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1 Research Institute, 2 Department of Medicine, and 3 Department of Pathology, National Cardiovascular Center, Suita, Osaka 565; and 4 Division of Hypertension and Cardiorenal Disease, Dokkyo University Medical School of Medicine, Mibu, Tochigi 321-0293, Japan
In the present study we investigated
the form of expression, action, second messenger, and the cellular
location of urocortin, a member of the corticotropin-releasing factor
(CRF) family, in the heart. Urocortin mRNA, as shown by quantitative
RT-PCR analysis, is expressed in the cultured rat cardiac nonmyocytes
(NMC) as well as myocytes (MC) in the heart, whereas CRF receptor type 2
(CRF-R2), presumed urocortin receptor mRNA, is predominantly expressed in MC compared with NMC. Urocortin mRNA expression is higher
in left ventricular (LV) hypertrophy than in normal LV, whereas
CRF-R2 mRNA expression is markedly depressed in LV hypertrophy compared with normal LV. Urocortin more potently increased the cAMP
levels in both MC and NMC than did CRF, and its effect was more potent
in MC than in NMC. Urocortin significantly increased protein synthesis
by [14C]Phe incorporations and atrial natriuretic peptide
secretion in MC and collagen and increased DNA synthesis by
[3H]prolin and [3H]Thy incorporations in
NMC. An immunohistochemical study revealed that urocortin
immunoreactivity was observed in MC in the normal human heart and that
it was more intense in the MC of the human failing heart than in MC of
the normal heart. These results, together with the recent evidence of
urocortin for positive inotropic action, suggest that increased
urocortin in the diseased heart may modulate the pathophysiology of
cardiac hypertrophy or failing heart, at least in part, via cAMP
signaling pathway.
heart failure; myocytes; hypertrophy; natriuretic peptides
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