TY - JOUR
T1 - Influence of diabetes on norepinephrine-induced inositol 1,4,5-trisphosphate levels in rat aorta
AU - Abebe, Worku
AU - MacLeod, Kathleen M.
N1 - Funding Information:
This work was supportedb y a grant from the British Columbiaa nd Yukon Heart Foundation.T he authorsw ish to thankD r. John Langlandsfo r his experta dvicer egardingth e I(1,4,5)3P assay.
PY - 1991
Y1 - 1991
N2 - The effects of norepinephrine on total tissue levels of inositol 1,4,5-triphosphate were measured by protein binding assay in aortas from rats with chronic streptozotocin-induced diabetes and from age-matched control rats. In both control and diabetic aortas, norepinephrine induced a rapid, transient and concentration-dependent elevation of inositol 1,4,5-trisphosphate content during contraction. Maximum production of inositol 1,4,5-trisphosphate in response to norepinephrine was greater in diabetic than in control aortas. However, the sensitivities of control and diabetic aortas to norepinephrine for inositol 1,4,5-trisphosphate production were not significantly different. Enhanced norepinephrine-induced production of inositol 1,4,5-trisphosphate in diabetic aortas may contribute to the increased maximum contractile responsiveness of these arteries to the agonist. However, since enhanced contractile responses of diabetic aortas to norepinephrine were also detected at times when inositol 1,4,5-trisphosphate levels were not significantly increased, other factors also appear to be involved in mediating enhanced contractions of diabetic arteries to norepinephrine.
AB - The effects of norepinephrine on total tissue levels of inositol 1,4,5-triphosphate were measured by protein binding assay in aortas from rats with chronic streptozotocin-induced diabetes and from age-matched control rats. In both control and diabetic aortas, norepinephrine induced a rapid, transient and concentration-dependent elevation of inositol 1,4,5-trisphosphate content during contraction. Maximum production of inositol 1,4,5-trisphosphate in response to norepinephrine was greater in diabetic than in control aortas. However, the sensitivities of control and diabetic aortas to norepinephrine for inositol 1,4,5-trisphosphate production were not significantly different. Enhanced norepinephrine-induced production of inositol 1,4,5-trisphosphate in diabetic aortas may contribute to the increased maximum contractile responsiveness of these arteries to the agonist. However, since enhanced contractile responses of diabetic aortas to norepinephrine were also detected at times when inositol 1,4,5-trisphosphate levels were not significantly increased, other factors also appear to be involved in mediating enhanced contractions of diabetic arteries to norepinephrine.
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U2 - 10.1016/0024-3205(91)90084-O
DO - 10.1016/0024-3205(91)90084-O
M3 - Article
C2 - 1886452
AN - SCOPUS:0025896155
SN - 0024-3205
VL - 49
SP - PL85-PL90
JO - Life Sciences
JF - Life Sciences
IS - 13
ER -
