Evidence for uneven distribution of L-type calcium channels in rat pulmonary circulation.
Experiments were performed on isolated, perfused rat lungs to determine the segmental sites of vasoconstriction in response to factors that 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, whereas capillary pressure was estimated by the double-occlusion technique. After equilibration, lungs were constricted with depolarizing PSS containing high K+ (35 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.
Walker
B R
BR
Department of Physiology, University of New Mexico School of Medicine, Albuquerque 87131-5321, USA.
D019796:15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid; D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester / Q000494:pharmacology; D000818:Animals; D001808:Blood Vessels / Q000378:metabolism; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000378:metabolism*; D066298:In Vitro Techniques; D008297:Male; D009543:Nifedipine / Q000494:pharmacology; D011188:Potassium / Q000494:pharmacology; D011450:Prostaglandin Endoperoxides, Synthetic / Q000494:pharmacology; D011652:Pulmonary Circulation / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D013928:Thromboxane A2 / Q000031:analogs & derivatives / Q000494:pharmacology; D014018:Tissue Distribution; D014661:Vasoconstriction; D014662:Vasoconstrictor Agents / Q000494:pharmacology
D002121:Calcium Channel Blockers; D015220:Calcium Channels; D011450:Prostaglandin Endoperoxides, Synthetic; D014662:Vasoconstrictor Agents; D013928:Thromboxane A2; D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; D019796:15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid; D009543:Nifedipine; D011188:Potassium