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Norepinephrine release in isolated arteries induced by K-free solution
The American Journal of Physiology
|February 1, 1977
Summary
Vascular smooth muscle contracture in K-free solution is mediated by neurogenic mechanisms involving norepinephrine release. This process is linked to Na+-K+-ATPase inhibition and can be blocked by phentolamine.
Area of Science:
- Vascular physiology
- Neuropharmacology
- Smooth muscle contractility
Background:
- Arteries with rich sympathetic innervation exhibit sustained contracture in K-free physiological salt solution (PSS).
- This phenomenon is influenced by nerve terminal integrity and adrenergic blockade.
Purpose of the Study:
- To elucidate the neurogenic mechanisms underlying K-free induced vascular smooth muscle contracture.
- To determine the temporal relationship between force development and norepinephrine (NE) release.
Main Methods:
- Utilized helical strips from rat tail/femoral and dog mesenteric arteries.
- Incubated arterial strips with 3H-labeled norepinephrine ([3H]NE) in PSS.
- Employed a superfusion system for isometric recordings and collection of superfusate to measure [3H]NE efflux.
Main Results:
- K-free PSS induced sustained contracture, blocked by phentolamine and absent in nerve-ablated arteries.
- Force development was temporally correlated with NE release in rat tail and dog mesenteric arteries.
- Both force development and NE release were potentiated by ouabain.
Conclusions:
- A neurogenic mechanism, involving norepinephrine release from adrenergic nerves, plays a critical role in K-free vascular smooth muscle contracture.
- This release is associated with the inhibition of Na+-K+-ATPase, highlighting a key pathway in vascular regulation.