This study examined the
calcium dependency of contractions in arteries from rats made hypertensive by
aortic coarctation and in rats with genetic hypertensive (
stroke-prone spontaneously hypertensive rats). Mesenteric artery and aortic strips were suspended in tissue
baths for isometric force recording and contractions to two drugs were characterized: 1) a
phorbol ester, TPA (12-O-tetrade-canoylphorbol-13-
acetate), and 2) the
calcium channel agonist,
Bay K 8644. Thoracic aortae and mesenteric arteries from hypertensive rats were more sensitive to the contractile properties of the
protein kinase C activator TPA than comparable arteries from normotensive rats. In thoracic aortae from coarcted rats, the contractile activity of
Bay K 8644 was potentiated compared to normotensive values. In the presence of 19.2 mmol/L KCl, responses to
Bay K 8644 in thoracic aortae from normotensive rats were potentiated and did not differ from coarcted values. In contrast, contractions to
Bay K 8644 and TPA in abdominal aortae obtained below the coarctation were not different from normotensive values. Upon exposure to 26.2 mmol/L KCl, contractions to
Bay K 8644 in abdominal aortae were potentiated and those in aortae from coarcted rats did not differ from
sham values. Contractile responses to both drugs were blocked by
nifedipine and
verapamil and responses were attenuated in
calcium-free
solution. We conclude that
calcium channel function and its regulation by
protein kinase C contribute to altered vascular reactivity in
hypertension. Further, these abnormalities have a pressure dependency, because they did not occur in abdominal aortae from coarcted rats.