Etiology of essential hypertension.

Abstract

is not possible to study the etiology of essential hypertension without considering the role of inheritance. Unfortunately, a genetic approach to this problem has been hampered by the fact that not a single deleterious recurrent mutation has been detected in the structural idiomorphic genes which synthesize the enzymes of the renin angiotensinaldosterone and kallikrein-kinin systems in mammals. Similarly, physiologists and biochemists have been unable to discover a single polymorphic genetic system that relates to blood pressure (BP) regulation. Thus, unable to obtain a direct approach to the genetic sources, geneticists have used indirect epidemiological methods to investigate the genetics of BP in human populations. Models Polygenic ModelThe epidemiological evidence currently available indicates that the development of high BP in the population at large depends on the interaction of several genetic and environmental influences. The sources of genetic variation of the BP phenotype originate from polygenes, polymorphic genes, and possibly idiomorphic genes. The sources of ecological or environmental variation originate mainly from weight gain, salt (Na) intake, and psychosocial stress. All the genes may be grouped and explained on the basis of a polygenic model. Polygenic or multifactorial inheritance of a quantitative trait assumes that multiple factors, both inherited and acquired and acting independently, lead to a distribution that is correlated in relatives of patients. The distribution is continuous in the population at large and is the expression of the interaction of "minor" or "common" genes and multiple environmental factors. 1The degree of quantitative resemblance (correlation and regression coefficients) among relatives is proportional to the number of genes in common shared by all the individuals within the family. 2The polygenic evidence is the following-1) distribution of levels of BP in relatives of hypertensive patients, compared with controls, shows that the relatives of hypertensives have significant higher mean blood BP levels at all ages than the relatives of controls.3 ' * 2) After suitable adjustment for age and sex, it has been found that the tendency of the first degree relatives of hypertensive patients to resemble one another is the same at all levels of BP from the lowest to the highest ranges. The higher the pressure of the patient, the higher the pressure of the relative. 5 3) The degree of BP resemblance between relatives is a function of the corresponding degree of parentage. Firstdegree relatives (parents and sibling) show higher correlations and regression coefficients than the second-degree (uncles and grandfathers) and third-degree (cousin) relatives."All the correlation studies of BP between relatives have found low degrees of resemblance around r = 0.20, against an expected 0.50 for total genetic determination.7 This familial aggregation is present early in life; the maternal infant correlation at birth is also 0.20. This resemblance is maintained with increasing age until ...

Syncope in Childhood: A Case Control Clinical Study of the Familial Tendency to Faint

“…Arterial blood pressure is thought to be determined by a combination of multiple genetic influences plus environmental factors and is therefore said to be multifactorial. 3 Blood pressure in children resembles that of their parents -no single factor explains this association. 4 Syncope results from faulty blood pressure control and is the final result of several mechanisms including bradycardia from excessive vagal discharge and/or lack of sympathetic tone.…”

Comparison between Essential Hypertension and Pregnancy-induced Hypertension: a Genetic Perspective

“…There are a few monogenic diseases (inheritance hypertension) that have been defined as unusual hypertension. Although the available evidence strongly suggests that EH is a multifactorial inheritance disease [4], a causal gene for EH has not yet be clearly identified. There are many environmental factors that can affect EH, including obesity, diabetes, drinking and smoking.…”

The borderline hypertensive rat: A model for studying the mechanisms of environmentally induced hypertension.

“…Yet not all borderline hypertensives go on to the established phase of the disease (Julius & Esler, 1975). Cruz-Coke (1981) and others have suggested that genetics and environment interact to produce essential hypertension. In this view, genetic predisposition serves as a necessary but not generally sufficient condition for hypertension.…”