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Regulation of Tyrosine Hydroxylase Gene Expression in the Rat Carotid Body by Hypoxia
Author(s) -
CzyzykKrzeska Maria F.,
Bayliss Douglas A.,
Lawson Edward E.,
Millhorn David E.
Publication year - 1992
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1992.tb11376.x
Subject(s) - carotid body , tyrosine hydroxylase , endocrinology , medicine , hypoxia (environmental) , adrenal medulla , superior cervical ganglion , biology , in situ hybridization , adrenal gland , gene expression , glomus cell , tyrosine 3 monooxygenase , medulla , tyrosine , messenger rna , hypercapnia , catecholamine , chemistry , gene , stimulation , dopamine , biochemistry , organic chemistry , oxygen , acidosis
The activity (V max ) of tyrosine hydroxylase (TH; EC 1.14.16.2), the rate limiting enzyme in the synthesis of catecholamines, is increased in carotid body, superior cervical ganglion, and the adrenal medulla during hypoxia (i.e., reduced P a o 2 ). The present study was undertaken to determine if the increase in TH activity in these tissues during hypoxia is regulated at the level of TH mRNA. Adult rats were exposed to hypoxia (10% O 2 ) or room air for periods lasting from 1 to 48 h. The carotid bodies, superior cervical ganglia, and adrenals were removed and processed for in situ hybridization using 35 S‐labeled oligonucleotide probes. The concentration of TH mRNA was increased by hypoxia at all time points in carotid body type I cells, but not in cells of either superior cervical ganglion or adrenal medulla. The increase in TH mRNA in carotid body during hypoxia did not require innervation of the carotid body or intact adrenal glands. In addition, hypercapnia, another physiological stimulus of carotid body activity, failed to induce an increase in TH mRNA in type I cells. Our findings suggest that hypoxia stimulates TH gene expression in the carotid body by a mechanism that is intrinsic to type I cells.