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- Gao, XiangUppsala universitet,Institutionen för medicinsk cellbiologi (author)
Adenosine A1 receptor-dependent and independent pathways in modulating renal vascular responses to angiotensin II
- Article/chapterEnglish2015
Publisher, publication year, extent ...
- 2014-10-09
- Wiley,2015
- printrdacarrier
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- LIBRIS-ID:oai:DiVA.org:uu-230758
- https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-230758URI
- https://doi.org/10.1111/apha.12399DOI
- http://kipublications.ki.se/Default.aspx?queryparsed=id:130301635URI
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- Language:English
- Summary in:English
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- AIM: Renal afferent arterioles are the effector site for autoregulation of glomerular perfusion and filtration. There is synergistic interaction between angiotensin II (ANG II) and adenosine (Ado) in regulating arteriolar contraction, however, the mechanisms are not clear. In this context, this study investigated the contribution of A1 receptor dependent and independent signaling mechanisms.METHODS: Isolated perfused afferent arterioles from transgenic mice (A1+/+ and A1-/-) were used for vascular reactivity studies. Cultured vascular smooth muscle cells (VSMC) were used for phosphorylation studies of signaling proteins that induce arteriolar contraction.RESULTS: Maximal arteriolar contraction to ANG II was attenuated in A1-/- (22%) compared with A1+/+ (40%). Simultaneous incubation with low dose Ado (10-8 mol/L) enhanced ANG II-induced contraction in A1+/+ (58%), but also in A1-/- (42%). An Ado transporter inhibitor (NBTI) abolished this synergistic effect in A1-/-, but not in wild-type mice. Incubation with Ado+ANG II increased p38 phosphorylation in aortic VSMC from both genotypes, but treatment with NBTI only blocked phosphorylation in A1-/-. Combination of ANG II+Ado also increased MLC phosphorylation in A1+/+ but not significantly in A1-/-, and NBTI had no effects. In agreement, Ado+ANG II-induced phosphorylation of p38 and MLC in rat preglomerular VSMC was not affected by NBTI. However, during pharmacological inhibition of the A1 receptor simultaneous treatment with NBTI reduced phosphorylation of both p38 and MLC to control levels.CONCLUSION: Interaction between ANG II and Ado in VSMC normally involves A1 receptor signaling, but this can be compensated by receptor independent actions that phosphorylate p38 MAPK and MLC.
Subject headings and genre
- MEDICIN OCH HÄLSOVETENSKAP Medicinska och farmaceutiska grundvetenskaper Fysiologi hsv//swe
- MEDICAL AND HEALTH SCIENCES Basic Medicine Physiology hsv//eng
- afferent arteriole
- microcirculation
- vascular smooth muscle cell
- kidney
- p38 MAP kinase
- myosin light chain
Added entries (persons, corporate bodies, meetings, titles ...)
- Peleli, MariaKarolinska Institutet (author)
- Zollbrecht, ChristaKarolinska Institutet,Dept Physiology & Pharmacology (author)
- Patzak, AndreasCharité-Universitätsmedizin Berlin, Germany,Institute of Vegetative Physiology (author)
- Persson, ErikUppsala universitet,Institutionen för medicinsk cellbiologi(Swepub:uu)erikpers (author)
- Mattias, CarlströmKarolinska Institutet (author)
- Uppsala universitetInstitutionen för medicinsk cellbiologi (creator_code:org_t)
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- In:Acta Physiologica: Wiley213:1, s. 268-2761748-17081748-1716
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