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Acute leptin evokes physiological responses in rat carotid body type I cells (873.4)
Author(s) -
Pye Richard,
Ricker Ellen,
Jurcsisn Jennifer,
Barr Barbara,
Wyatt Christopher
Publication year - 2014
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.28.1_supplement.873.4
Subject(s) - leptin , carotid body , medicine , endocrinology , leptin receptor , chemistry , receptor , calcium , glomus cell , biology , obesity , electrophysiology
Leptin is a central stimulant of respiration and also contributes to obesity related sympathoactivation. Recently leptin receptors have been identified on type I cells from the carotid body. Our most recent data indicate that activation of these receptors with leptin initiates calcium signaling events and increases outward macroscopic currents in isolated type I cells. The acute (10 min) application of leptin (200 ng.ml ‐1 ) evoked calcium signaling responses in isolated type I cells. Cells significantly increased their Fura 2 F 340 /F 380 ratio by 0.09 ± 0.015 ratio units (n =24, P < 0.001). Leptin also increased the peak membrane currents in a subset (65 % ) of type I cells. At +10mV leptin (200ng.ml ‐1 ) increased peak macroscopic currents from 123 ± 19 pA.pF ‐1 to 198 ± 28 pA.pF ‐1 (n = 6, P < 0.02). The remaining 35% of type I cells were unresponsive to this concentration of leptin. Interestingly, leptin does not alter the rate of oxidative phosphorylation in isolated type I cells as measured by reduction of C 12 ‐resazurin to C 12‐ resorufin. These data suggest that changes in leptin signaling may potentially influence carotid body function at the level of the type I cell. Given the involvement of the carotid bodies in the control of breathing and sympathetic tone, this finding may be especially pertinent to obesity related pathologies such as obesity hypoventilation syndrome and essential hypertension. Grant Funding Source : Supported by NIH‐1RO1HL091836 & NIH‐ 1S10RR025075‐01