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Prevertebral sympathetic ganglion neurons projecting to mesenteric veins are less responsive to exogenous glucocorticoid in DOCA‐salt hypertension
Author(s) -
Shah Amit,
Houchin Timothy,
Kreulen David
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.695.18
Subject(s) - hyperpolarization (physics) , mesenteric arteries , medicine , endocrinology , anatomy , ganglion , vein , adrenergic neurons , artery , chemistry , adrenergic , receptor , organic chemistry , nuclear magnetic resonance spectroscopy
The superior mesenteric ganglion (SMG) contains sympathetic postganglionic neurons that innervate the blood vessels of the small intestine. In hypertension (HT), capacitance in veins may be reduced, resulting in a shift in blood volume to less compliant arteries. We investigated the properties of neurons of the SMG that project to mesenteric arteries or veins and compared these properties in intact ganglia from adult normotensive (NT) and DOCA‐salt HT rats. We inoculated segments of mesenteric veins and arteries with pseudorabies‐viral constructs that resulted in expression of fluorescent proteins in the somata. Intracellular recordings of identified vein and artery neurons revealed resting membrane potentials of −43 and −47 mV (n=19 and 13), cell input resistances of 63 and 76 MΩ, and membrane time constants of 12 and 13 ms. These properties were not significantly different between NT and HT rats (n=98 neurons total). Application of the glucocorticoid, hydrocortisone 21‐hemisuccinate (100 μM), resulted in a 5mV hyperpolarization (n=7) in artery neurons from NT and HT rats, and in vein neurons from NT rats. When applied during recording of vein neurons from HT rats, however, the amplitude of this hyperpolarization was reduced to 1mV (n=9) P=0.0005. This result suggests that neurons projecting to mesenteric veins are differentially modulated in DOCA‐salt HT.