Y. Asada et al., Dynamic Ca2+ signalling in rat arterial smooth muscle cells under the control of local renin-angiotensin system, J PHYSL LON, 521(2), 1999, pp. 497-505
1. We visualized the changes in intracellular Ca2+ concentration ([Ca2+](i)
), using fluo-3 as an indicator, in individual smooth muscle cells within i
ntact rat tail artery preparations.
2. On average in about 45% of the vascular smooth muscle cells we found spo
ntaneous Ca2+ waves and oscillations (similar to 0.13 Hz), which we refer t
o here as Ca2+ ripples because the peak amplitude of [Ca2+](i) was about on
e-seventh of that of Ca2+ oscillations evoked by noradrenaline.
3. We also found another pattern of spontaneous Ca2+ transients often in gr
oups of two to three cells. They were rarely observed and are referred to a
s Ca2+ flashes because their peak amplitude was nearly twice as large as th
at in noradrenaline-evoked responses.
4. Sympathetic nerve activity was not considered responsible for the Ca2+ r
ipples, and they were abolished by inhibitors of either the Ca2+ pump in th
e sarcoplasmic reticulum (cyclopiazonic acid) or phospholipase C (U-73122).
5. Both angiotensin antagonists ([Sar(1),Ile(8)]-angiotensin II and losarta
n) and an angiotensin converting enzyme inhibitor (captopril) inhibited the
Ca2+ ripples.
6. The extracellular Ca2+-dependent tension borne by unstimulated arterial
rings was reduced by the angiotensin antagonist by similar to 50%.
7. These results indicate that the Ca2+ ripples are generated via inositol
1,4,5-trisphosphate-induced Ca2+ release from the intracellular Ca2+ stores
in response to locally produced angiotensin II, which contributes to the m
aintenance of vascular tone.