Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
1999-3-29
pubmed:abstractText
Estrogen is known to exert a protective effect against cardiovascular disease. However, women with diabetes have three times the risk as compared with age-matched non-diabetic women. Our previous study on aortic rings of ovariectomized (OVX) female rats treated with 17-beta-estradiol (E2) demonstrated that the beneficial effect of estrogen is related to the basal release of NO from endothelial cells. In the present study, in order to understand why estrogen protection is abolished in diabetes, we tested vascular responses in OVX, streptozotocin-diabetic female rats and their non-diabetic controls receiving or not E2 replacement. Concentration-response curves to norepinephrine (NE) showed attenuation of the contractile response in E2-treated diabetic, with respect to non-diabetic preparations. This response was further impaired in diabetic, E2-deprived rats. The basal release of NO, as evaluated by concentration-related responses to N(G)-methyl-L-arginine acetate in NE-precontracted aortic rings, was found to be impaired in E2-treated diabetic rats, no further effect being induced by E2 deprivation. The endothelium-dependent relaxation produced by carbachol did not change between groups, whereas the relaxation produced by histamine was enhanced by both diabetes and E2 deprivation. However, E2 treatment counteracted the response to histamine only in preparations from non-diabetic animals. Finally, the relaxation induced by sodium nitroprusside, an endothelium-independent relaxant agent, was comparable between groups. These findings suggest that the lack of protective effects of estrogen in diabetes may be mainly ascribed to the failure of estrogen to reverse the impaired basal release of NO and the abnormal relaxation to histamine, which are observed in the aorta of diabetic rats.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0024-3205
pubmed:author
pubmed:issnType
Print
pubmed:volume
64
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
741-9
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:10075106-Animals, pubmed-meshheading:10075106-Aorta, pubmed-meshheading:10075106-Carbachol, pubmed-meshheading:10075106-Diabetes Mellitus, Experimental, pubmed-meshheading:10075106-Dose-Response Relationship, Drug, pubmed-meshheading:10075106-Enzyme Inhibitors, pubmed-meshheading:10075106-Estradiol, pubmed-meshheading:10075106-Female, pubmed-meshheading:10075106-Histamine, pubmed-meshheading:10075106-Muscle, Smooth, Vascular, pubmed-meshheading:10075106-Muscle Contraction, pubmed-meshheading:10075106-NG-Nitroarginine Methyl Ester, pubmed-meshheading:10075106-Nitric Oxide, pubmed-meshheading:10075106-Nitroprusside, pubmed-meshheading:10075106-Ovariectomy, pubmed-meshheading:10075106-Rats, pubmed-meshheading:10075106-Rats, Sprague-Dawley, pubmed-meshheading:10075106-Streptozocin, pubmed-meshheading:10075106-Superoxide Dismutase
pubmed:year
1999
pubmed:articleTitle
Diabetes abolishes the vascular protective effects of estrogen in female rats.
pubmed:affiliation
Institute of Pharmacological Sciences, University of Milan, Italy.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't