HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Asada, Y. Articles by Iino, M. Search for Related Content PubMed PubMed Citation Articles by Asada, Y. Articles by Iino, M.

Dynamic Ca²⁺ signalling in rat arterial smooth muscle cells under the control of local renin-angiotensin system

Yukinori Asada *¹, Toshiko Yamazawa *, Kenzo Hirose *, Tomonori Takasaka ¹ and Masamitsu Iino *

We visualized the changes in intracellular Ca²⁺ concentration ([Ca²⁺]_i), using fluo-3 as an indicator, in individual smooth muscle cells within intact rat tail artery preparations.

On average in about 45 % of the vascular smooth muscle cells we found spontaneous Ca²⁺ waves and oscillations (~0·13 Hz), which we refer to here as Ca²⁺ ripples because the peak amplitude of [Ca²⁺]_i was about one-seventh of that of Ca²⁺ oscillations evoked by noradrenaline.

We also found another pattern of spontaneous Ca²⁺ transients often in groups of two to three cells. They were rarely observed and are referred to as Ca²⁺ flashes because their peak amplitude was nearly twice as large as that in noradrenaline-evoked responses.

Sympathetic nerve activity was not considered responsible for the Ca²⁺ ripples, and they were abolished by inhibitors of either the Ca²⁺ pump in the sarcoplasmic reticulum (cyclopiazonic acid) or phospholipase C (U-73122).

Both angiotensin antagonists ([Sar¹,Ile⁸]-angiotensin II and losartan) and an angiotensin converting enzyme inhibitor (captopril) inhibited the Ca²⁺ ripples.

The extracellular Ca²⁺-dependent tension borne by unstimulated arterial rings was reduced by the angiotensin antagonist by ~50 %.

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 maintenance of vascular tone.