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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.
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Failli et al. (2005) studied this question.
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