TY - JOUR
T1 - Effects of glycosylated hemoglobin on vascular responses in vitro
AU - Oltman, Christine L.
AU - Gutterman, David D.
AU - Scott, Eric C.
AU - Bocker, Jennifer M.
AU - Dellsperger, Kevin C.
N1 - Funding Information:
We thank Gilbert Falcon for technical assistance during portions of this study. Supported by: NIH RO1 HL51308 KCD) and VA Merit Review DDG). Dr. Oltman was supported by a National Research Service Award F32HL09198 and T32HL07121). Ms. Bocker was supported by a pre-doctoral American Heart Association Fellowship. Drs. Gutterman and Dellsperger are Established Investigators of the American Heart Association.
PY - 1997/4
Y1 - 1997/4
N2 - Vascular responses to endothelium-dependent vasodilators are greatly impaired in vivo, while isolated blood vessels from animals with diabetes mellitus demonstrate less consistent degrees of impairment. Glycation of proteins, such as hemoglobin, has been implicated in the vascular abnormalities associated with diabetes. Objective: The purpose of this study was to test the hypothesis that glycosylated hemoglobin is capable of reducing endothelium-dependent vasodilator responses, possibly explaining impaired dilation observed in vivo. Methods: To test this hypothesis, the effect of glycosylated hemoglobin (GH) on vascular responses was studied in several vascular beds, including ventricular microvessels and coronary, mesenteric, femoral, and renal arteries. Coronary arterioles were isolated and mounted between two glass pipettes in a pressurized (30 cmH2O) organ chamber. Isolated artery segments were studied using a standard isometric ring technique. Results: In ventricular microvessels, 10 nM nGH (non-GH) and GH both attenuated the relaxation to Ach. A lower concentration, 1 nM nGH or GH, did not alter dilation to Ach. In coronary, fernoral, mesenteric and renal artery segments, endothelium-dependent responses were not altered by the presence of 10 or 100 nM nGH or GH. Conclusion: In coronary microvessels, and coronary, femoral, mesenteric and renal arteries, GH is not responsible for the impaired endothelial function associated with diabetes mellitus.
AB - Vascular responses to endothelium-dependent vasodilators are greatly impaired in vivo, while isolated blood vessels from animals with diabetes mellitus demonstrate less consistent degrees of impairment. Glycation of proteins, such as hemoglobin, has been implicated in the vascular abnormalities associated with diabetes. Objective: The purpose of this study was to test the hypothesis that glycosylated hemoglobin is capable of reducing endothelium-dependent vasodilator responses, possibly explaining impaired dilation observed in vivo. Methods: To test this hypothesis, the effect of glycosylated hemoglobin (GH) on vascular responses was studied in several vascular beds, including ventricular microvessels and coronary, mesenteric, femoral, and renal arteries. Coronary arterioles were isolated and mounted between two glass pipettes in a pressurized (30 cmH2O) organ chamber. Isolated artery segments were studied using a standard isometric ring technique. Results: In ventricular microvessels, 10 nM nGH (non-GH) and GH both attenuated the relaxation to Ach. A lower concentration, 1 nM nGH or GH, did not alter dilation to Ach. In coronary, fernoral, mesenteric and renal artery segments, endothelium-dependent responses were not altered by the presence of 10 or 100 nM nGH or GH. Conclusion: In coronary microvessels, and coronary, femoral, mesenteric and renal arteries, GH is not responsible for the impaired endothelial function associated with diabetes mellitus.
KW - Acetylcholine
KW - Coronary vasculature
KW - Diabetes
KW - Dog
KW - Glycosylated hemoglobin
KW - Microcirculation
KW - arteries
UR - http://www.scopus.com/inward/record.url?scp=0030909706&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0030909706&partnerID=8YFLogxK
U2 - 10.1016/S0008-6363(97)00016-3
DO - 10.1016/S0008-6363(97)00016-3
M3 - Article
C2 - 9217888
AN - SCOPUS:0030909706
SN - 0008-6363
VL - 34
SP - 179
EP - 184
JO - Cardiovascular Research
JF - Cardiovascular Research
IS - 1
ER -