ABSTRACT: Recent data suggest that AT2 receptors in smooth muscle cells (VSMCs) of adult vessels may counterbalance AT1 receptor activity by inhibiting cell growth. The role of AT2 receptors in VSMC proliferation was investigated by using an in vitro organ culture model in which the sprouting of tubular structures was assessed. In preparations with endothelium, tubular growth was unaffected by angiotensin II (Ang II) but was inhibited by 50 ±9% by losartan and was increased by 110 ±15% by the AT2 antagonist PD123177. In endothelium-deprived preparations, growth inhibition (−49.1 ±0.5%) was observed when angiotensin II was added together with losartan 1uM, whereas stimulation (59.8 ± 14%) was induced by angiotensin II with 1uM PD123177. In cultured VSMCs angiotensin II slightly promoted growth that was inhibited by losartan but was unaffected by PD123177. AT1a, AT1b, and AT2 mRNA expression was demonstrated in cells isolated from tubular structures grown from intact and endothelium-deprived rings, but only AT1a and AT1b mRNA was detected in cultured VSMCs. In conclusion, this paper proposes an in vitro organ culture model in which the expression of AT2 receptors in VSMCs is preserved and demonstrates AT2 receptor-mediated inhibition of VSMC proliferation in adult vessels.

Inhibition of vascular smooth muscle cell growth by angiotensin type 2 receptor stimulation in an in vitro organ culture model / L. BROGELLI; A. PARENTI; FABRIZIO LEDDA. - In: JOURNAL OF CARDIOVASCULAR PHARMACOLOGY. - ISSN 0160-2446. - STAMPA. - 39(5):(2002), pp. 739-745.

Inhibition of vascular smooth muscle cell growth by angiotensin type 2 receptor stimulation in an in vitro organ culture model

PARENTI, ASTRID;LEDDA, FABRIZIO
2002

Abstract

ABSTRACT: Recent data suggest that AT2 receptors in smooth muscle cells (VSMCs) of adult vessels may counterbalance AT1 receptor activity by inhibiting cell growth. The role of AT2 receptors in VSMC proliferation was investigated by using an in vitro organ culture model in which the sprouting of tubular structures was assessed. In preparations with endothelium, tubular growth was unaffected by angiotensin II (Ang II) but was inhibited by 50 ±9% by losartan and was increased by 110 ±15% by the AT2 antagonist PD123177. In endothelium-deprived preparations, growth inhibition (−49.1 ±0.5%) was observed when angiotensin II was added together with losartan 1uM, whereas stimulation (59.8 ± 14%) was induced by angiotensin II with 1uM PD123177. In cultured VSMCs angiotensin II slightly promoted growth that was inhibited by losartan but was unaffected by PD123177. AT1a, AT1b, and AT2 mRNA expression was demonstrated in cells isolated from tubular structures grown from intact and endothelium-deprived rings, but only AT1a and AT1b mRNA was detected in cultured VSMCs. In conclusion, this paper proposes an in vitro organ culture model in which the expression of AT2 receptors in VSMCs is preserved and demonstrates AT2 receptor-mediated inhibition of VSMC proliferation in adult vessels.
2002
39(5)
739
745
L. BROGELLI; A. PARENTI; FABRIZIO LEDDA
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Utilizza questo identificatore per citare o creare un link a questa risorsa: https://hdl.handle.net/2158/311749
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