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Characteristics of impaired endothelium-dependent relaxation of rat aorta after streptozotocin-induced diabetes.
Zhongguo Yao Li Xue Bao. 1999 Sep; 20(9):844-50.ZY

Abstract

AIM

To study whether impaired endothelium-dependent relaxation (EDR) in early diabetic mellitus in response to different receptor-mediated and nonreceptor-mediated vasodilators ran parallel and its possible mechanism.

METHODS

Isometric tension recording in aortic rings from streptozotocin (Str)-induced diabetic and age-matched nondiabetic rats.

RESULTS

EDR induced by receptor agonist acetylcholine (ACh), histamine (His) or bradykinin (BK) were all significantly reduced in diabetic rings compared with control rings, whereas nonreceptor agonist calcimycin-induced EDR was well reserved in diabetic rings [IC50 control: (0.13 +/- 0.07) mumol.L-1 diabetic: (0.14 +/- 0.06) mumol.L-1, P > 0.05, n = 7]. Cyclopiazonic acid (CPA) which also is a nonreceptor mediated endothelium-dependent vasorelaxant and cells' capacitative Ca2+ entry stimulant, failed to trigger EDR in diabetic rings. Pretreatment with N omega-nitro-L-arginine methylester (L-NAME, 0.3 mmol.L-1) not only abolished all of the EDR elicited by above mentioned vasodilators in either of diabetic or control rings, but also leveled responses triggered by each of the agonists between diabetic and control rings. Upon the maximal EDR induced by ACh (1 mol.L-1) or CPA (3 mumol.L-1) in phenylephrine (1 mumol.L-1) precontracted rings, calcimycin (1 mumol.L-1) further relaxed diabetic rings, but contracted control preparations. When endothelium was denuded, relaxation evoked by sodium nitroprusside and contractions triggered by CPA or His were all identical between diabetic and control rings.

CONCLUSION

Receptor agonists but not nonreceptor agonists-induced EDR are commonly impaired in 4-wk Str-induced diabetic rat aorta, and this defective effect is attributable to the low formation of EDRF/NO which is related to impaired capacitative Ca2+ entry pathway in endothelium.

Authors+Show Affiliations

Department of Pharmacology, Faculty of Medicine, Zhejiang University, Hangzhou 310031, China. shenjz@mail.hz.zj.cnNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

11245095

Citation

Shen, J Z., and X F. Zheng. "Characteristics of Impaired Endothelium-dependent Relaxation of Rat Aorta After Streptozotocin-induced Diabetes." Zhongguo Yao Li Xue Bao = Acta Pharmacologica Sinica, vol. 20, no. 9, 1999, pp. 844-50.
Shen JZ, Zheng XF. Characteristics of impaired endothelium-dependent relaxation of rat aorta after streptozotocin-induced diabetes. Zhongguo Yao Li Xue Bao. 1999;20(9):844-50.
Shen, J. Z., & Zheng, X. F. (1999). Characteristics of impaired endothelium-dependent relaxation of rat aorta after streptozotocin-induced diabetes. Zhongguo Yao Li Xue Bao = Acta Pharmacologica Sinica, 20(9), 844-50.
Shen JZ, Zheng XF. Characteristics of Impaired Endothelium-dependent Relaxation of Rat Aorta After Streptozotocin-induced Diabetes. Zhongguo Yao Li Xue Bao. 1999;20(9):844-50. PubMed PMID: 11245095.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Characteristics of impaired endothelium-dependent relaxation of rat aorta after streptozotocin-induced diabetes. AU - Shen,J Z, AU - Zheng,X F, PY - 2001/3/14/pubmed PY - 2001/5/22/medline PY - 2001/3/14/entrez SP - 844 EP - 50 JF - Zhongguo yao li xue bao = Acta pharmacologica Sinica JO - Zhongguo Yao Li Xue Bao VL - 20 IS - 9 N2 - AIM: To study whether impaired endothelium-dependent relaxation (EDR) in early diabetic mellitus in response to different receptor-mediated and nonreceptor-mediated vasodilators ran parallel and its possible mechanism. METHODS: Isometric tension recording in aortic rings from streptozotocin (Str)-induced diabetic and age-matched nondiabetic rats. RESULTS: EDR induced by receptor agonist acetylcholine (ACh), histamine (His) or bradykinin (BK) were all significantly reduced in diabetic rings compared with control rings, whereas nonreceptor agonist calcimycin-induced EDR was well reserved in diabetic rings [IC50 control: (0.13 +/- 0.07) mumol.L-1 diabetic: (0.14 +/- 0.06) mumol.L-1, P > 0.05, n = 7]. Cyclopiazonic acid (CPA) which also is a nonreceptor mediated endothelium-dependent vasorelaxant and cells' capacitative Ca2+ entry stimulant, failed to trigger EDR in diabetic rings. Pretreatment with N omega-nitro-L-arginine methylester (L-NAME, 0.3 mmol.L-1) not only abolished all of the EDR elicited by above mentioned vasodilators in either of diabetic or control rings, but also leveled responses triggered by each of the agonists between diabetic and control rings. Upon the maximal EDR induced by ACh (1 mol.L-1) or CPA (3 mumol.L-1) in phenylephrine (1 mumol.L-1) precontracted rings, calcimycin (1 mumol.L-1) further relaxed diabetic rings, but contracted control preparations. When endothelium was denuded, relaxation evoked by sodium nitroprusside and contractions triggered by CPA or His were all identical between diabetic and control rings. CONCLUSION: Receptor agonists but not nonreceptor agonists-induced EDR are commonly impaired in 4-wk Str-induced diabetic rat aorta, and this defective effect is attributable to the low formation of EDRF/NO which is related to impaired capacitative Ca2+ entry pathway in endothelium. SN - 0253-9756 UR - https://www.unboundmedicine.com/medline/citation/11245095/Characteristics_of_impaired_endothelium_dependent_relaxation_of_rat_aorta_after_streptozotocin_induced_diabetes_ DB - PRIME DP - Unbound Medicine ER -