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Daniel Landau
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Chen Chayat Department of Pediatrics A, Shraga Segal Department of Microbiology and Immunology, Department of Pathology, Laboratory for Molecular Medicine and Israeli Rat Genome Center, Faculty of Health Sciences, Soroka University Medical Center, Ben Gurion University, PO Box 151, Beer Sheva 84101, Israel

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Nili Zucker
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Eli Golomb Department of Pediatrics A, Shraga Segal Department of Microbiology and Immunology, Department of Pathology, Laboratory for Molecular Medicine and Israeli Rat Genome Center, Faculty of Health Sciences, Soroka University Medical Center, Ben Gurion University, PO Box 151, Beer Sheva 84101, Israel

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Channa Yagil Department of Pediatrics A, Shraga Segal Department of Microbiology and Immunology, Department of Pathology, Laboratory for Molecular Medicine and Israeli Rat Genome Center, Faculty of Health Sciences, Soroka University Medical Center, Ben Gurion University, PO Box 151, Beer Sheva 84101, Israel

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Yoram Yagil Department of Pediatrics A, Shraga Segal Department of Microbiology and Immunology, Department of Pathology, Laboratory for Molecular Medicine and Israeli Rat Genome Center, Faculty of Health Sciences, Soroka University Medical Center, Ben Gurion University, PO Box 151, Beer Sheva 84101, Israel

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Yael Segev Department of Pediatrics A, Shraga Segal Department of Microbiology and Immunology, Department of Pathology, Laboratory for Molecular Medicine and Israeli Rat Genome Center, Faculty of Health Sciences, Soroka University Medical Center, Ben Gurion University, PO Box 151, Beer Sheva 84101, Israel

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Cardiac remodeling is a key event in both diabetic and hypertensive heart diseases. In the present study, we investigated early myocardial changes in an animal model, the male Sabra rat model (SBH/y) of salt-induced hypertension-rendered diabetic with streptozotocin. Control non-diabetic (C), diabetic (D), and D or C rats made hypertensive by salt loading (DS or CS) were studied after 6 weeks. M-mode echocardiography revealed that left ventricular internal dimension during diastole and systole were significantly increased in D and DS, but not in C or CS. Concurrently, we found in D and DS an increase in cardiac β-myosin heavy chain, atrial natriuretic peptide, skeletal α-actin mRNA, type III collagen, and transforming growth factor-β. Myocardial angiotensin-converting enzyme (ACE) mRNA levels were increased while ACE2 mRNA levels were decreased in both D and DS groups. Cardiac angiotensin-1 (AT1) receptor protein levels were unchanged but the levels of phosphorylated (p) ERK and Jun-NH2-protein kinase (JNK) were increased in D and DS. In conclusion, we detected early cardiac changes in diabetic rats that were unrelated to hypertension. The increase in ACE, the decrease in ACE2, and the increase in cardiac pERK and pJNK suggest an increase in free angiotensin II and AT1R signaling in the diabetic myocardium as a possible mechanism contributing to cardiac remodeling in diabetes.

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-08-0040
Volume/Issue:
Volume 197: Issue 1
Free access