Hypertension, Vol 21, 195-203, Copyright © 1993 by American Heart Association
S Orlov, TJ Resink, J Bernhardt, F Ferracin and FR Buhler
This study examined 45Ca uptake, 45Ca efflux, and the distribution of
exchangeable 45Ca in confluent, quiescent cultures of aortic smooth muscle
cells (VSMCs) from normotensive Wistar-Kyoto (WKY) rats and spontaneously
hypertensive rats (SHRs). These parameters were investigated under basal
conditions and after addition of angiotensin II (Ang II) and low (LDL) and
high (HDL) density lipoproteins. Basal 45Ca uptake was approximately 50%
greater in VSMCs from SHRs (p < 0.005 versus WKY). Calcium antagonists
(diltiazem or nifedipine) abolished this difference. The 45Ca uptake
response to Ang II was approximately twofold greater in SHR than in WKY
VSMCs (p < 0.05), and Ang II-induced increments of 45Ca uptake were
weakly inhibited (by approximately 15- 25%) by calcium antagonists.
Lipoproteins also stimulated 45Ca uptake in VSMCs, and the apparent
affinity of this process was approximately fivefold greater for LDL than
for HDL. Calcium antagonists did not inhibit either LDL- or HDL-induced
45Ca uptake. SHR and WKY VSMCs did not differ with respect to 45Ca uptake
induced by either LDL or HDL. The initial size of the slowly exchangeable
pool of intracellular Ca2+ was approximately 35% greater in SHR VSMCs (p
< 0.05 versus WKY). Ang II-induced mobilization of intracellular calcium
(measured as the decrease in 45Ca content of the slowly exchangeable pool)
was threefold greater in SHR VSMCs (p < 0.005 versus WKY). LDL and HDL
marginally stimulated 45Ca efflux from this pool (< or = 20% above
control) and to comparable extents in both SHR and WKY VSMCs.(ABSTRACT
TRUNCATED AT 250 WORDS)
ARTICLES
Vascular smooth muscle cell calcium fluxes. Regulation by angiotensin II and lipoproteins
Department of Research, Basel University Hospital, Switzerland.
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