Hypertension, Vol 21, 204-209, Copyright © 1993 by American Heart Association
CJ Clark, G Milligan, AR McLellan and JM Connell
We compared guanine nucleotide regulatory protein (G protein) levels and
function in plasma membranes from resistance vessels (mesenteric arteries)
isolated from spontaneously hypertensive (SHR) and normotensive Wistar
rats. G protein function was deduced from studies of adenylate cyclase
activity. Although the basal level of adenylate cyclase activity (+/- Mn2+
ions) was significantly greater in SHR membranes, addition of agents that
function via the stimulatory G protein--i.e., NaF (10(-2) M),
(-)-isoproterenol (10(-4) M), and prostaglandin E1 (10(-5) M)--resulted in
a significantly lower stimulatory response in SHR membranes. Ligands that
function via the inhibitory G protein--i.e., adrenaline (10(-5)
M)/propranolol (10(-5) M) (this combination being equivalent to an alpha
2-receptor agonist), carbachol (10(-3) M), and serotonin (10(-5) M)--were
responsible for only slight inhibitory responses in both SHR and Wistar rat
membranes, which were not significantly different. Western blotting
identified the presence of Gs, Gi2, and Gi3 alpha-subunits in rat vascular
smooth muscle, but there were no differences in the levels of these G
protein alpha-subunits found in SHR and Wistar rat plasma membranes. The
levels of the beta-subunit in the two sets of membranes were also similar.
In conclusion, there is a reduced response in adenylate cyclase activity to
agents that function via the stimulatory G protein in SHR membranes.
However, this is not a consequence of altered levels of the different G
protein subunits.
ARTICLES
Guanine nucleotide regulatory proteins in the spontaneously hypertensive rat
MRC Blood Pressure Unit, Western Infirmary, Glasgow, Scotland, UK.
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