| Research Abstract |
1. We found that growth factors such as fetal calf serum, platelet-derived growth factor, epidermal growth factor, angiotensin II, endothelin-1, endothelin-2 and endothelin-3 were inducible of an enhanced increase of c-myc mRNA in vascular smooth muscle cells from spontaneously hypertensive rats as compared with that from Wistar-Kyoto rats. However, transforming growth factor-beta1 did not induce c-myc gene expression. Calcium antagonists such as nifedipine and diltiazem, were able to inhibit the enhanced c-myc gene expression and DNA synthesis induced by growth factors in vascular smooth muscle cells from spontaneously hypertensive rats.
2. We examined angiotensin II (ANGII) induced changes of inositol-1, 4, 5-triphosphate (Ins (1, 4, 5) P_3) in cultured vascular smooth muscle cells (VSMC) from spontaneously hypertensive rats (SHR) and Wistar Kyoto rats (WKY) using a specific protein binding assay system. We observed a rapid biphasic Ins (1, 4, 5) P_3 response peaked at 5 and 30 seconds after ANGII stimulation. At every period of time the Ins (1, 4, 5) P_3 level of SHR was two to five fold higher than that of WKY. Thus, the assay specific for Ins (1, 4, 5) P_3 revealed complex 1ms (1, 4, 5) P_3 response after ANGII stimulation and suggested a need for further studies on the Ins (1, 4, 5) P_3 metabolism following agonist stimulation in VSMC. The enhanced Ins (1, 4, 5) P_3 response in VSMC from SHR may contribute the enhanced expression of c-myc gene in VSMC from SHR.
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