Genetic, common household and non-familial environmental factors contribute about 33, 15 and 50% of blood pressure (BP) variance, respectively. Although usually considered to be additive, the environmental impact on the expression of hypertension may also interact with genetic components. Even factors such as gender and age may exert an additive (subtractive) or interactive effect. These interactions usually lead to phenotypic amplification. 2. In some instances, the environmental impact is allele-dependent (putative locus of salt-sensitivity), and there are other occasions when phenotypic expression may be environmentally dependent. Environmental temperature appears to be another environmental modifier of BP. 3. Increased sensitivity to this environmental factor has been observed in hypertension, and a locus of thermosensitivity segregates with BP in mice. Candidate genes of environmental susceptibility are proposed to include tumour necrosis factor and the heat shock protein (HSP) family. An abnormal accumulation of HSP27 and HSP70 messenger RNA has been described in rodent (mice, rat) models of hypertension as well as in human subjects. Segregation of the HSP27 and HSP70 polymorphism with BP has been determined in at least some crosses. 4. These candidate genes of environmental susceptibility may also be involved in determining heart weight in addition to BP.
