| Inhibition of nitric oxide synthase by NG-nitro-L-arginine causes a preferential decrease in pancreatic islet blood flow in normal rats and spontaneously diabetic GK rats. | |
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MedLine Citation:
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PMID: 7520863 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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To elucidate the effect of nitric oxide (NO) on the blood flow of the pancreatic islets, the NO synthase inhibitor NG-nitro-L-arginine (N-arg; 25 mg/kg BW) was administered iv to rats 10 min before pancreatic blood flow was measured with a nonradioactive microsphere technique. In male Sprague-Dawley rats, N-arg induced a marked decrease in islet blood flow (16 +/- 4 vs. 44 +/- 8 microliters/min.g pancreas; P < 0.001) and a less pronounced decrease in whole pancreatic blood flow (0.27 +/- 0.04 vs. 0.43 +/- 0.06 ml/min.g; P < 0.05), leading to a markedly decreased fractional islet blood flow (5.5 +/- 0.9% vs. 10.3 +/- 1.3%; P < 0.02). In a second experiment, injection of D-glucose (300 mg/kg BW, iv) in male Sprague-Dawley rats induced a selective increase in islet blood flow (P < 0.05). Such an increase has previously been shown to be mediated by a vagal cholinergic mechanism. Administration of N-arg to these rats resulted in decreased pancreatic (P < 0.05), islet (P < 0.001), and fractional (P < 0.001) islet blood flow, which did not differ from those observed in normoglycemic rats after treatment with N-arg. Furthermore, we studied the mechanism behind the previously described increase in islet blood perfusion, mediated by the vagus nerve, in F1-hybrids of the GK (Goto-Kakizaki) rat, a spontaneous animal model of noninsulin-dependent diabetes mellitus. Administration of N-arg to female GK rats resulted in decreases in islet (P < 0.001), pancreatic (P < 0.01), and fractional islet blood flow (P < 0.001) to the levels observed in female Wistar rats treated in parallel. These data are consistent with the possibility that NO is an important physiological regulator of islet blood flow. Furthermore, the vagally dependent high levels of islet blood flow demonstrated in the GK rat appear to be mediated by a mechanism involving NO. |
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Authors:
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A M Svensson; C G Ostenson; S Sandler; S Efendic; L Jansson |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Endocrinology Volume: 135 ISSN: 0013-7227 ISO Abbreviation: Endocrinology Publication Date: 1994 Sep |
Date Detail:
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Created Date: 1994-09-26 Completed Date: 1994-09-26 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 0375040 Medline TA: Endocrinology Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 849-53 Citation Subset: AIM; IM |
Affiliation:
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Department of Medical Cell Biology, Uppsala University, Sweden. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Amino Acid Oxidoreductases
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antagonists & inhibitors* Animals Arginine / analogs & derivatives*, pharmacology Diabetes Mellitus, Experimental / genetics, physiopathology* Female Islets of Langerhans / blood supply* Male Nitric Oxide Synthase Nitroarginine Rats Rats, Mutant Strains Rats, Sprague-Dawley Rats, Wistar Reference Values Regional Blood Flow / drug effects |
| Chemical | |
Reg. No./Substance:
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2149-70-4/Nitroarginine; 74-79-3/Arginine; EC 1.14.13.39/Nitric Oxide Synthase; EC 1.4.-/Amino Acid Oxidoreductases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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