Angiotensin II stimulates nitric oxide production in pulmonary artery endothelium via the type 2 receptor

Olson, Susan C.; Oeckler, Richard A.; Li, Xinmei; Du, Litong; Traganos, Frank; Zhao, Xiangmin; Burke-Wolin, T.

doi:10.1152/ajplung.00312.2003

Cited by 31 publications

(41 citation statements)

References 49 publications

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“…Recent reports indicate the presence of AT2R in coronary and pulmonary endothelial cells. 34,35 Also, aldosterone actions on human endothelial cells has been demonstrated, 36 making the endothelium another potential target of aldosterone-regulated AT2R expression.…”

Section: Discussionmentioning

confidence: 99%

High-Salt Diet Inhibits Expression of Angiotensin Type 2 Receptor in Resistance Arteries

et al. 2005

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Abstract-Recent studies suggested that type 2 angiotensin receptor (AT2R) could contribute to regulation of blood pressure and/or vascular remodeling. A key question relates to the effects of potential modulators of vascular AT2R expression. In the present work, we evaluated if high salt intake (70 mmol/L NaCl in drinking water) could modulate rat mesenteric artery AT2R function and expression. Angiotensin II dose-response curves were studied in rat perfused pressurized small-diameter arteries in the presence of losartan (AT1R antagonist Key Words: mineralocorticoid Ⅲ sodium Ⅲ hypertension Ⅲ vascular remodeling Ⅲ apoptosis T he renin-angiotensin-aldosterone system (RAAS) regulates vascular tone, body fluid volume, electrolyte balance, hormonal secretion, and neuronal activity. The biological effects of angiotensin II (Ang II), the main effector peptide in the vasculature, are mediated by at least 2 receptor isofoms. 1,2 The type 1 receptor (AT1R) mediates vasoconstriction, sympathetic facilitation, and trophic effects. The type 2 receptor (AT2R) is widely expressed during fetal development, whereas in the adult its expression has been detected in many different vessel types, including mesenteric, coronary, and renal arteries. 3-6 AT2R has opposite effects to those of AT1R, ie, it promotes cell apoptosis and inhibits cell proliferation. 6,7 AT2R also attenuates the pressor action of Ang II 8 and mediates vasodilation. 9,10 Recently, it has been shown that Ang II relaxes small mesenteric arteries via AT2R when AT1R are blocked. [11][12][13] Interestingly, the expression of AT2R is increased in several pathologic conditions such as vascular injury, 14 cardiac remodeling, congestive heart failure, and myocardial infarction. 15,16 It has been suggested that in adults the presence of AT2R in vascular tissues may be playing a role in vascular tone and/or tissue remodeling. [17][18][19] Therefore, a key and complex question that arises is how AT1R and AT2R expression are modulated. Several studies indicate interaction between Ang II and aldosterone, affecting the expression of ATRs. The expression of AT1R appears to be induced by Ang II in vascular smooth muscle, 4 and mineralocorticoids potentiate the action of Ang II in cultured rat vascular smooth muscle cells (VSMCs) by increasing the number of AT1R. 20,21 However, there are few data concerning the physiological regulation of AT2R expression. Dietary sodium depletion, which increases RAAS activity, enhances renal AT2 receptor function 10,22 and expression in both young and mature adult rats, mainly in the glomeruli and interstitial cells. 23 Induction of AT2R-mediated modulation of blood pressure was described in rats fed with a synthetic diet, an effect attributed to the stimulation of the RAAS. 8 Bonnet et al 24 have shown that Ang II infusion in the rat induces the expression of AT2R in the mesenteric vasculature. Nevertheless, it is not clear whether Ang II directly mediates the increased AT2R expression or if it is secondary to direct aldosterone action on arte...

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Section: Discussionmentioning

confidence: 99%

High-Salt Diet Inhibits Expression of Angiotensin Type 2 Receptor in Resistance Arteries

et al. 2005

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“…Aortic banding seems to induce up-regulation of the AT 2 receptor through increased circulating ANG II via the AT 1 receptor, thereby activating a vasodilatory pathway in vessels through the AT 2 receptor via the kinin/NO/cyclic GMP system. Olson et al (2004) found that ANG II stimulated an increase in NOS mRNA, protein expression, and NO production via AT 2 receptors, whereas signaling via the AT 1 receptor negatively regulated NO production in pulmonary endothelial cells. According to Zhao et al (2005), ANG II stimulates an increase in NOS mRNA levels, eNOS protein expression, and NO production via the AT 2 receptor, whereas ANG II seems to down-regulate eNOS protein expression via an AT 1 receptor-linked pathway involving the G ␣ q protein/phosphatidylinositol phospholipase C/Ca 2ϩ /protein kinase C-␣ signaling pathway in bovine pulmonary artery endothelial cells.…”

Section: Angiotensin-induced Endothelium-derived Relaxing Factomentioning

confidence: 95%

Interaction of Endothelial Nitric Oxide and Angiotensin in the Circulation

2007

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“…These results suggest that the relaxing factor induced by Ang II might be NO. NO production by AT 2 receptor activation on endothelial cells has also been reported in canine coronary arteries (Seyedi et al, 1995), rat aorta (Gohlke et al, 1998;Pueyo et al, 1998), rat skeletal muscle microcirculation (Nora et al, 1998), and porcine and rat pulmonary arteries (Hill-Kapturczak et al, 1999;Olson et al, 2004).…”

Section: Discussionmentioning

confidence: 86%

Role of angiotensin II receptor subtypes in porcine basilar artery: Functional, radioligand binding, and cell culture studies

et al. 2006

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We aimed to clarify responsiveness to angiotensin (Ang) II in the porcine basilar artery and the role of Ang II receptor subtypes by functional, radioligand binding, and cell culture studies. Ang II induced more potent contractions in the proximal part than in the distal part of isolated porcine basilar arteries. The contraction induced by Ang II was inhibited by the Ang II type 1 (AT 1 ) receptor antagonist losartan, but the Ang II type 2 (AT 2 ) receptor antagonist PD123319 enhanced it. After removal of the endothelium, the effect of losartan remained but the effect of PD123319 was abolished. The specific binding site of [ 3 H]Ang II on the smooth muscle membrane was inhibited by losartan, but not by PD123319. Stimulation of angiotensin II increased nitric oxide (NO) production in cultured basilar arterial endothelial cells. This production was inhibited by PD123319 and the NO synthase inhibitor L-N G -nitroarginine. These results suggest that the contraction induced by Ang II might be mediated via the activation of AT 1 receptors on the basilar arterial smooth muscle cells and be modulated via the activation of AT 2 receptors on the endothelial cells, followed by NO production.

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Angiotensin II stimulates nitric oxide production in pulmonary artery endothelium via the type 2 receptor

Cited by 31 publications

References 49 publications

High-Salt Diet Inhibits Expression of Angiotensin Type 2 Receptor in Resistance Arteries

High-Salt Diet Inhibits Expression of Angiotensin Type 2 Receptor in Resistance Arteries

Interaction of Endothelial Nitric Oxide and Angiotensin in the Circulation

Role of angiotensin II receptor subtypes in porcine basilar artery: Functional, radioligand binding, and cell culture studies

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