Linked Life Data

6311651

Source:http://linkedlifedata.com/resource/pubmed/id/6311651

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
1983-11-23
pubmed:abstractText
To more fully characterize the alterations in myocardial adrenergic and cholinergic receptors induced by the diabetic state, we investigated the binding characteristics of (--) [3H] dihydroalprenolol to beta adrenergic receptors (bAR), [3H] prazosin to alpha adrenergic receptors (aAR), and [3H] quinuclidinyl-benzilate to muscarinic cholinergic receptors (MCR) in myocardial membranes derived from rats 8 wk after treatment with streptozotocin. We also studied an equal number of animals from three control groups: free-eating nondiabetics, pair-weighted nondiabetics, and streptozotocin-treated animals treated daily with insulin. Diabetic hearts demonstrated 27% fewer bAR (P less than 0.01) and 31% fewer aAR (P less than 0.01) than free-eating controls, without changes in MCR, and without changes in antagonist affinity, agonist affinity, or agonist slope factor (pseudo-Hill coefficient) for any class of receptors. Food restriction had no effect on receptor characteristics, and treatment of diabetic rats with insulin prevented any downregulation of cardiac bAR or aAR. The parallel decrease in both bAR and aAR suggests that streptozotocin-induced hypothyroidism is not the primary causative factor of bAR downregulation in this model, since hypothyroidism produces upregulation of aAR. Furthermore, the lack of change in cardiac MCR suggests that the adrenergic receptor alterations are not the result of nonspecific abnormalities of protein synthesis in the diabetic heart. Further studies are required to establish the physiologic significance of these receptor alterations, but these data support the hypothesis that altered adrenergic receptor properties may underlie, at least in part, the chronotropic and inotropic abnormalities of cardiac performance that are associated with the diabetic state.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0012-1797
pubmed:author
pubmed:issnType
Print
pubmed:volume
32
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
881-6
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:6311651-Animals, pubmed-meshheading:6311651-Blood Glucose, pubmed-meshheading:6311651-Body Weight, pubmed-meshheading:6311651-Cell Membrane, pubmed-meshheading:6311651-Diabetes Mellitus, Experimental, pubmed-meshheading:6311651-Diabetic Diet, pubmed-meshheading:6311651-Dihydroalprenolol, pubmed-meshheading:6311651-Insulin, pubmed-meshheading:6311651-Male, pubmed-meshheading:6311651-Myocardium, pubmed-meshheading:6311651-Organ Size, pubmed-meshheading:6311651-Prazosin, pubmed-meshheading:6311651-Quinuclidinyl Benzilate, pubmed-meshheading:6311651-Rats, pubmed-meshheading:6311651-Rats, Inbred Strains, pubmed-meshheading:6311651-Receptors, Adrenergic, alpha, pubmed-meshheading:6311651-Receptors, Adrenergic, beta, pubmed-meshheading:6311651-Receptors, Cholinergic, pubmed-meshheading:6311651-Receptors, Muscarinic
pubmed:year
1983
pubmed:articleTitle
Effects of experimental diabetes on adrenergic and cholinergic receptors of rat myocardium.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't