C-peptide increases forearm blood flow in patients with type 1 diabetes via a nitric oxide-dependent mechanism
1 Section of Clinical Physiology, Department of Surgical Sciences and 2 Section of Cardiology, Department of Medicine, Karolinska Hospital, S-171 76 Stockholm, Sweden Submitted 2 January 2003 ; accepted in final form 4 June 2003 Proinsulin C-peptide has been shown to increase muscle blood flow in ty...
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| Veröffentlicht in: | American journal of physiology: endocrinology and metabolism 2003-10, Vol.285 (4), p.E864-E870 |
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| container_title | American journal of physiology: endocrinology and metabolism |
| container_volume | 285 |
| creator | Johansson, Bo-Lennart Wahren, John Pernow, John |
| description | 1 Section of Clinical Physiology, Department of Surgical Sciences and 2 Section of Cardiology, Department of Medicine, Karolinska Hospital, S-171 76 Stockholm, Sweden
Submitted 2 January 2003
; accepted in final form 4 June 2003
Proinsulin C-peptide has been shown to increase muscle blood flow in type 1 diabetic patients. The underlying mechanism is not fully understood. The aim of this study was to evaluate if the vasodilator effect of C-peptide is mediated by nitric oxide (NO). Eleven type 1 diabetic patients were studied two times and randomized to administration of intravenous and intra-arterial infusion of C-peptide or saline. Forearm blood flow (FBF) was measured by venous occlusion plethysmography during infusion of C-peptide or saline before, during, and after NO synthase (NOS) blockade. Endothelium-dependent and -independent vasodilatation was evaluated by administration of acetylcholine and sodium nitroprusside, respectively. FBF increased by 35% during intravenous C-peptide ( P < 0.01) but not during saline infusion (2%, not significant). NOS blockade resulted in a more pronounced reduction in FBF during intravenous C-peptide than during saline infusion (41 vs. 26%, P < 0.05). Intra-arterial C-peptide failed to increase FBF during NOS blockade. However, when C-peptide was given after the recovery from NOS blockade, FBF rose by 30% ( P < 0.001). The vasodilator effects of acetylcholine and nitroprusside were not influenced by C-peptide. It is concluded that the stimulatory effect of C-peptide on FBF in type 1 diabetic patients is mediated via the NO system and that C-peptide increases basal endothelial NO levels.
acetylcholine; insulin; N G -monomethyl- L -arginine; sodium nitroprusside; venous occlusion plethysmography
Address for reprint requests and other correspondence: B.-L. Johansson, Dept. of Surgical Sciences, Division of Clinical Physiology N1:05, Karolinska Hospital, SE-171 76 Stockholm, Sweden. |
| doi_str_mv | 10.1152/ajpendo.00001.2003 |
| format | Article |
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Submitted 2 January 2003
; accepted in final form 4 June 2003
Proinsulin C-peptide has been shown to increase muscle blood flow in type 1 diabetic patients. The underlying mechanism is not fully understood. The aim of this study was to evaluate if the vasodilator effect of C-peptide is mediated by nitric oxide (NO). Eleven type 1 diabetic patients were studied two times and randomized to administration of intravenous and intra-arterial infusion of C-peptide or saline. Forearm blood flow (FBF) was measured by venous occlusion plethysmography during infusion of C-peptide or saline before, during, and after NO synthase (NOS) blockade. Endothelium-dependent and -independent vasodilatation was evaluated by administration of acetylcholine and sodium nitroprusside, respectively. FBF increased by 35% during intravenous C-peptide ( P < 0.01) but not during saline infusion (2%, not significant). NOS blockade resulted in a more pronounced reduction in FBF during intravenous C-peptide than during saline infusion (41 vs. 26%, P < 0.05). Intra-arterial C-peptide failed to increase FBF during NOS blockade. However, when C-peptide was given after the recovery from NOS blockade, FBF rose by 30% ( P < 0.001). The vasodilator effects of acetylcholine and nitroprusside were not influenced by C-peptide. It is concluded that the stimulatory effect of C-peptide on FBF in type 1 diabetic patients is mediated via the NO system and that C-peptide increases basal endothelial NO levels.
acetylcholine; insulin; N G -monomethyl- L -arginine; sodium nitroprusside; venous occlusion plethysmography
Address for reprint requests and other correspondence: B.-L. Johansson, Dept. of Surgical Sciences, Division of Clinical Physiology N1:05, Karolinska Hospital, SE-171 76 Stockholm, Sweden.</description><identifier>ISSN: 0193-1849</identifier><identifier>EISSN: 1522-1555</identifier><identifier>DOI: 10.1152/ajpendo.00001.2003</identifier><identifier>PMID: 12799312</identifier><language>eng</language><publisher>United States</publisher><subject>Acetylcholine - pharmacology ; Adult ; Blood Flow Velocity - drug effects ; C-Peptide - administration & dosage ; Diabetes Mellitus, Type 1 - metabolism ; Diabetes Mellitus, Type 1 - physiopathology ; Forearm - blood supply ; Forearm - physiopathology ; Humans ; Infusions, Intravenous ; Insulin - administration & dosage ; Male ; Nitric Oxide - metabolism ; Nitric Oxide Synthase - antagonists & inhibitors ; Nitric Oxide Synthase - metabolism ; Nitroprusside - pharmacology ; omega-N-Methylarginine - pharmacology ; Regional Blood Flow - drug effects ; Vasodilator Agents - administration & dosage</subject><ispartof>American journal of physiology: endocrinology and metabolism, 2003-10, Vol.285 (4), p.E864-E870</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c425t-48e4bebe22253dda0d2d9057724af632554c7636fe92d2d18f9969f7da595ceb3</citedby><cites>FETCH-LOGICAL-c425t-48e4bebe22253dda0d2d9057724af632554c7636fe92d2d18f9969f7da595ceb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,3026,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12799312$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:1937781$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Johansson, Bo-Lennart</creatorcontrib><creatorcontrib>Wahren, John</creatorcontrib><creatorcontrib>Pernow, John</creatorcontrib><title>C-peptide increases forearm blood flow in patients with type 1 diabetes via a nitric oxide-dependent mechanism</title><title>American journal of physiology: endocrinology and metabolism</title><addtitle>Am J Physiol Endocrinol Metab</addtitle><description>1 Section of Clinical Physiology, Department of Surgical Sciences and 2 Section of Cardiology, Department of Medicine, Karolinska Hospital, S-171 76 Stockholm, Sweden
Submitted 2 January 2003
; accepted in final form 4 June 2003
Proinsulin C-peptide has been shown to increase muscle blood flow in type 1 diabetic patients. The underlying mechanism is not fully understood. The aim of this study was to evaluate if the vasodilator effect of C-peptide is mediated by nitric oxide (NO). Eleven type 1 diabetic patients were studied two times and randomized to administration of intravenous and intra-arterial infusion of C-peptide or saline. Forearm blood flow (FBF) was measured by venous occlusion plethysmography during infusion of C-peptide or saline before, during, and after NO synthase (NOS) blockade. Endothelium-dependent and -independent vasodilatation was evaluated by administration of acetylcholine and sodium nitroprusside, respectively. FBF increased by 35% during intravenous C-peptide ( P < 0.01) but not during saline infusion (2%, not significant). NOS blockade resulted in a more pronounced reduction in FBF during intravenous C-peptide than during saline infusion (41 vs. 26%, P < 0.05). Intra-arterial C-peptide failed to increase FBF during NOS blockade. However, when C-peptide was given after the recovery from NOS blockade, FBF rose by 30% ( P < 0.001). The vasodilator effects of acetylcholine and nitroprusside were not influenced by C-peptide. It is concluded that the stimulatory effect of C-peptide on FBF in type 1 diabetic patients is mediated via the NO system and that C-peptide increases basal endothelial NO levels.
acetylcholine; insulin; N G -monomethyl- L -arginine; sodium nitroprusside; venous occlusion plethysmography
Address for reprint requests and other correspondence: B.-L. Johansson, Dept. of Surgical Sciences, Division of Clinical Physiology N1:05, Karolinska Hospital, SE-171 76 Stockholm, Sweden.</description><subject>Acetylcholine - pharmacology</subject><subject>Adult</subject><subject>Blood Flow Velocity - drug effects</subject><subject>C-Peptide - administration & dosage</subject><subject>Diabetes Mellitus, Type 1 - metabolism</subject><subject>Diabetes Mellitus, Type 1 - physiopathology</subject><subject>Forearm - blood supply</subject><subject>Forearm - physiopathology</subject><subject>Humans</subject><subject>Infusions, Intravenous</subject><subject>Insulin - administration & dosage</subject><subject>Male</subject><subject>Nitric Oxide - metabolism</subject><subject>Nitric Oxide Synthase - antagonists & inhibitors</subject><subject>Nitric Oxide Synthase - metabolism</subject><subject>Nitroprusside - pharmacology</subject><subject>omega-N-Methylarginine - pharmacology</subject><subject>Regional Blood Flow - drug effects</subject><subject>Vasodilator Agents - administration & dosage</subject><issn>0193-1849</issn><issn>1522-1555</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNptkUFv3CAUhFHVqNmm_QM9VJx689aAsc2xWiVNpEi9JGeEzSMmtQ0F3M3--7Jdp3spF56Yb0YPDUKfSLklhNOv6tnDrN22zIdsaVmyN2iTBVoQzvlbtCmJYAVpK3GJ3sf4nLGGV_QduiS0EYIRukHzrvDgk9WA7dwHUBEiNi4PYcLd6JzGZnT7LGKvkoU5Rby3acDp4AETrK3qIGXPb6uwwrNNwfbYveTAQsNxv2zBE_SDmm2cPqALo8YIH9f7Cj3eXD_sbov7H9_vdt_ui76iPBVVC1UHHVBKOdNalZpqUfKmoZUyNaOcV31Ts9qAoFkirRGiFqbRigveQ8euUHHKjXvwSyd9sJMKB-mUlevTzzyB5K3gTZv5LyfeB_drgZjkZGMP46hmcEuUDasJbxjJID2BfXAxBjD_okkpj63ItRX5txV5bCWbPq_pSzeBPlvWGjIgTsBgn4a9DSD9cIjWje7pIG-WcXyAl_SaTFsuK3nd1pX02py_-j_v6zJnD_sDLbGxBQ</recordid><startdate>20031001</startdate><enddate>20031001</enddate><creator>Johansson, Bo-Lennart</creator><creator>Wahren, John</creator><creator>Pernow, John</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>ADTPV</scope><scope>AOWAS</scope></search><sort><creationdate>20031001</creationdate><title>C-peptide increases forearm blood flow in patients with type 1 diabetes via a nitric oxide-dependent mechanism</title><author>Johansson, Bo-Lennart ; Wahren, John ; Pernow, John</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c425t-48e4bebe22253dda0d2d9057724af632554c7636fe92d2d18f9969f7da595ceb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Acetylcholine - pharmacology</topic><topic>Adult</topic><topic>Blood Flow Velocity - drug effects</topic><topic>C-Peptide - administration & dosage</topic><topic>Diabetes Mellitus, Type 1 - metabolism</topic><topic>Diabetes Mellitus, Type 1 - physiopathology</topic><topic>Forearm - blood supply</topic><topic>Forearm - physiopathology</topic><topic>Humans</topic><topic>Infusions, Intravenous</topic><topic>Insulin - administration & dosage</topic><topic>Male</topic><topic>Nitric Oxide - metabolism</topic><topic>Nitric Oxide Synthase - antagonists & inhibitors</topic><topic>Nitric Oxide Synthase - metabolism</topic><topic>Nitroprusside - pharmacology</topic><topic>omega-N-Methylarginine - pharmacology</topic><topic>Regional Blood Flow - drug effects</topic><topic>Vasodilator Agents - administration & dosage</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Johansson, Bo-Lennart</creatorcontrib><creatorcontrib>Wahren, John</creatorcontrib><creatorcontrib>Pernow, John</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>SwePub</collection><collection>SwePub Articles</collection><jtitle>American journal of physiology: endocrinology and metabolism</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Johansson, Bo-Lennart</au><au>Wahren, John</au><au>Pernow, John</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>C-peptide increases forearm blood flow in patients with type 1 diabetes via a nitric oxide-dependent mechanism</atitle><jtitle>American journal of physiology: endocrinology and metabolism</jtitle><addtitle>Am J Physiol Endocrinol Metab</addtitle><date>2003-10-01</date><risdate>2003</risdate><volume>285</volume><issue>4</issue><spage>E864</spage><epage>E870</epage><pages>E864-E870</pages><issn>0193-1849</issn><eissn>1522-1555</eissn><abstract>1 Section of Clinical Physiology, Department of Surgical Sciences and 2 Section of Cardiology, Department of Medicine, Karolinska Hospital, S-171 76 Stockholm, Sweden
Submitted 2 January 2003
; accepted in final form 4 June 2003
Proinsulin C-peptide has been shown to increase muscle blood flow in type 1 diabetic patients. The underlying mechanism is not fully understood. The aim of this study was to evaluate if the vasodilator effect of C-peptide is mediated by nitric oxide (NO). Eleven type 1 diabetic patients were studied two times and randomized to administration of intravenous and intra-arterial infusion of C-peptide or saline. Forearm blood flow (FBF) was measured by venous occlusion plethysmography during infusion of C-peptide or saline before, during, and after NO synthase (NOS) blockade. Endothelium-dependent and -independent vasodilatation was evaluated by administration of acetylcholine and sodium nitroprusside, respectively. FBF increased by 35% during intravenous C-peptide ( P < 0.01) but not during saline infusion (2%, not significant). NOS blockade resulted in a more pronounced reduction in FBF during intravenous C-peptide than during saline infusion (41 vs. 26%, P < 0.05). Intra-arterial C-peptide failed to increase FBF during NOS blockade. However, when C-peptide was given after the recovery from NOS blockade, FBF rose by 30% ( P < 0.001). The vasodilator effects of acetylcholine and nitroprusside were not influenced by C-peptide. It is concluded that the stimulatory effect of C-peptide on FBF in type 1 diabetic patients is mediated via the NO system and that C-peptide increases basal endothelial NO levels.
acetylcholine; insulin; N G -monomethyl- L -arginine; sodium nitroprusside; venous occlusion plethysmography
Address for reprint requests and other correspondence: B.-L. Johansson, Dept. of Surgical Sciences, Division of Clinical Physiology N1:05, Karolinska Hospital, SE-171 76 Stockholm, Sweden.</abstract><cop>United States</cop><pmid>12799312</pmid><doi>10.1152/ajpendo.00001.2003</doi></addata></record> |
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| ispartof | American journal of physiology: endocrinology and metabolism, 2003-10, Vol.285 (4), p.E864-E870 |
| issn | 0193-1849 1522-1555 |
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| source | MEDLINE; American Physiological Society; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Acetylcholine - pharmacology Adult Blood Flow Velocity - drug effects C-Peptide - administration & dosage Diabetes Mellitus, Type 1 - metabolism Diabetes Mellitus, Type 1 - physiopathology Forearm - blood supply Forearm - physiopathology Humans Infusions, Intravenous Insulin - administration & dosage Male Nitric Oxide - metabolism Nitric Oxide Synthase - antagonists & inhibitors Nitric Oxide Synthase - metabolism Nitroprusside - pharmacology omega-N-Methylarginine - pharmacology Regional Blood Flow - drug effects Vasodilator Agents - administration & dosage |
| title | C-peptide increases forearm blood flow in patients with type 1 diabetes via a nitric oxide-dependent mechanism |
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