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Role of L‐type calcium channels in acute alcohol intoxication‐induced enhancement of lymphatic calcium transient magnitude.
Author(s) -
SouzaSmith Flavia M.,
Breslin Jerome W.,
Molina Patricia
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.681.6
Subject(s) - nifedipine , chemistry , calcium , contraction (grammar) , voltage dependent calcium channel , medicine , lymphatic system , alcohol , endocrinology , anesthesia , pathology , biochemistry
We previously demonstrated that acute alcohol intoxication (AAI) increases the magnitude of Ca 2+ transients in pumping lymphatic vessels (LV). We tested whether sarcolemmal Ca 2+ entry or Ca 2+ release from the SR contribute to the AAI‐induced increase in Ca 2+ transient magnitude. AAI was produced by intragastric administration of 30% alcohol to conscious, unrestrained rats through surgically implanted catheters. Isovolumic administration of water (vehicle) served as control. Mesenteric LVs were isolated, cannulated and loaded with Fura‐2 AM to measure changes in intracellular Ca 2+ . Measurements were performed at a basal intraluminal pressure of 2 cm H 2 O and during pressure steps to 6 and 10 cm H 2 O. Nifedipine (ND‐10 −7 M) was used to block L‐type Ca 2+ channels and xestospongin C (XC‐10 −6 M) was used to inhibit SR Ca 2+ release. The results show that ND reduced Ca 2+ transient magnitude of LV from AAI and vehicle groups at all pressures studied, and also reduced contraction frequency (CF) of LV from the vehicle group. Treatment with XC did not significantly change any of the Ca 2+ parameters in either LVs from the AAI or vehicle group. These data suggest that L‐type Ca 2+ channels contribute to the AAI‐induced increase in lymphatic Ca 2+ transient magnitude. We speculate that alcohol may activate a nifedipine‐insensitive pathway to maintain CF.