Abstract
Angiotensin II (Ang II), the primary effector of the renin-angiotensin system, is a multifunctional hormone that plays an important role in vascular function. In addition to its classical vasoconstrictor action, more recent studies demonstrated thatAng II stimulates the growth of a number of cell types, including vascular smooth muscle cells (SMC) (reviewed in [1–3]). In vivo studies have shown that chronic infusion of Ang II leads to the development of vascular hypertrophy in rats, whereas administration of angiotensin-converting enzyme (ACE) inhibitors or Ang II receptor antagonists prevents or regresses vascular hypertrophy in models of genetic and experimental hypertension [4]. Consistent with in vivo data, several laboratories have shown that Ang II stimulates protein synthesis and induces cellular hypertrophy, but not cell proliferation, in cultured aortic SMC [5–9]. Ang II also induces directed migration (chemotaxis) of vascular SMC [10, 11], although its effect is less prominent than that of platelet-derived growth factor (PDGF). The cellular mechanisms underlying these diverse actions of Ang II are not clearly understood but are likely to involve the activation of distinct signaling pathways. (Mol Cell Biochem 212: 99–109, 2000)
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Meloche, S., Pelletier, S., Servant, M.J. (2000). Functional cross-talk between the cyclic AMP and Jak/STAT signaling pathways in vascular smooth muscle cells. In: Rupp, H., Maisch, B. (eds) Control of Gene Expression by Catecholamines and the Renin-Angiotensin System. Developments in Molecular and Cellular Biochemistry, vol 33. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-4351-0_12
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