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Endothelin-1(1-31) induces spreading depolarization in rats.

D Jorks¹, S Major, A I Oliveira-Ferreira

¹Department of Experimental Neurology, Charité University Medicine Berlin, Berlin, Germany.

Acta Neurochirurgica. Supplement

|December 1, 2010

Summary

Endothelin-1(1-31) is less potent than endothelin-1 (ET-1) in inducing spreading depolarization (SD) and cerebral vasoconstriction. This suggests ET-1(1-31) may be a safer therapeutic target after subarachnoid hemorrhage.

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Area of Science:

Neuroscience
Pharmacology
Cerebrovascular Physiology

Background:

Endothelin-1 (ET-1) induces cerebral vasospasm and spreading depolarization (SD) post-aneurysmal subarachnoid hemorrhage (aSAH).
ET-1(1-31) is an alternate metabolic intermediate in ET-1 generation.
Investigating ET-1(1-31)'s role in SD is crucial for understanding aSAH pathophysiology.

Purpose of the Study:

To compare the efficacy of ET-1(1-31) and ET-1 in inducing SD.
To evaluate ET-1(1-31) as a potential therapeutic target in aSAH.

Main Methods:

Topical brain application of increasing ET-1, ET-1(1-31), or vehicle concentrations in 29 rats.
Recording of regional cerebral blood flow (rCBF) and direct current electrocorticogram (DC-ECoG) during superfusion.

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Statistical analysis using two-tailed Fisher's Exact Test to compare SD induction efficacy.

Main Results:

Both ET-1 and ET-1(1-31) induced SD at 10(-6) M.
ET-1 was significantly more potent in inducing SD at concentrations below 10(-6) M (P<0.001).
ET-1(1-31) demonstrated significantly lower efficacy in inducing SD compared to ET-1.

Conclusions:

ET-1(1-31) is less potent than ET-1 in inducing SD, suggesting it's a weaker vasoconstrictor.
ET-1(1-31) may represent a safer therapeutic target than ET-1 post-aSAH.
Shifting metabolism towards ET-1(1-31) could mitigate ET-1-induced vasoconstriction and SD while preserving beneficial ETA receptor activation.