components of the renin-angiotensin system. We therefore genotyped Flemish Study on Environment, Genes and Health Outcomes participants for the angiotensinogen (AGT) C-532T and G-6A promoter polymorphisms as well as for the intronic A1166C polymorphism in the angiotensin II type-1 receptor gene (AT1R).…”