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Chronic intermittent hypoxia decreases the levels of corticotropin‐releasing hormone receptor 2 in the nucleus of the solitary tract in rats
Author(s) -
Wang Lei,
Mifflin Steve
Publication year - 2017
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.31.1_supplement.841.15
Subject(s) - endocrinology , medicine , corticotropin releasing hormone , receptor , solitary tract , hormone , hypoxia (environmental) , in situ hybridization , chemistry , messenger rna , biochemistry , organic chemistry , oxygen , gene
Corticotropin‐releasing hormone (CRH) has been suggested to play a role in the nucleus of the solitary tract (NTS) to regulate sympathetic activity and cardiovascular function but the distribution of CRH receptors in the NTS is not fully understood. In this study, we used RNAscope in situ hybridization and CD IGS rats to examine the mRNA levels of CRH receptor type 1 (CRHR1) and CRH receptor type 2 (CRHR2) in regions of the NTS (13.68 mm – 14.76 mm caudal to bregma) implicated in the regulation of sympathetic and cardiovascular function. The results showed that both CRHR1 and CRHR2 were expressed in the NTS. In general, there was higher mRNA levels of CRHR2 compared to CRHR1 in the NTS with CRHR2 being 319% ± 69% greater than CRHR1. The higher levels of CRHR2 compared to CRHR1 was mainly observed in the middle portion of the NTS we examined (13.8 mm – 14.28 mm caudal to bregma). We investigated whether CRHR1 and CRHR2 levels were influenced by chronic intermittent hypoxia (CIH), a model of sleep apnea associated with sympathetic excitation and hypertension in rats. We found that CIH did not affect the mRNA levels of CRHR1 but significantly decreased the mRNA levels of CRHR2 in the NTS by 34% ± 14%. These results demonstrate that both CRHR1 and CRHR2 mRNAs are expressed in the NTS and suggest that dys‐regulation of CRHR2 may contribute to CIH‐induced hypertension. Support or Funding Information NIH HL088052