Short-term streptozotocin-induced diabetes induces blood pressure decreaseassociated with reduced aortic Ca-45(2+) uptake and selective depression of the sustained noradrenergic contraction

To test the hypothesis that diabetes can selectively affect the intracellul ar and extracellular components of the noradrenergic vascular response in r ats, we studied changes in blood pressure, in vitro vascular contraction a nd Ca-45(2+) uptake in experimental diabetes induced by injection of 60 mg/ kg of streptozotocin (STZ). One week after induction of diabetes mean blood pressure decreased significantly from 106 +/- 3 mmHg to 89 +/- 2 mmHg. Aft er incubation in Ca2+ = 1.6 mM, contraction of STZ aortic rings to 10(-7) M of norepinephrine was preserved in its intracellular component (Control: 2 31 +/- 28, STZ: 274 +/- 22 mgForce/mgTissue, NS) but depressed in its extra cellular component (Control: 277 +/- 24, STZ: 133 +/- 33 mgForce/mgTissue, P < 0.05). Uptake of Ca-45(2+) in the same rings was depressed in both comp onents. Norepinephrine contractions due to extracellular Ca2+ (prior deplet ion of norepinephrine-sensitive Ca2+ stores) unexpectedly exhibited a initi al component whose magnitude in control rings was similar to the response d ue to intracellular Ca2+ (extra: 503 +/- 65 mg, intra: 411 +/- 30 mgForce/m gTissue), and was not depressed in STZ preparations (399 +/- 62 mgForce/mgT issue). The sustained contraction to norepinephrine in extracellular Ca2+ w as significantly reduced in STZ aortas (1163 +/- 92 vs. 528 +/- 95 mgForce/ mgTissue). We conclude that: 1) Short-term streptozotocin-induced diabetes features reduced blood pressure along with deficient aortic Ca-45 uptake an d contraction to norepinephrine, and 2) Only the sustained phase of the nor epinephrine contraction, dependent on extracellular Ca2+, was depressed in the diabetic rats and could possibly be associated with the observed fall i n blood pressure.