Cosegregation of the renin allele of the spontaneously hypertensive rat with an increase in blood pressure.
The spontaneously hypertensive rat (SHR) exhibits alterations in the renin-angiotensin-aldosterone system which are similar to those that characterize patients with "nonmodulating" hypertension, a common and highly heritable form of essential hypertension. Accordingly, we determined whether the inheritance of a DNA restriction fragment length polymorphism (RFLP) marking the renin gene of the SHR was associated with greater blood pressure than inheritance of a RFLP marking the renin gene of a normotensive control rat. In an F2 population derived from inbred SHR and inbred normotensive Lewis rats, we found the blood pressure in rats that inherited a single SHR renin allele to be significantly greater than that in rats that inherited only the Lewis renin allele. To the extent that the SHR provides a suitable model of "nonmodulating" hypertension, these findings raise the possibility that a structural alteration in the renin gene, or a closely linked gene, may be a pathogenetic determinant of increased blood pressure in one of the most common forms of essential hypertension in humans.
Kurtz
T W
TW
Department of Laboratory Medicine, University of California, San Francisco 94143.
Simonet
L
L
Kabra
P M
PM
Wolfe
S
S
Chan
L
L
Hjelle
B L
BL
D000483:Alleles; D000595:Amino Acid Sequence; D000818:Animals; D001794:Blood Pressure; D005260:Female; D006973:Hypertension / Q000209:etiology* / Q000235:genetics; D008297:Male; D012150:Polymorphism, Restriction Fragment Length; D051381:Rats; D011917:Rats, Inbred Lew; D011918:Rats, Inbred SHR; D012083:Renin / Q000235:genetics*
D012083:Renin