Evidence for uneven distribution of l-type calcium channels in the
rat pulmonary circulation.
Walker, Benjimen R.
Department of Physiology, University of New Mexico, School of
Medicine, Albuquerque, NM 87131-5321
APStracts 2:0262H, 1995.
Experiments were performed on isolated, perfused rat lungs to
determine the segmental sites of vasoconstriction in response to
factors which open voltage sensitive, L-type calcium channels on
vascular smooth muscle cells. Lungs from male Sprague-Dawley rats
were perfused at constant flow with a physiological saline solution
(PSS) containing albumin. Measurements were made of pulmonary
arterial and venous pressure, while capillary pressure was estimated
by the double occlusion technique. Following equilibration, lungs
were constricted with depolarizing PSS containing high K+ (35 mM or
45 mM). With both stimuli, approximately 80% of the observed increase
in vascular resistance occurred on the arterial side of the
circulation. Both nifedipine and verapamil reversed this response,
however reversal was more consistent in the arterial segment. In
additional experiments, the L-type channel activator (-) BAY K 8644
caused increased resistance in the arterial, but not the venous
segment. Another group of lungs constricted with the thromboxane
mimetic U-46619 demonstrated equal arterial and venous
vasoconstriction. In U-46619 constricted lungs, nifedipine caused a
28% reversal of the agonist-induced increase in arterial resistance,
but was without effect on the venous circulation. These data suggest
that a greater density of L-type calcium channels may exist within
the arterial segment of the pulmonary circulation than in the veins.
Received 21 April 1995; accepted in final form 15 June 1995.
APS Manuscript Number H381-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 6 July 1995.