1. Distribution of atrial natriuretic peptide and its effects on contraction and intracellular calcium in ventricular myocytes from streptozotocin-induced diabetic rat.
- Author
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Howarth FC, Adem A, Adeghate EA, Al Ali NA, Al Bastaki AM, Sorour FR, Hammoudi RO, Ghaleb NA, Chandler NJ, and Dobrzynski H
- Subjects
- Animals, Atrial Natriuretic Factor blood, Diabetes Mellitus, Experimental pathology, Heart Ventricles drug effects, Heart Ventricles pathology, Male, Muscle Cells drug effects, Myocardial Contraction drug effects, Rats, Rats, Wistar, Streptozocin toxicity, Atrial Natriuretic Factor pharmacology, Atrial Natriuretic Factor physiology, Diabetes Mellitus, Experimental physiopathology, Heart Ventricles physiopathology, Muscle Cells physiology, Myocardial Contraction physiology
- Abstract
The distribution of atrial natriuretic peptide (ANP) in blood plasma and cardiac muscle and its effects on ventricular myocyte contraction and intracellular free calcium concentration [Ca2+]i in the streptozotocin (STZ)-induced diabetic rat have been investigated. Blood plasma concentration and heart atrial and ventricular contents of ANP were significantly increased in STZ-treated rats compared to age-matched controls. STZ treatment increased the number of ventricular myocytes immunolabeled with antibodies against ANP. In control myocytes the percentage of cells that labeled positively and negatively were 17% versus 83%, respectively. However, in myocytes from STZ-treated rat the percentages were 52% versus 53%. Time to peak (TPK) shortening was significantly and characteristically prolonged in myocytes from STZ-treated rats (360+/-5 ms) compared to controls (305+/-5 ms). Amplitude of the Ca2+ transient was significantly increased in myocytes from STZ-treated rats compared to controls (0.39+/-0.02 versus 0.29+/-0.02 fura-2 RU in controls) and treatment with ANP reduced the amplitude of the Ca2+ transient to control levels. ANP may have a protective role in STZ-induced diabetic rat heart.
- Published
- 2005
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