December 1, 1997Journal of Hypertension
Role of calcium influx and intracellular calcium stores in angiotensin II-mediated calcium hyper-responsiveness in smooth muscle from spontaneously hypertensive rats
Population
Primary cultured unpassaged vascular smooth muscle cells from mesenteric arteries of spontaneously…
Comparison
Angiotensin II stimulation, with or without… vs Cells from normotensive Wistar and Wistar-Kyoto…
Design
Preclinical
Authors
Discussion
Loading...
Member takes
Implication
Supports mechanistic studies of calcium handling in genetic hypertension models; leaves open human translation.
Structured PICO
P
Population
Primary cultured unpassaged vascular smooth muscle cells from mesenteric arteries of spontaneously hypertensive rats (SHR), Wistar and Wistar-Kyoto (WKY) rats aged 17 weeks
I
Intervention
Angiotensin II stimulation, with or without calcium channel antagonists (nitrendipine and diltiazem), extracellular Ca2+ depletion, or thapsigargin
C
Comparator
Cells from normotensive Wistar and Wistar-Kyoto (WKY) rats
O
Outcome
Cytosolic free Ca2+ concentration ([Ca2+]i) responses measured by fura-2 methodologysurrogate
In spontaneously hypertensive rats, elevated basal intracellular calcium may be partly due to increased calcium influx, while angiotensin II-induced hyper-responsiveness primarily depends on intracellular calcium mobilization.
Cite This Study
Touyz et al. (1997) studied this question.