title: Dynamic Ca2+ signalling in rat arterial smooth muscle cells under the control of local renin-angiotensin system.
abstract: 1. 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. 2. On average in about 45 % of the vascular smooth muscle cells we found spontaneous Ca2+ waves and oscillations ( approximately 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. 3. 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. 4. 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). 5. Both angiotensin antagonists ([Sar1,Ile8]-angiotensin II and losartan) 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 approximately 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 maintenance of vascular tone.
authors.affiliation: Department of Pharmacology, Graduate School of Medicine, The University of Tokyo, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Asada
authors.forename: T
authors.initials: T
authors.lastname: Yamazawa
authors.forename: K
authors.initials: K
authors.lastname: Hirose
authors.forename: T
authors.initials: T
authors.lastname: Takasaka
authors.forename: M
authors.initials: M
authors.lastname: Iino
mesh_terms: D015059:1-Sarcosine-8-Isoleucine Angiotensin II / Q000494:pharmacology; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000814:Aniline Compounds; D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology; D001158:Arteries; D002118:Calcium / Q000378:metabolism; D020013:Calcium Signaling / Q000502:physiology*; D000252:Calcium-Transporting ATPases / Q000037:antagonists & inhibitors / Q000378:metabolism; D002216:Captopril / Q000494:pharmacology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D004963:Estrenes / Q000494:pharmacology; D005071:Evoked Potentials / Q000502:physiology; D005456:Fluorescent Dyes; D007211:Indoles / Q000494:pharmacology; D019808:Losartan / Q000494:pharmacology; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000166:cytology / Q000502:physiology*; D010507:Periodicity; D010726:Phosphodiesterase Inhibitors / Q000494:pharmacology; D011760:Pyrrolidinones / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D012084:Renin-Angiotensin System / Q000502:physiology*; D012519:Sarcoplasmic Reticulum / Q000201:enzymology; D013268:Stimulation, Chemical; D013623:Tail / Q000098:blood supply; D010738:Type C Phospholipases / Q000037:antagonists & inhibitors / Q000378:metabolism; D014661:Vasoconstriction / Q000502:physiology; D014966:Xanthenes
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D000814:Aniline Compounds; D000959:Antihypertensive Agents; D004791:Enzyme Inhibitors; D004963:Estrenes; D005456:Fluorescent Dyes; D007211:Indoles; D010726:Phosphodiesterase Inhibitors; D011760:Pyrrolidinones; D014966:Xanthenes; C060229:1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione; C059715:Fluo-3; D015059:1-Sarcosine-8-Isoleucine Angiotensin II; D002216:Captopril; D010738:Type C Phospholipases; D000252:Calcium-Transporting ATPases; D019808:Losartan; D002118:Calcium; C000543:cyclopiazonic acid