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Insulin attenuates norepinephrine-induced venoconstriction. An ultrasonographic study
A Grover1, C Padginton, M F Wilson
1Department of Medicine, State University of New York at Buffalo, Millard Fillmore Hospitals, USA.
Hypertension (Dallas, Tex. : 1979)
|April 1, 1995
Summary
Insulin causes veins to widen, a process that can be blocked by methylene blue. This study quantifies insulin's venodilator effects using ultrasound measurements of venous diameter.
Area of Science:
- Vascular Physiology
- Pharmacology
Background:
- Insulin's effects on blood vessels are not fully understood.
- Direct, quantitative assessment of insulin's impact on venous tone is needed.
Purpose of the Study:
- To quantitatively assess insulin's effects on venous diameter.
- To investigate the mechanism of insulin-induced vasodilation.
Main Methods:
- Utilized a modified ultrasonographic technique to measure venous diameter in healthy subjects.
- Administered incremental doses of norepinephrine to induce venoconstriction.
- Combined norepinephrine with incremental doses of insulin to assess vasodilation.
- Investigated the role of guanylate cyclase inhibition using methylene blue.
Main Results:
- Norepinephrine caused dose-dependent venoconstriction.
- Insulin significantly increased venous diameter in a dose-dependent manner when combined with norepinephrine.
- Methylene blue inhibited the venodilator effect of insulin, suggesting a role for guanylate cyclase.
Conclusions:
- Insulin exerts a venodilator effect, increasing venous diameter.
- This venodilator effect appears to be mediated, at least in part, by the guanylate cyclase pathway.