Effect of the Endothelium on the Response to Phorbol Ester in Smooth Muscle from Spontaneously Hypertensive Rats.
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Problem: The phorbol ester-induced contractile response of blood vessels from spontaneously hypertensive rats (SHR) is greater than that from normotensive Wistar-Kyoto rats (WKY), which suggests that protein kinase C activity is abnormally high in vascular smooth muscle from SHR. However, the role of the overlying endothelium in these responses has not been tested. Hypothesis: The response of vascular smooth muscle to protein kinase C activation is influenced by the presence of the endothelium. Methods: We examined the isotonic contraction of aortic rings (with or without endothelium) from 12-14-week-old SHR and WKY in response to KCl, norepinephrine, and the phorbol ester PDBu (with and without staurosporine). We also tested these responses in the presence of L-NMMA. Results: PDBu (1nM-1 mM) dose-dependently increased contractile force, with an EC50 of 100nM. Aortic rings from SHR were more sensitive than those from WKY at all doses tested. Removal of the endothelium abolished this difference: the sensitivity of aortic rings from WKY increased and the contractility of rings from SHR decreased. Preincubation with L-NMMA (10-5M) for 20min also abolished the difference in contractile response in the same fashion. The response to norepinephrine was increased by L-NMMA in both SHR and WKY. Conclusions: The difference between SHR and WKY in phorbol ester-induced contraction of aortic rings is due to a difference in endothelial cell function, rather than to a difference in vascular smooth muscle. We suggest that PKC may mediate the release from endothelial cells of a vasodilator, which may be nitric oxide. This effect may be abnormally weak in the endothelium of SHR. (Hypertens Res 1994; 17: 193-197)
- 日本高血圧学会の論文
日本高血圧学会 | 論文
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