Key result
Diabetes fails to alter adrenoceptor-mediated platelet aggregation despite enhanced ADP responses.
Why the study?
Diabetes influences cardiac and vascular sensitivity to adrenoceptor stimulation, but its effect on platelet adrenoceptor-mediated aggregation responses is unclear.
Does diabetes alter the influence of adrenoceptor stimulation on platelet aggregation in rats?
Does diabetes alter the influence of adrenoceptor stimulation on platelet aggregation in rats?
Unlike the heart and vasculature, the influence of adrenoceptor stimulation on platelet aggregation is not altered by diabetes in a rat model.
Adrenoceptor effects on platelet aggregation remain intact in diabetic rats; leaves open relevance to human diabetes and cardiovascular outcomes.
Studies of cardiac and vascular responses have previously demonstrated that diabetes influences the sensitivity of these tissues to adrenoceptor stimulation. Adrenoceptors are also present on platelets where they modulate aggregatory responses. The present study investigates the influence of diabetes on these platelet adrenoceptor-mediated responses. 2. Rats were made diabetic with streptozotocin and platelet aggregatory responses to ADP were examined 2 or 12 weeks later. Aggregation to ADP of platelets from 2-week-diabetic rats was similar to that of platelets from age-matched controls, but platelets from 12-week-diabetic animals exhibited an enhanced aggregation to ADP. 3. In all groups studied, beta-adrenoceptor stimulation with isoprenaline caused a concentration-dependent inhibition of aggregation to ADP, whilst alpha-adrenoceptor stimulation with adrenaline was found to potentiate aggregation to ADP. The degree of inhibition or potentiation was found to remain unchanged by diabetes of either 2 or 12 weeks duration. 4. Previously reported increases in cardiac beta-adrenoceptor sensitivity and aortic alpha-adrenoceptor sensitivity were confirmed 2-week-diabetic animals, but these sensitivity changes were not observed in 12-week-diabetic rats. 5. The results indicate that, unlike the heart and vasculature, the influences of adrenoceptor stimulation on platelet aggregation are not altered by diabetes, even when aggregation to ADP is enhanced.
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Austin et al. (1995) studied Diabetes. Diabetes (streptozotocin-induced) vs. Age-matched controls was evaluated on Platelet aggregatory responses to ADP and adrenoceptor stimulation. Diabetes of 2 or 12 weeks duration did not alter the degree of inhibition or potentiation of platelet aggregation by adrenoceptor stimulation, despite enhanced aggregation to ADP at 12 weeks.
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