H. Nielsen et al., EFFECTS OF DIABETES, INSULIN-TREATMENT, AND OSMOLALITY ON CONTRACTILITY OF ISOLATED RAT RESISTANCE ARTERIES, Pharmacology & toxicology, 77(3), 1995, pp. 209-215
The effects of osmolality, diabetes, and insulin-treatment on microvas
cular contractility were examined in mesenteric resistance arteries (i
nternal diameter approximately 250 mu m) isolated from streptozotocin-
induced diabetic rats, streptozotocin-induced diabetic rats treated wi
th 1-3 U insulin/day during the week before being killed, and age- and
sex-matched control rats. Vessels were mounted in a microvascular myo
graph for isometric tension recording and responses were generated in
physiological salt solutions with varying amounts of glucose or mannit
ol added. The passive response (expressed as the diameter the vessels
would maintain if relaxed and exposed to a transmural pressure of 100
mmHg), the maximal response to noradrenaline, and the response produce
d by partial depolarization with 50 mmol/l potassium were not dependen
t on glucose or mannitol concentrations of the bathing medium; also, t
hese responses were not dissimilar in vessels from the three groups of
rats tested. The sensitivity to noradrenaline, however, was inversely
related to the concentration of glucose (P<0.01) and mannitol (P<0.01
) of the bathing medium without significant differences in slopes of r
egression lines between rat groups. Moreover, Vessels from streptozoto
cin-induced diabetic rats were less sensitive to noradrenaline than we
re vessels from control rats; vessels from insulin-treated streptozoto
cin-induced diabetic animals had the lowest sensitivity to noradrenali
ne. These data suggest that osmolality, diabetes, and insulin-treatmen
t independently affect microvascular sensitivity to the endogenous neu
rotransmitter, noradrenaline.