1.
Prostacyclin elicits potent vasodilation and inhibition of platelet aggregation through binding to its membrane receptor. The impairment of
prostacyclin receptor activity is implicated in various human
cardiovascular diseases. We recently succeeded in molecular cloning of
cDNA for the mouse, rat, and human
prostacyclin receptors. 2. In the present study, we examined the
mRNA expression of the
prostacyclin receptor in various rat tissues, and further investigated its gene expression in the hypertrophied cardiac ventricles of
stroke-prone spontaneously hypertensive rats (SHRSP). 3. In rat tissues, a single
RNA band of approximately 3.7 kb was detected by northern blotting analysis using rat
prostacyclin receptor cDNA as a probe. In adult Wistar rats, abundant
mRNA expression was observed in the aorta, lung and spleen. Substantial amounts of transcript were expressed in the heart, pancreas, thymus and stomach. In contrast, no
mRNA expression was detected in the brain. 4. We further examined the
mRNA expression of the
prostacyclin receptor in the ventricles of 21 week old SHRSP. The ventricles of SHRSP showed remarkable
hypertrophy, compared with those of age-matched Wistar-Kyoto (WKY) rats. The expression of
prostacyclin receptor mRNA in the hypertrophied ventricles of SHRSP was almost equivalent to that in the ventricles of WKY. 5. The present study revealed the gene expression of the
prostacyclin receptor in various rat tissues, and further demonstrated the receptor
mRNA expression in hypertensive
cardiac hypertrophy. The present study will give a clue to investigate the clinical implication of
prostacyclin and its receptor.