OBJECTIVE: The chromosomal location of candidate genes for a disease, especially if the disease is multifactorial, is an important datum. The objective of the present study was to determine the chromosomal location of candidate hypertensinogenic genes, both in humans and in the rat, a species widely used for animal models of human hypertension. The type 1 angiotensin II receptor (AT1) genes are obvious hypertension candidate genes, whereas the SA gene has recently been shown to cosegregate with hypertension in the rat. DESIGN: The chromosomal location of the relevant genes was determined using somatic cell hybrids segregating either human chromosomes or rat chromosomes. The presence of the human or rat genes was determined by the Southern blot method, using rat probes. RESULTS: A single AT1 gene (AT1) was detected in the human genome, and was assigned to chromosome 3, whereas two non-syntenic genes were detected in the rat genome, corresponding to the previously identified A and B subtypes. They were assigned to the rat chromosome 17 (At1a) and 2 (AT1b). The Sa gene was assigned to human chromosome 16 and rat chromosome 1, disclosing a new synteny group retained on rat chromosome 1 and human chromosome 16. CONCLUSIONS: These chromosomal assignments should be useful for linkage analyses of genes controlling blood pressure. The genes that we studied, and the chromosomes that we identified, deserve special attention in such linkage analyses.
OBJECTIVE: The chromosomal location of candidate genes for a disease, especially if the disease is multifactorial, is an important datum. The objective of the present study was to determine the chromosomal location of candidate hypertensinogenic genes, both in humans and in the rat, a species widely used for animal models of humanhypertension. The type 1 angiotensin II receptor (AT1) genes are obvious hypertension candidate genes, whereas the SA gene has recently been shown to cosegregate with hypertension in the rat. DESIGN: The chromosomal location of the relevant genes was determined using somatic cell hybrids segregating either human chromosomes or rat chromosomes. The presence of the human or rat genes was determined by the Southern blot method, using rat probes. RESULTS: A single AT1 gene (AT1) was detected in the human genome, and was assigned to chromosome 3, whereas two non-syntenic genes were detected in the rat genome, corresponding to the previously identified A and B subtypes. They were assigned to the rat chromosome 17 (At1a) and 2 (AT1b). The Sa gene was assigned to human chromosome 16 and rat chromosome 1, disclosing a new synteny group retained on rat chromosome 1 and human chromosome 16. CONCLUSIONS: These chromosomal assignments should be useful for linkage analyses of genes controlling blood pressure. The genes that we studied, and the chromosomes that we identified, deserve special attention in such linkage analyses.