z-logo
Premium
Leptin activates rat carotid body Type I cells and brainstem astroglial cells
Author(s) -
Mariephtali,
Kasymov Vitaliy,
Mohamed-Ali Vidya,
Kasparov Sergey,
Gourine Alexander V
Publication year - 2012
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.26.1_supplement.1128.4
Subject(s) - carotid body , leptin , brainstem , medicine , endocrinology , blood pressure , leptin receptor , receptor , optogenetics , sympathetic nervous system , chemistry , biology , obesity , neuroscience , electrophysiology
Obesity is strongly associated with significant increases in muscle vasoconstrictor sympathetic activity which may contribute to the development of obesity‐related hypertension. Sympathetic tone and blood pressure can be reflexly increased by activation of peripheral chemoreceptors in the Carotid Bodies. Similarly, we have recently shown that optogenetic activation of ventral medullary astrocytes results in sympathoexcitation and increases in blood pressure. Leptin and leptin receptors have been recently found to be expressed both in Carotid Body Type I cells and in astroglial cells. Here, we explored whether these receptors are functional and whether leptin is capable of triggering activation of Carotid Body Type I cells and brainstem astroglial cells in vitro. RESULTS In Carotid Body dissociated cultures and primary cultured brainstem astrocytes loaded with Ca 2+ indicator Fura‐2, application of recombinant rat leptin evoked dose‐dependent increase in [Ca 2+ ] i . The responses had long latency (approximately 500 sec.) and [Ca 2+ ] i oscillations were sustained for prolonged periods. CONCLUSIONS These data suggest that sustained high levels of circulating leptin in obesity have the potential to activate Carotid Body Type I cells and brainstem astroglial cells, leading to increases in sympathetic tone and blood pressure.

This content is not available in your region!

Continue researching here.

Having issues? You can contact us here