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Adenosine A(1)-rece...
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Gao, XiangUppsala universitet,Integrativ Fysiologi
(författare)
Adenosine A(1)-receptor deficiency diminishes afferent arteriolar and blood pressure responses during nitric oxide inhibition and angiotensin II treatment
- Artikel/kapitelEngelska2011
Förlag, utgivningsår, omfång ...
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American Physiological Society,2011
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printrdacarrier
Nummerbeteckningar
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LIBRIS-ID:oai:DiVA.org:uu-167644
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https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-167644URI
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https://doi.org/10.1152/ajpregu.00268.2011DOI
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http://kipublications.ki.se/Default.aspx?queryparsed=id:123741760URI
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Språk:engelska
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Sammanfattning på:engelska
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Klassifikation
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Ämneskategori:ref swepub-contenttype
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Ämneskategori:art swepub-publicationtype
Anmärkningar
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Adenosine mediates tubuloglomerular feedback responses via activation of A(1)-receptors on the renal afferent arteriole. Increased preglomerular reactivity, due to reduced nitric oxide (NO) production or increased levels of ANG II and reactive oxygen species (ROS), has been linked to hypertension. Using A(1)-receptor knockout (A(1)(-/-)) and wild-type (A(1)(+/+)) mice we investigated the hypothesis that A(1)-receptors modulate arteriolar and blood pressure responses during NO synthase (NOS) inhibition or ANG II treatment. Blood pressure and renal afferent arteriolar responses were measured in nontreated mice and in mice with prolonged N(omega)-nitro-L-arginine methyl ester hydrochloride (L-NAME) or ANG II treatment. The hypertensive responses to L-NAME and ANG II were clearly attenuated in A(1)(-/-) mice. Arteriolar contractions to L-NAME (10(-4) mol/l; 15 min) and cumulative ANG II application (10(-12) to 10(-6) mol/l) were lower in A(1)(-/-) mice. Simultaneous treatment with tempol (10(-4) mol/l; 15 min) attenuated arteriolar responses in A(1)(+/+) but not in A(1)(-/-) mice, suggesting differences in ROS formation. Chronic treatment with L-NAME or ANG II did not alter arteriolar responses in A(1)(-/-) mice, but enhanced maximal contractions in A(1)(+/+) mice. In addition, chronic treatments were associated with higher plasma levels of dimethylarginines (asymmetrical and symmetrical) and oxidative stress marker malondialdehyde in A(1)(+/+) mice, and gene expression analysis showed reduced upregulation of NOS-isoforms and greater upregulation of NADPH oxidases. In conclusion, adenosine A(1)-receptors enhance preglomerular responses during NO inhibition and ANG II treatment. Interruption of A(1)-receptor signaling blunts L-NAME and ANG II-induced hypertension and oxidative stress and is linked to reduced responsiveness of afferent arterioles.
Ämnesord och genrebeteckningar
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preglomerular function
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hypertension
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oxidative stress
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tubuloglomerular feedback
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reactive oxygen species
Biuppslag (personer, institutioner, konferenser, titlar ...)
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Patzak, Andreas
(författare)
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Sendeski, Mauricio
(författare)
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Scheffer, Peter G.
(författare)
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Teerlink, Tom
(författare)
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Sällström, JohanUppsala universitet,Institutionen för medicinsk cellbiologi(Swepub:uu)josal227
(författare)
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Fredholm, Bertil B.Karolinska Institutet
(författare)
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Persson, A. Erik G.Uppsala universitet,Integrativ Fysiologi(Swepub:uu)erikpers
(författare)
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Carlström, MattiasKarolinska Institutet,Uppsala universitet,Integrativ Fysiologi(Swepub:uu)macar229
(författare)
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Uppsala universitetIntegrativ Fysiologi
(creator_code:org_t)
Sammanhörande titlar
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Ingår i:American Journal of Physiology. Regulatory Integrative and Comparative Physiology: American Physiological Society301:6, s. R1669-R16810363-61191522-1490
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