Experimental models of genetic hypertension are used to develop paradigms t
o study human essential hypertension while removing some of the complexity
inherent in the study of human subjects. Since 1991 several quantitative tr
ait loci responsible for blood pressure regulation have been identified in
various rat crosses. More recently, a series of interesting quantitative tr
ait loci influencing cardiac hypertrophy, stroke, metabolic syndrome and re
nal damage has also been described. It is recognized that the identificatio
n of large chromosomal regions containing a quantitative trait locus is onl
y a first step towards gene identification. The next step is the production
of congenic strains and substrains to confirm the existence of the quantit
ative trait locus and to narrow down the chromosomal region of interest. Se
veral congenic strains have already been produced, with further refinement
of the methodology currently in progress. The ultimate goal is to achieve p
ositional cloning of the causal gene, a task which has so far been elusive.
There are several areas of cross-fertilization between experimental and hum
an genetics of hypertension, with a successful transfer of two loci directl
y from rats to humans and with new pharmacogenetic approaches which may be
utilized in both experimental and clinical settings. J Hypertens 1998, 16:1
859-1869 (C) 1998 Lippincott Williams & Wilkins.