Effect of intracellular ph on ferret pulmonary arterial smooth
muscle cell calcium homeostasis and pressure.
Farrukh, Imad S., John R. Hoidal, and William H. Barry.
Division of Respiratory, Critical Care and Occupational Medicine
and Division of Cardiology, Departments of Internal Medicine, the
Veterans Affairs Medical Center and the University of Utah Health
Science Center, Salt Lake City, Utah.
APStracts 2:0409A, 1995.
In this study we investigated the role of Na+/H+ antiport in
regulating cytosol pH (pHi) in isolated and cultured ferret pulmonary
artery smooth muscle cells (PSMC). We also studied the effects of
modulating pHi on cytosol calcium ([Ca++]i) in PSMC and on the
pulmonary arterial pressure (PPA) of isolated ferret lungs. PHi was
modulated by the NH4Cl washout method. To eliminate the contribution
of Cl-/HCO3- exchangers the PSMC and isolated lungs were perfused in
HCO3--free buffer. Blocking the Na+/H+ antiporter decreased baseline
pHi and prevented the recovery from NH4Cl washout-induced
intracellular acidosis. Intracellular alkalinization caused an
initial transient increase in both [Ca++]i and PPA that were
dependent on extracellular Ca++ ([Ca++]o) entry. Maintaining cytosol
alkalinization caused another increase in PPA that was not associated
with an increase with [Ca++]i. Intracellular acidosis also caused an
increase in [Ca++]i and PPA. The cytosol acidosis-induced increase in
[Ca++]i and PPA were mediated by both [Ca++]o influx and release of
stored [Ca++]i. Cytosol acidosis also appears to have direct effect
on the smooth muscle contractile elements. Both cytosol alkalosis and
acidosis increased vascular reactivity.
Received 19 April 1995; accepted in final form 13 September 1995.
APS Manuscript Number A427-5.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 31 October 95