Key result
Insulin or triiodothyronine treatment prevented diabetes-induced depressions of mechanical and biochemical indexes of ventricular relaxation in spontaneously hypertensive rats.
Why the study?
Does insulin or triiodothyronine treatment prevent diabetes-induced impairment of ventricular relaxation in spontaneously hypertensive rats?
Does insulin or triiodothyronine treatment prevent diabetes-induced impairment of ventricular relaxation in spontaneously hypertensive rats?
Hypertrophic ventricles in spontaneously hypertensive rats are more susceptible to diabetes-induced relaxation impairment, which can be prevented by insulin or triiodothyronine, suggesting a role for diabetes-associated hypothyroidism.
Animal models link diabetes to impaired relaxation in LVH via Ca2+ uptake; leaves open human translation and therapeutic targeting.
Diabetes, and possibly the hypothyroidism that attends diabetes, impairs mechanical relaxation of ventricular muscle, in part by depressing the rate of Ca2+ uptake by sarcoplasmic reticulum. Left ventricular hypertrophy exacerbates the adverse effects of diabetes on cardiac performance, but its effects on relaxation variables have not been well characterized. We examined the impact of streptozotocin-induced diabetes (8 weeks) on ventricular pressure load-dependent relaxation and sarcoplasmic reticular calcium uptake of hearts from spontaneously hypertensive rats and Wistar-Kyoto rats. Subsets of diabetic hypertensive rats were treated with either insulin (10 units/kg/day) or triiodothyronine (8-10 micrograms/kg/day). Diabetes impaired load-dependent relaxation and depressed sarcoplasmic reticular calcium uptake only in spontaneously hypertensive rat hearts. Either insulin or triiodothyronine treatment prevented the diabetes-induced depressions of both mechanical and biochemical indexes of relaxation. The results suggest that 1) hypertrophic ventricles of spontaneously hypertensive rats are more susceptible to the detrimental effects of diabetes on relaxation indexes than are the nonhypertrophic Wistar-Kyoto rat ventricles, and 2) the hypothyroidism that attends diabetes may contribute to the impaired relaxation of diabetic spontaneously hypertensive rat left ventricle.
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Davidoff et al. (1990) studied Diabetes and hypertension (animal model). Insulin or triiodothyronine vs. Untreated diabetic spontaneously hypertensive rats was evaluated on Ventricular pressure load-dependent relaxation and sarcoplasmic reticular calcium uptake. Insulin or triiodothyronine treatment prevented diabetes-induced depressions of mechanical and biochemical indexes of ventricular relaxation in spontaneously hypertensive rats.