In order to elucidate further the abnormal myocardial Ca2+ metabolism in 
diabetes mellitus, voltage-gated Ca2+ channels and beta-receptors were 
quantified in myocardial membranes of short- and long-term diabetic rats. 
Diabetes was induced by an injection of streptozotocin (STZ). Animals were 
killed 2, 4, 7, 90 and 200 days after STZ. A group of diabetic animals were 
treated with insulin for 20 days following 180 days of untreated diabetes. 
Diabetic animals developed low triiodothyronine syndrome. During short-term 
diabetes, the maximum binding capacity (MBC) for Ca2+ channels was reduced by 
25% at day 4 (p < 0.05) and the beta-receptor MBC was reduced by 48% (p < 0.05). 
A normalizing tendency was observed at day 7 for both receptor types; 
insulin-treated rats did not differ from controls at that time. After 90 and 200 
days of untreated diabetes the Ca2+ channel MBC had increased by 36% and 27%, 
respectively (p < 0.05). Twenty days of strictly regulated blood glucose 
following 180 days of untreated diabetes totally normalized the Ca2+ channel 
MBC. This is in contrast to a previous report where insulin treatment did not 
normalize the Ca2+ channel MBC. Total beta-receptor MBCs did not differ from 
control values 90 and 200 days after STZ. In conclusion, an increase in rat 
myocardial Ca2+ channel MBC during long-term diabetes was fully normalized by 
short-term insulin treatment. The increase in sarcolemmal Ca2+ channels could 
serve to compensate for a defect coupling of the beta-receptor to adenylate 
cyclase. An elevated Ca2+ channel number may, at least theoretically, lead to 
increased Ca2+ flow across the cardiac sarcolemma and in this way contribute to 
the diabetic cardiomyopathy by increasing the intracellular Ca2+ concentration.