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Temporal Response of Na+/H+ exchanger 1(NHE1) Expression and Right Ventricular Hypertrophy in Rats Exposed to Chronic Hypoxia (CH)
Author(s) -
Pisarcik Sarah Elizabeth,
Shimoda Larissa A.
Publication year - 2006
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.20.4.a403-a
Subject(s) - ventricle , right ventricular hypertrophy , medicine , muscle hypertrophy , sodium–hydrogen antiporter , cardiology , ventricular hypertrophy , ventricular pressure , myocyte , left ventricular hypertrophy , chemistry , pulmonary hypertension , endocrinology , blood pressure , sodium , organic chemistry
CH causes pulmonary hypertension, which leads to right ventricular hypertrophy and failure. Increased activity of Na + /H + exchanger (NHE) via the specific isoform NHE1, a ubiquitously distributed membrane protein that plays a key role in regulating intracellular pH, is a primary factor mediating hypertropic responses of ventricular myocytes. There is evidence that increased NHE1 activity is required for left ventricular hypertrophy and failure in several models. However, little is known about the role of NHE1 in right ventricular hypertrophy during CH. In this study, we sought to determine whether the effects of CH on right ventricular physical aspects correlated with an increase in NHE1 expression. Adult, male Wistar rats were exposed to normoxia or CH (10% O 2 ) for 1, 3, 7, or 21 days. Under anesthesia, right ventricular pressure was measured via closed chest cardiac puncture with a needle tip pressure transducer. The hearts were then removed, right ventricle and left ventricle + septum weights measured, RNA isolated via Trizol extraction, and RT‐PCR performed using primers designed specifically for NHE1. With exposure to CH, we found a gradual increase in the mean right ventricular pressure. The right ventricle/left ventricle + septum weight ratio also increased significantly. Overall, expression of NHE1 increased in the right ventricles of rats exposed to CH, where as left ventricle tissue showed no significant change in NHE1 expression. From these results we conclude that exposure to CH caused a time‐dependent increase in right ventricular pressure and hypertrophy that was associated with an increase in NHE1 expression.