The B2 subunit of vascular H+-ATPase is chronically regulated by angiotensin II in immortalized rat proximal tubule cells (2007)
- Authors:
- USP affiliated authors: SOUZA, MARIA OLIVEIRA DE - ICB ; MALNIC, GERHARD - ICB
- Unidade: ICB
- Assunto: FISIOLOGIA
- Language: Inglês
- Imprenta:
- Publisher: Sociedade Brasileira de Nefrologia
- Publisher place: Rio de Janeiro
- Date published: 2007
- Source:
- Título do periódico: Abstracts
- Conference titles: World Congress of Nephrology
-
ABNT
CARRARO-LACROIX, L. R. et al. The B2 subunit of vascular H+-ATPase is chronically regulated by angiotensin II in immortalized rat proximal tubule cells. 2007, Anais.. Rio de Janeiro: Sociedade Brasileira de Nefrologia, 2007. . Acesso em: 24 abr. 2024. -
APA
Carraro-Lacroix, L. R., Bezerra, C. N. A., Oliveira-Souza, M., & Malnic, G. (2007). The B2 subunit of vascular H+-ATPase is chronically regulated by angiotensin II in immortalized rat proximal tubule cells. In Abstracts. Rio de Janeiro: Sociedade Brasileira de Nefrologia. -
NLM
Carraro-Lacroix LR, Bezerra CNA, Oliveira-Souza M, Malnic G. The B2 subunit of vascular H+-ATPase is chronically regulated by angiotensin II in immortalized rat proximal tubule cells. Abstracts. 2007 ;[citado 2024 abr. 24 ] -
Vancouver
Carraro-Lacroix LR, Bezerra CNA, Oliveira-Souza M, Malnic G. The B2 subunit of vascular H+-ATPase is chronically regulated by angiotensin II in immortalized rat proximal tubule cells. Abstracts. 2007 ;[citado 2024 abr. 24 ] - Colchicine impairs the dose-dependent stimulatory effect of ANG II or AVP on acid subcellular vesicle traafficking in MDCK cells
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- Colchicina inibe ação da AVP no tráfego de vesículas ácidas subcelulares, em células MDCK
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- Activation of the AT1 receptor-beta-arrestin signaling pathway inhibits NHE3 activity in the renal proximal tubule
- Arginine vasopressin stimulates H+ - ATPase in MDCK cells via V1 (cell Ca2+) and V2 (cAMP) receptors
- The role of β-adrenergic overstimulation in the early stages of renal injury
- Papel da angiotensina II e da proteína quinase C (PKC) na modulação do PH intracelular (PHI) em células renais
- Papel da proteína Kinase C e do cálcio citosólico na velocidade de extrusão de H+ das células MDCK
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