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Alterations in atrial reactivity in a strain of spontaneously diabetic rats
Author(s) -
Durante William,
Sunahara Fred A.,
Sen Amar K.
Publication year - 1989
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1989.tb12571.x
Subject(s) - chronotropic , medicine , endocrinology , phenylephrine , isoprenaline , adenosine , propranolol , inotrope , stimulation , agonist , chemistry , adenosine receptor , diabetes mellitus , receptor , heart rate , blood pressure
1 The present study examined the reactivity of atria from control and spontaneously diabetic rats to various adrenoceptor agonists and to adenosine. 2 Isoprenaline (1.5 nM‐1500 n m ) produced concentration‐dependent increases in inotropy which were unchanged in diabetic atria. However, the sensitivity to isoprenaline‐induced changes in chronotropy was reduced in diabetic preparations. 3 In the presence of propranolol (2 μ m ), phenylephrine (0.2 μ m ‐100 μ m ) produced concentration‐dependent increases in both inotropy and chronotropy; however, atria from diabetic rats exhibited a much greater maximal response. The diabetic state did not alter the sensitivity to phenylephrine. 4 Adenosine (0.15 μ m ‐300 μ m ) produced concentration‐dependent decreases in both inotropy and chronotropy which were unchanged in diabetic atria. 5 Radioligand binding studies revealed that both α 1 ‐and β‐adrenoceptor populations were substantially reduced in atria from diabetic rats. However, there was no change in receptor affinity for either adrenoceptor. 6 These results show that diabetes leads to an alteration in atrial reactivity to adrenoceptor stimulation. Future studies examining steps following hormone‐receptor coupling are required in order to characterize this defect.