Am J Physiol Cell Physiol Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Cell Physiol 257: C122-C128, 1989;
0363-6143/89 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Rembold, C. M.
Right arrow Articles by Murphy, R. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Rembold, C. M.
Right arrow Articles by Murphy, R. A.

AJP - Cell Physiology, Vol 257, Issue 1 C122-C128, Copyright © 1989 by American Physiological Society

ARTICLES

Histamine concentration and Ca2+ mobilization in arterial smooth muscle

C. M. Rembold and R. A. Murphy
Department of Medicine, University of Virginia Health Sciences Center, Charlottesville 22908.

Smooth muscle contraction is dependent on Ca2+ entry from the extracellular space or release from intracellular stores. The sensitivity of these Ca2+ sources to agonist concentration was evaluated by measuring myoplasmic [Ca2+] (as estimated by aequorin), myosin phosphorylation, and isometric stress in the swine carotid media. High histamine concentrations produced transient elevations in [Ca2+] and phosphorylation with rapid generation of near maximal stress. Lower histamine concentrations produced much smaller [Ca2+] and phosphorylation transients, and stress development was slower. Peak [Ca2+] was proportional to the rate of stress development. Steady-state [Ca2+], phosphorylation, and stress values (which are dependent on extracellular Ca2+) were more sensitive to histamine concentration than was the peak [Ca2+] response both in the presence and absence of extracellular CaCl2 (measures of intracellular Ca2+ release). This result suggests that the mechanism for Ca2+ influx from the extracellular space is more sensitive to histamine than intracellular Ca2+ release. These results are also consistent with the hypothesis that agonist-releasable sarcoplasmic reticular Ca2+ is the major contributor to initial phosphorylation transients that enhance the rate of stress development.


This article has been cited by other articles:


Home page
 Am. J. Physiol. Cell Physiol.Home page
R. Wang, Q. Li, and D. D. Tang
Role of vimentin in smooth muscle force development
Am J Physiol Cell Physiol, September 1, 2006; 291(3): C483 - C489.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
D. D. Tang and J. Tan
Downregulation of profilin with antisense oligodeoxynucleotides inhibits force development during stimulation of smooth muscle
Am J Physiol Heart Circ Physiol, October 1, 2003; 285(4): H1528 - H1536.
[Abstract] [Full Text] [PDF]

Home page
 HypertensionHome page
H. Xie, I. Laher, and J. A. Bevan
Intracellular Ca2+ Release in Flow-Induced Contraction of Venous Smooth Muscle
Hypertension, December 1, 1995; 26(6): 1051 - 1055.
[Abstract] [Full Text]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online