Nielsen H, Bonnema S J, Flyvbjerg A
Institute of Pharmacology, Aarhus County Hospital, Denmark.
Pharmacol Toxicol. 1995 Sep;77(3):209-15. doi: 10.1111/j.1600-0773.1995.tb01014.x.
The effects of osmolality, diabetes, and insulin-treatment on microvascular contractility were examined in mesenteric resistance arteries (internal diameter approximately 250 microns) isolated from streptozotocin-induced diabetic rats, streptozotocin-induced diabetic rats treated with 1-3 U insulin/day during the week before being killed, and age- and sex-matched control rats. Vessels were mounted in a microvascular myograph for isometric tension recording and responses were generated in physiological salt solutions with varying amounts of glucose or mannitol 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 produced by partial depolarization with 50 mmol/l potassium were not dependent on glucose or mannitol concentrations of the bathing medium; also, these 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 regression lines between rat groups. Moreover, vessels from streptozotocin-induced diabetic rats were less sensitive to noradrenaline than were vessels from control rats; vessels from insulin-treated streptozotocin-induced diabetic animals had the lowest sensitivity to noradrenaline. These data suggest that osmolality, diabetes, and insulin-treatment independently affect microvascular sensitivity to the endogenous neurotransmitter, noradrenaline.