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This Article Full Text Full Text (PDF) All Versions of this Article: 571/2/451    most recent jphysiol.2005.101352v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Goossens, G. H. Articles by Karpe, F. Search for Related Content PubMed PubMed Citation Articles by Goossens, G. H. Articles by Karpe, F. Related Collections Integrative

¹ Department of Human Biology, Nutrition and Toxicology Research Institute Maastricht (NUTRIM), Maastricht University, Maastricht, The Netherlands
² Oxford Centre for Diabetes, Endocrinology and Metabolism, Nuffield Department of Clinical Medicine, University of Oxford, Oxford, UK

We investigated the functional roles of circulating and locally produced angiotensin II (Ang II) in fasting and postprandial adipose tissue blood flow (ATBF) regulation and examined the interaction between Ang II and nitric oxide (NO) in ATBF regulation. Local effects of the pharmacological agents (or contralateral saline) on ATBF, measured with ¹³³Xe wash-out, were assessed using the recently developed microinfusion technique. Fasting and postprandial (75 g glucose challenge) ATBF regulation was investigated in nine lean healthy subjects (age, 29 ± 3 years; BMI, 23.4 ± 0.7 kg m^–2) using local Ang II stimulation, Ang II type 1 (AT₁) receptor blockade, and angiotensin-converting enzyme (ACE) inhibition. Furthermore, NO synthase (NOS) blockade alone and in combination with AT₁ receptor blockade was used to examine the interaction between Ang II and NO. Ang II induced a dose-dependent decrease in ATBF (10^–9M: –16%, P= 0.04; 10^–7M: –33%, P < 0.01; 10^–5M: –53%P < 0.01). Fasting ATBF was not affected by ACE inhibition, but was increased by 55% (P < 0.01) by AT₁ receptor blockade. NOS blockade induced a 30% (P= 0.001) decrease in fasting ATBF. Combined AT₁ receptor and NOS blockade increased ATBF by 40% (P= 0.003). ACE inhibition and AT₁ receptor blockade did not affect the postprandial increase in ATBF. We therefore conclude that circulating Ang II is a major regulator of fasting ATBF, and a major proportion of the Ang II-induced decrease in ATBF is NO independent. Locally produced Ang II does not appear to regulate ATBF. Ang II appears to have no major effect on the postprandial enhancement of ATBF.

(Received 4 November 2005; accepted after revision 4 January 2006; first published online 5 January 2006)
Corresponding author G. H. Goossens: Department of Human Biology, Nutrition and Toxicology Research Institute Maastricht (NUTRIM), Maastricht University, Maastricht, The Netherlands. Email: g.goossens{at}hb.unimaas.nl