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Characterization of contractile function in diabetic hypertensive cardiomyopathy in adult rat ventricular myocytes
L E Wold1, D P Relling, P B Colligan
1Department of Pharmacology, Physiology and Therapeutics, University of North Dakota School of Medicine, Grand Forks, ND 58203, USA.
Insights
Diabetic cardiomyopathy and hypertensive cardiomyopathy worsen heart function. Combining diabetes and hypertension severely impairs cardiac contractility at the single myocyte level, increasing cardiovascular risk.
Area of Science:
- Cardiovascular physiology
- Diabetology
- Hypertension research
Background:
- Diabetes and hypertension independently cause myocardial dysfunction, increasing cardiovascular morbidity and mortality.
- The combined effect of diabetes and hypertension on cardiac function is often more severe than either condition alone.
Purpose of the Study:
- To investigate the impact of combined diabetes and hypertension on cardiac contractile function at the single ventricular myocyte level.
- To characterize the specific cellular mechanisms underlying diabetic hypertensive cardiomyopathy.
Main Methods:
- Adult spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats were induced into diabetes using streptozotocin (STZ).
- Ventricular myocyte contractile properties, including peak shortening (PS), time-to-peak shortening (TPS), time-to-90% relengthening (TR90), and maximal shortening/relengthening velocities (+/-dL/dt), were assessed.
- Responsiveness to extracellular calcium (Ca2+) and stimulus frequency-response curves were evaluated.
Main Results:
- Diabetic hypertensive rats (SHR-STZ) exhibited enlarged hearts, hyperglycemia, and elevated blood pressure.
- Myocytes from SHR-STZ showed depressed peak shortening and prolonged contraction/relaxation times compared to controls.
- Impaired calcium responsiveness was observed in diabetic myocytes (WKY-STZ), while hypertensive myocytes (SHR, SHR-STZ) displayed reduced maximal shortening/relengthening velocities.
- The SHR-STZ group demonstrated an altered stimulus frequency-peak shortening relationship, indicating significant contractile dysfunction.
Conclusions:
- The combination of diabetes and hypertension leads to a greater impairment of cardiac contractile function at the single myocyte level than either condition individually.
- Diabetic hypertensive cardiomyopathy involves complex alterations in myocyte mechanics, calcium handling, and responsiveness to stimulation.
- These findings underscore the critical need for integrated management strategies for patients with both diabetes and hypertension to mitigate severe cardiac outcomes.
Abstract:
Diabetes and hypertension both produce myocardial dysfunction that accelerates cardiovascular morbidity and mortality. Coexistence of the two often results in a more severe cardiomyopathy than either process alone. The purpose of this study was to characterize the contractile function of diabetic hypertensive cardiomyopathy at the single myocyte level. Adult spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats were made diabetic with a single injection (55 mg/kg) of streptozotocin (STZ). Contractile properties of ventricular myocytes were evaluated, including peak shortening (PS), time-to-peak shortening (TPS), time-to-90% relengthening (TR90) and maximal velocities of shortening/relengthening (+/-dL/d t). The experimental animals exhibited enlarged heart size, elevated blood glucose and systolic blood pressure. PS was unchanged (SHR), enhanced (WKY-STZ) or depressed (SHR-STZ) compared to control (WKY). Myocytes from all experimental groups displayed prolonged TPS and TR90 compared to the WKY group, although only those from the hypertensive groups (SHR, SHR-STZ) were associated with reduced +/-dL/d t. Additionally, myocytes from the WKY-STZ but not the SHR or the SHR-STZ groups exhibited impaired responsiveness to increased extracellular Ca2+. Myocytes from the SHR-STZ group displayed a leftward shift of the stimulus frequency-peak shortening response curve compared to the WKY group. These results confirmed observations at the multicellular levels that combination of diabetes and hypertension results in a greater impairment of cardiac contractile function than is seen with either disease alone.
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