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aDepartment of Preclinical and Clinical Pharmacology and bDepartment of Anatomy, Histology & Forensic Medicine, University of Florence, Florence, Italy
Address for correspondence: Prof. Daniele Bani, Department of Anatomy, Histology and Forensic Medicine, Viale G. Pieraccini 6, I-50139, Florence, Italy. Voice: (+39) 0554271390; fax: (+39) 0554271385. daniele.bani{at}unifi.it
We tested the effects of relaxin on [Ca2+]i response to angiotensin II in smooth muscle (vSMC) and endothelial cells isolated from hypertensive (SHR) and normotensive (WKY) rats. Relaxin markedly reduced the [Ca2+]i response of vSMCs from WKY, but not from SHR rats. Western blots showed that cGMP-dependent protein kinase G was reduced in vSMCs from SHR as compared with WKY rats. Relaxin also blunted the [Ca2+]i response in endothelial cells from WKY, but not from SHR rats. However, in endothelial cells from SHR and WKY rats, protein kinase G was nearly unexpressed, thus accounting for an alternative pathway of the intracellular response to nitric oxide and relaxin. Hence, vSMCs and endothelial cells in SHR rats show a deficiency response to nitric oxide that may render them insensitive to relaxin.
Key Words: endothelial cells • smooth muscle cells • SHR • calcium • nitric oxide • protein kinase G
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