Journal of Applied Physiology AJP: Renal Physiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

J Appl Physiol 76: 1098-1105, 1994;
8750-7587/94 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
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 Vanelli, G.
Right arrow Articles by Hussain, S. N.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Vanelli, G.
Right arrow Articles by Hussain, S. N.

Journal of Applied Physiology, Vol 76, Issue 3 1098-1105, Copyright © 1994 by American Physiological Society

ARTICLES

Contribution of potassium channels to active hyperemia of the canine diaphragm

G. Vanelli, H. Y. Chang, A. G. Gatensby and S. N. Hussain
Division of Critical Care, Royal Victoria Hospital, Montreal, Quebec, Canada.

Glibenclamide, iberiotoxin, and apamin (blockers of ATP-sensitive, large-conductance, and small-conductance Ca(2+)-activated K+ channels, respectively) were infused into the diaphragmatic vasculature of anesthetized indomethacin-treated dogs to assess the contribution of K+ channels to active hyperemia. Diaphragmatic blood flow (Qphr) and O2 uptake (VO2di) were measured at rest and during 2 min of continuous left phrenic nerve stimulation at 0.5, 1, 2, and 4 Hz. These measurements were repeated before (control) and after the infusion of a selective K+ channel blocker in three groups of animals. Glibenclamide at 10(-5) M significantly attenuated Qphr at rest and in response to all stimulation frequencies. Whereas resting VO2di remained unchanged, glibenclamide infusion significantly reduced VO2di in response to all stimulation frequencies. The slope of the linear relationship between Qphr and VO2di, however, was not affected by glibenclamide. By comparison, infusion of iberiotoxin (10(-7) M) in a second group reduced Qphr at rest and in response to 0.5- and 1-Hz stimulation, whereas Qphr measured in response to 2- and 4-Hz stimulation remained similar to control values. Apamin (10(-6) M) infusion in a third group reduced only resting Qphr with no effect on active hyperemia during phrenic nerve stimulation. Neither iberiotoxin nor apamin influenced resting or stimulated VO2di. In all groups diaphragmatic tension measured after the infusion of K+ channel blockers remained similar to control values. These results indicate that K+ channels, especially those sensitive to glibenclamide, modulate the increase in Qphr and VO2di in response to moderate augmentation of metabolic demands.


This article has been cited by other articles:


Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
D. J. Duncker, H. H. Oei, F. Hu, R. Stubenitsky, and P. D. Verdouw
Role of KATP+ channels in regulation of systemic, pulmonary, and coronary vasomotor tone in exercising swine
Am J Physiol Heart Circ Physiol, January 1, 2001; 280(1): H22 - H33.
[Abstract] [Full Text] [PDF]

Home page
 HypertensionHome page
W. F. Jackson
Ion Channels and Vascular Tone
Hypertension, January 1, 2000; 35(1): 173 - 178.
[Abstract] [Full Text] [PDF]


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