PMID- 12100359 OWN - NLM STAT- MEDLINE DCOM- 20030108 LR - 20140728 IS - 0001-6772 (Print) IS - 0001-6772 (Linking) VI - 175 IP - 3 DP - 2002 Jul TI - Attenuation of the exercise-induced increase in skeletal muscle Flt-1 mRNA by nitric oxide synthase inhibition. PG - 201-9 AB - We investigated the vascular endothelial growth factor (VEGF) receptor [fms-like-tyrosine kinase (Flt-1 and fetal liver kinase-1 (Flk-1)] response to acute exercise. In female Wistar rats, the VEGF receptor messenger RNA (mRNA) response to a single acute exercise bout was examined using semi-quantitative Northern blot from the left gastrocnemius muscles at rest and post-exercise at 0, 1, 2, 4, 8, 16, 24 and 48 h. Exercise altered both Flt-1 and Flk-1 mRNA, with significant increases in Flt-1 mRNA at 1 and 24 h. However, post-hoc analysis was unable to discern the time point where a significant increase in Flk-1 mRNA occurred. To investigate the regulation of Flt-1 mRNA by exercise we examined if nitric oxide synthase (NOS) inhibition alters the Flt-1 mRNA response. Eight groups [ CONDITION: Rest or Exercise; Drug: Saline, 30 mg kg(-1)N(omega)-nitro-L-arginine methyl ester (L-NAME), 300 mg kg(-1) L-NAME or 300 mg kg(-1) D-NAME] were used to determine the effect of NOS inhibition on the Flt-1 mRNA response to exercise. L-NAME, a known NOS inhibitor, attenuated the exercise-induced increase in Flt-1 mRNA by approximately 50%. These findings suggest that: (1) exercise alters Flt-1 and Flk-1 gene expression; and (2) NO is important in the regulation of the Flt-1 gene response to exercise. FAU - Gavin, T P AU - Gavin TP AD - Department of Medicine, University of California San Diego, La Jolla, CA, USA. FAU - Wagner, P D AU - Wagner PD LA - eng GR - HL-09624/HL/NHLBI NIH HHS/United States GR - HL-17731/HL/NHLBI NIH HHS/United States PT - Comparative Study PT - Journal Article PT - Research Support, Non-U.S. Gov't PT - Research Support, U.S. Gov't, P.H.S. PL - England TA - Acta Physiol Scand JT - Acta physiologica Scandinavica JID - 0370362 RN - 0 (Endothelial Growth Factors) RN - 0 (Enzyme Inhibitors) RN - 0 (Extracellular Matrix Proteins) RN - 0 (Intercellular Signaling Peptides and Proteins) RN - 0 (Lymphokines) RN - 0 (RNA, Messenger) RN - 0 (RNA, Ribosomal, 18S) RN - 0 (Vascular Endothelial Growth Factor A) RN - 0 (Vascular Endothelial Growth Factors) RN - EC 1.14.13.39 (Nitric Oxide Synthase) RN - EC 2.7.10.1 (Flt1 protein, rat) RN - EC 2.7.10.1 (Vascular Endothelial Growth Factor Receptor-1) RN - EC 2.7.10.1 (Vascular Endothelial Growth Factor Receptor-2) RN - V55S2QJN2X (NG-Nitroarginine Methyl Ester) SB - IM MH - Animals MH - Endothelial Growth Factors MH - Enzyme Inhibitors/pharmacology MH - Extracellular Matrix Proteins/drug effects/*genetics MH - Female MH - Gene Expression/drug effects/physiology MH - Gene Expression Regulation/drug effects/physiology MH - Intercellular Signaling Peptides and Proteins MH - Lymphokines MH - Muscle, Skeletal/*physiology MH - NG-Nitroarginine Methyl Ester/analogs & derivatives/pharmacology MH - Nitric Oxide Synthase/*antagonists & inhibitors MH - Physical Exertion/*physiology MH - RNA, Messenger/metabolism MH - RNA, Ribosomal, 18S/genetics MH - Rats MH - Rats, Wistar MH - Reproducibility of Results MH - Sensitivity and Specificity MH - Vascular Endothelial Growth Factor A MH - Vascular Endothelial Growth Factor Receptor-1/genetics MH - Vascular Endothelial Growth Factor Receptor-2/genetics MH - Vascular Endothelial Growth Factors EDAT- 2002/07/09 10:00 MHDA- 2003/01/09 04:00 CRDT- 2002/07/09 10:00 PHST- 2002/07/09 10:00 [pubmed] PHST- 2003/01/09 04:00 [medline] PHST- 2002/07/09 10:00 [entrez] AID - 987 [pii] AID - 10.1046/j.1365-201X.2002.00987.x [doi] PST - ppublish SO - Acta Physiol Scand. 2002 Jul;175(3):201-9. doi: 10.1046/j.1365-201X.2002.00987.x.