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Rabbit aorta: electrical properties and agonist-induced depolarization.

G Haeusler¹, J E De Peyer

¹Department of Pharmaceutical Research, E. Merck, Darmstadt, F.R.G.

European Journal of Pharmacology

|July 18, 1989

Summary

Noradrenaline and angiotensin II cause depolarization in rabbit aorta smooth muscle cells, suggesting electromechanical coupling contributes to vasoconstriction. This contrasts with previous findings, highlighting a novel mechanism for blood vessel contraction.

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Area of Science:

Vascular smooth muscle electrophysiology
Cardiovascular pharmacology

Background:

Smooth muscle cells maintain a resting membrane potential crucial for vascular tone.
Understanding the electrical activity of aortic myocytes is key to comprehending vasoconstriction mechanisms.

Purpose of the Study:

To investigate the electrophysiological effects of noradrenaline and angiotensin II on rabbit aorta smooth muscle.
To determine the coupling mechanisms involved in vasoconstriction induced by these agents.

Main Methods:

Measurement of membrane potential and cable properties in rabbit aortic smooth muscle.
Application of noradrenaline, methoxamine, B-HT 920, and angiotensin II.
Analysis of current-voltage relationships and space constants.

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Main Results:

Noradrenaline and angiotensin II caused concentration-dependent depolarization of aortic myocytes.
Alpha 1-adrenoceptor stimulation by noradrenaline decreased membrane resistance and the space constant.
Angiotensin II acted as a partial agonist, inducing depolarization similar to alpha 1-agonists.

Conclusions:

Depolarization occurs in rabbit aorta smooth muscle upon stimulation with noradrenaline and angiotensin II.
Electromechanical coupling may play a significant role in vasoconstriction, alongside pharmacomechanical coupling.
These findings challenge previous assumptions about the mechanisms of vasoconstriction in this vascular bed.