Yukiko Nomura and Masahisa Asano*
Department of Pharmacology, Nagoya City University Medical School, Mizuho-cho,
Mizuho-ku, Nagoya 467-8601, Japan
* To whom correspondence and reprints requests should be addressed.
Abstract: The superficial buffer barrier function of the sarcoplasmic
reticulum (SR) during rest and that during stimulation with Bayﾊkﾊ8644,
an agonist of L-type Ca2+ channels, were compared in endothelium-denuded
strips of tail arteries from 13-week-old normotensive Wistar-Kyoto rats
(WKY) and spontaneously hypertensive rats (SHR), by measuring the effects
of cyclopiazonic acid (CPA) and thapsigargin that inhibit SR Ca2+-ATPase
and the effect of ryanodine that depletes SR Ca2+. The addition
of 10ﾊmM CPA induced a transient contraction
that was not significantly different between WKY and SHR. The CPA-induced
contraction was strongly inhibited by 100ﾊnM nifedipine and was abolished
by Ca2+-free solution in both strains. Thapsigargin (100ﾊnM)
or ryanodine (10ﾊmM) induced similar, small transient
contractions in the two strains. The addition of Bayﾊkﾊ8644 (1-100ﾊnM) almost
failed to induce a contraction in both WKY and SHR. When the strips were
preincubated with 10ﾊmM CPA, 100ﾊnM thapsigargin
or 10ﾊmM ryanodine, Bayﾊkﾊ8644 induced similar
concentration-dependent contractions in the two strains. The amount of Ca2+
stored in the SR, as estimated from the 20ﾊmM caffeine-induced contraction,
was not significantly different between WKY and SHR. Our results suggest
that the SR of rat tail arteries can buffer a large amount of Ca2+
that enters the cell during the rest and the Bayﾊkﾊ8644 stimulation, and
these functions are not altered in SHR.
Keywords: Superficial buffer barrier function, Sarcoplasmic reticulum
Ca2+-ATPase,
Ca2+ influx via L-type Ca2+ channels, Tail artery,
Spontaneously hypertensive rats (SHR)