TY - JOUR

T1 - Streptozotocin-induced diabetes decreases conducted vasoconstrictor response in mouse cremaster arterioles.

AU - Rai, A

AU - Riemann, M

AU - Gustafsson, F

AU - Holstein-Rathlou, N H

AU - Torp-Pedersen, C

N1 - Keywords: Animals; Arterioles; Blood Glucose; Body Weight; Diabetes Mellitus, Experimental; Male; Mice; Mice, Inbred C57BL; Potassium Chloride; Vasoconstriction

PY - 2008

Y1 - 2008

N2 - A conducted vasomotor response (CVR) is characterized by the spread of vasoconstriction or vasodilatation both up- and downstream from a local stimulation site in the microcirculation. It is believed to coordinate vasomotor responses within the microcirculation, and to contribute to the control of the major feed arteries to a given organ or tissue. Microvascular disease is a common and severe complication in diabetes, and we therefore studied CVR in streptozotocin (STZ) diabetic mice to examine whether changes in CVR might have a role in the pathophysiology of microvascular dysfunction in diabetes. The mouse cremasteric arterioles were stimulated locally with KCl and the resulting local response as well as conducted responses at 500 microm and 1000 microm were measured in control and STZ treated mice. Diabetes (n=8) induced by intraperitoneal injection of STZ in a dose of 100 mg/kg (mean blood glucose 16.8+/-2.1 mmol/l) decreased the conduction of vasoconstriction from 27.3+/-1.1% to 21.4+/-1.6% at 500 microm (p<0.01) and from 17.4+/-1.0% to 9.8+/-1.1% at 1000 microm (p<0.01) as compared with control (n=9). Treatment with either the protein kinase C beta II inhibitor (LY341684) or the oxygen radical scavenger tempol, did not improve the decreased conduction of vasoconstriction, but when administered together, the conduction of vasoconstriction was improved from 21.4+/-1.6% to 26.5+/-0.8% at 500 microm and 9.8+/-1.1% to 16.5+/-0.7% at 1000 microm (p<0.01). We conclude that STZ induced diabetes reduces conducted vasoconstriction to KCl in mouse cremasteric arterioles, and combined treatment with both an oxygen radical scavenger and a protein kinase C beta II inhibitor improves the reduced conducted vasoconstriction.

AB - A conducted vasomotor response (CVR) is characterized by the spread of vasoconstriction or vasodilatation both up- and downstream from a local stimulation site in the microcirculation. It is believed to coordinate vasomotor responses within the microcirculation, and to contribute to the control of the major feed arteries to a given organ or tissue. Microvascular disease is a common and severe complication in diabetes, and we therefore studied CVR in streptozotocin (STZ) diabetic mice to examine whether changes in CVR might have a role in the pathophysiology of microvascular dysfunction in diabetes. The mouse cremasteric arterioles were stimulated locally with KCl and the resulting local response as well as conducted responses at 500 microm and 1000 microm were measured in control and STZ treated mice. Diabetes (n=8) induced by intraperitoneal injection of STZ in a dose of 100 mg/kg (mean blood glucose 16.8+/-2.1 mmol/l) decreased the conduction of vasoconstriction from 27.3+/-1.1% to 21.4+/-1.6% at 500 microm (p<0.01) and from 17.4+/-1.0% to 9.8+/-1.1% at 1000 microm (p<0.01) as compared with control (n=9). Treatment with either the protein kinase C beta II inhibitor (LY341684) or the oxygen radical scavenger tempol, did not improve the decreased conduction of vasoconstriction, but when administered together, the conduction of vasoconstriction was improved from 21.4+/-1.6% to 26.5+/-0.8% at 500 microm and 9.8+/-1.1% to 16.5+/-0.7% at 1000 microm (p<0.01). We conclude that STZ induced diabetes reduces conducted vasoconstriction to KCl in mouse cremasteric arterioles, and combined treatment with both an oxygen radical scavenger and a protein kinase C beta II inhibitor improves the reduced conducted vasoconstriction.

U2 - 10.1055/s-0028-1083813

DO - 10.1055/s-0028-1083813

M3 - Journal article

C2 - 18792878

VL - 40

SP - 651

EP - 654

JO - Hormone and Metabolic Research

JF - Hormone and Metabolic Research

SN - 0018-5043

IS - 9

ER -