Positive feedback regulation of angiotensin II-AT 1B receptor gene expression in rat adrenal glands

Wagner, Charlotte; Kurtz, Armin

doi:10.1007/s004240050639

Cited by 4 publications

(3 citation statements)

References 20 publications

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“…APJ are structurally related to angiotensin II receptors. 1,28 Apelin acts initially in a paracrine manner and subsequently in an autocrine fashion to stimulate APJ signaling in embryonic and tumor angiogenesis. 29 Our data suggest that apelin may enhance APJ receptor expression, like the angiotensin I-AT1B signal.…”

Section: Discussionmentioning

confidence: 99%

Retardation of Retinal Vascular Development in Apelin-Deficient Mice

Kasai

Shintani

Kato

et al. 2008

ATVB

120

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Objective-Apelin is an endogenous ligand for the G protein-coupled receptor, APJ, and participates in multiple physiological processes. To identify the roles of endogenous apelin, we investigated the phenotype of apelin-deficient (apelin-KO) mice. Methods and Results-Apelin-KO mice showed impaired retinal vascularization and ocular development, which were analyzed by histology, immunohistochemistry, real-time polymerase chain reaction, and the mouse corneal micropocket assay. Apelin-KO mice showed significantly impaired retinal vascularization in the early postnatal period. Retinal apelin/APJ mRNAs were transiently upregulated during the first 2 postnatal weeks but were undetectable in adults. There were no differences in VEGF or FGF2 mRNA expression, or in the morphology and localization of GFAP-positive astrocytes, in the apelin-KO retinas at P5. The corneal pocket assay showed that angiogenic responses to VEGF and FGF2 were remarkably decreased in apelin-KO mice. The reduced responses to VEGF and FGF2 in apelin-KO mice were partially restored by apelin, but apelin alone did not induce angiogenesis. Conclusions-Our See accompanying article on page 1687Apelin/APJ mRNAs are expressed in multiple tissues, primarily in vascular endothelial cells, where they may contribute to angiogenesis. 8,9 Apelin stimulates the proliferation and migration of RF/6A cells, an endothelial cell line of monkey retina, thereby demonstrating angiogenic-like effects. 9 Similarly, apelin is a potent angiogenic factor required for the normal vascular development of frog embryos. 8 During mouse and frog embryonic development, the APJ receptor is highly expressed in endothelial precursor cells and in nascent vascular structures. Apelin is a potent angiogenic factor in 2 in vivo angiogenesis assays, the frog embryo and the chicken chorioallantoic membrane (CAM) assay. 8 More recently, Kidoya et al showed that the apelin/APJ system is involved in the regulation of blood vessel diameter during angiogenesis. 10 In the mouse, the formation of retinal vessels begins at birth and follows a centrifugal extension of retinal vessels from the optic disc to the periphery of the retina. Interestingly, retinal expression of APJ mRNA is observed during the formation of retinal vessels and traces the centrifugal extension of the superficial vasculature bed, whereas that of apelin mRNA is localized in "tip cells," an endothelial subpopulation that forms cell protrusions and directs the polarized extension of the vascular network. 11 In a mouse model of hypoxia-induced retinopathy of prematurity, APJ mRNA transcripts are localized in endothelial cells, and their expression traces the centripetal extension of the retinal network from the periphery of the retina to the optic disc. 12 These findings suggest that apelin/APJ signaling is involved in regulating retinal vascularization.Ocular developmental vascularization is a complex process, which requires the strict coordination of numerous molecular and cellular interactions. Retinal vascularization is contro...

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Section: Discussionmentioning

confidence: 99%

Retardation of Retinal Vascular Development in Apelin-Deficient Mice

Kasai

Shintani

Kato

et al. 2008

ATVB

120

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“…Increased receptor binding of ANG II during sodium depletion and ANG II infusion was originally attributed to a positive feedback effect of ANG II on its receptors (227). Although molecular biological studies supported the receptor-inducing effect of ANG II (267), and this mechanism seems to explain upregulation of AT 1B receptors (573), the effect of sodium depletion is primarily induced via an ANG II-AT 1 receptor-independent mechanism (63,573). Furthermore, in extra-adrenal tissues of other species, and even in the zona glomerulosa of dogs, prolonged low-dose infusion of ANG II reduces the responsiveness of the target tissue to ANG II (40).…”

Section: B Regulation Of Adrenal Angiotensin Receptorsmentioning

confidence: 99%

Control of Aldosterone Secretion: A Model for Convergence in Cellular Signaling Pathways

Spät

Hunyady

2004

Physiological Reviews

422

351

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Aldosterone secretion by glomerulosa cells is stimulated by angiotensin II (ANG II), extracellular K(+), corticotrophin, and several paracrine factors. Electrophysiological, fluorimetric, and molecular biological techniques have significantly clarified the molecular action of these stimuli. The steroidogenic effect of corticotrophin is mediated by adenylyl cyclase, whereas potassium activates voltage-operated Ca(2+) channels. ANG II, bound to AT(1) receptors, acts through the inositol 1,4,5-trisphosphate (IP(3))-Ca(2+)/calmodulin system. All three types of IP(3) receptors are coexpressed, rendering a complex control of Ca(2+) release possible. Ca(2+) release is followed by both capacitative and voltage-activated Ca(2+) influx. ANG II inhibits the background K(+) channel TASK and Na(+)-K(+)-ATPase, and the ensuing depolarization activates T-type (Ca(v)3.2) Ca(2+) channels. Activation of protein kinase C by diacylglycerol (DAG) inhibits aldosterone production, whereas the arachidonate released from DAG in ANG II-stimulated cells is converted by lipoxygenase to 12-hydroxyeicosatetraenoic acid, which may also induce Ca(2+) signaling. Feedback effects and cross-talk of signal-transducing pathways sensitize glomerulosa cells to low-intensity stimuli, such as physiological elevations of [K(+)] (< or =1 mM), ANG II, and ACTH. Ca(2+) signaling is also modified by cell swelling, as well as receptor desensitization, resensitization, and downregulation. Long-term regulation of glomerulosa cells involves cell growth and proliferation and induction of steroidogenic enzymes. Ca(2+), receptor, and nonreceptor tyrosine kinases and mitogen-activated kinases participate in these processes. Ca(2+)- and cAMP-dependent phosphorylation induce the transfer of the steroid precursor cholesterol from the cytoplasm to the inner mitochondrial membrane. Ca(2+) signaling, transferred into the mitochondria, stimulates the reduction of pyridine nucleotides.

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“…20 AT 1a and AT 1b mRNAs as well as NOS II and ␤-actin mRNAs were measured by RNase protection assay as previously described. 20,21 Radioligand Binding Assays Then the cells were washed with ice-cold PBS and solubilized with 1N NaOH. Radioactivity was measured by ␥ counting.…”

Section: Cell Culturementioning

confidence: 99%

Downregulation of Angiotensin II Type 1 Receptors During Sepsis

et al. 2001

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Abstract-Our study aimed to characterize the mechanisms underlying the attenuated cardiovascular responsiveness toward the renin-angiotensin system during sepsis. For this purpose, we determined the effects of experimental Gram-negative and Gram-positive sepsis in rats. We found that sepsis led to a ubiquitous upregulation of NO synthase isoform II expression and to pronounced hypotension. Despite increased plasma renin activity and plasma angiotensin (Ang) II levels, plasma aldosterone concentrations were normal, and the blood pressure response to exogenous Ang II was markedly diminished in septic rats. Mimicking the fall of blood pressure during sepsis by short-term infusion of the NO donor sodium nitroprusside in normal rats did not alter their blood pressure response to exogenous Ang II. Therefore, we considered the possibility of an altered expression of Ang II receptors during sepsis. It turned out that Ang II type 1 receptor expression was markedly downregulated in all organs of septic rats. Further in vitro studies with rat renal mesangial cells showed that NO and a combination of proinflammatory cytokines (interleukin-1␤, tumor necrosis factor-␣, and interferon-␥) downregulated Ang II type 1 receptor expression in a synergistic fashion. In summary, our data suggest that sepsis causes a systemic downregulation of Ang II type 1 receptors that is likely mediated by proinflammatory cytokines and NO. We suggest that this downregulation of Ang II type 1 receptors is the main reason for the attenuated responsiveness of blood pressure and of aldosterone formation to Ang II and, therefore, contributes to the characteristic septic shock. (Hypertension. 2001;38:177-182.)

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Positive feedback regulation of angiotensin II-AT 1B receptor gene expression in rat adrenal glands

Cited by 4 publications

References 20 publications

Retardation of Retinal Vascular Development in Apelin-Deficient Mice

Retardation of Retinal Vascular Development in Apelin-Deficient Mice

Control of Aldosterone Secretion: A Model for Convergence in Cellular Signaling Pathways

Downregulation of Angiotensin II Type 1 Receptors During Sepsis

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