Hypertension, Vol 19, 446-455, Copyright © 1992 by American Heart Association
T Osanai and MJ Dunn
We tested the hypothesis that increased systemic vascular resistance in
spontaneously hypertensive rats may be secondary to enhanced phospholipase
C activity in response to vasoconstrictor stimuli. Activation of
phospholipase C by angiotensin II (Ang II), thromboxane A2, arginine
vasopressin, and endothelin-1 was compared in cultured glomerular mesangial
cells and mesenteric vascular smooth muscle cells taken from 13- to
14-week-old hypertensive and normotensive Wistar- Kyoto rats (blood
pressure, 185 +/- 1 versus 135 +/- 2 mm Hg). Phospholipase C was assessed
by measuring cytosolic free calcium and by the accumulation of radiolabeled
inositol phosphates. Basal cytosolic calcium did not differ between
mesangial cells taken from both strains but was greater in smooth muscle
cells from hypertensive rats (210.1 +/- 8.2 versus 149.2 +/- 4.7 nM). The
responsiveness of cytosolic calcium and inositol phosphate accumulation to
Ang II was significantly enhanced in mesangial cells from hypertensive rats
(10(-7) M Ang II: peak increase of calcium, 1,266 +/- 181 versus 603 +/- 93
nM; percent increment of inositol phosphates at 1 minute, 266 +/- 26 versus
98 +/- 10%). Vascular smooth muscle cells from hypertensive rats, when
compared with normotensive rats, showed a similar augmentation of Ang
II-stimulated intracellular calcium and inositol phosphates. Thromboxane
A2-induced enhancement of intracellular calcium and inositol phosphate
accumulation in vascular smooth muscle cells was also greater in
hypertensive animals. However, the responses to vasopressin and endothelin
in mesangial or vascular smooth muscle cells did not differ between the
normotensive and hypertensive animals. There was no significant difference
in Ang II receptor number and affinity between hypertensive- and
normotensive-derived mesangial cells. We conclude that genetically
increased blood pressure in rats may be secondary to enhanced post-receptor
signaling in glomerular mesangial cells activated by Ang II and to enhanced
signaling in vascular smooth muscle cells stimulated by either Ang II or
thromboxane A2.
ARTICLES
Phospholipase C responses in cells from spontaneously hypertensive rats
Department of Medicine, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106.
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