[Absence of point mutation in the third intracellular loop of alpha 1B- and alpha 1D adrenergic receptor in the aortae of spontaneously hypertensive rats].

ABSTRACT

Our previous experiments showed that the basal level of inositol phosphates (IPs) accumulation in the aorta was higher in spontaneously hypertensive rats (SHR) than in WKY rats. According to the constitutive activity hypothesis for G-protein coupling receptors, we inferred that point mutations might possibly exsit in the third intracellular loop of alpha 1B- and/or alpha 1D-adrenergic receptor (AR), the main subtypes of alpha 1-AR mediating phosphatidylinositol hydrolysis in SHR aortae. This inference, however, was not demonstrated by the results of our PCR-SSCP analyses, which indicated that the increased basal level of IPs accumulation in the isolated aortae from SHR does not result from constitutive activity of alpha 1B- and alpha 1D-AR induced by point mutations of the third intracellular loop of the genes.