Decreased Ca2+ influx into the endothelium contributes to the decrease in endothelium-dependent relaxation in the aorta of streptozotocin-induced diabetic mice.
Experiments were designed to investigate the role of Ca2+ influx into the endothelium in the relaxation of mouse aorta caused by acetylcholine (ACh) in streptozotocin (STZ)-induced diabetic and age-matched control mice. When Ca2+ was added to the bath, Ca2+ caused a transient contraction followed by relaxation in Ca(2+)-free medium containing 2 x 10(-6) M prostaglandin F2 alpha (PGF2 alpha) and 10(-5) M ACh in the control experiments. On the other hand, Ca2+ showed a long lasting contraction in STZ-induced diabetic rats. These results suggest that influx of Ca2+ into the endothelium is significantly attenuated in the diabetic vessels, and production or release of relaxing factor is markedly decreased.
Kamata
K
K
Department of Physiology and Morphology, Hoshi University, Tokyo, Japan.
Sugiura
M
M
Kasuya
Y
Y
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects; D002118:Calcium / Q000378:metabolism* / Q000494:pharmacology; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism* / Q000503:physiopathology; D015237:Dinoprost / Q000494:pharmacology; D004730:Endothelium, Vascular / Q000378:metabolism* / Q000502:physiology; D066298:In Vitro Techniques; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D009126:Muscle Relaxation / Q000502:physiology; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology*; D051381:Rats
D015237:Dinoprost; D000109:Acetylcholine; D002118:Calcium