Electrophysiological mechanisms of arterial muscle activation: alterations associated with cerebral vasospasm and hypertension.
The active state of arterial muscle can be regulated by electrical events occurring at the plasma membrane. Factors which affect the level of the resting membrane potential can markedly alter resting tone, and sensitivity and contractility to agonists. The relative K+ conductance (gk) appears to be a principle factor in this regard. Reduction of gk induces generation of action potentials with concomitant mechanical activity. Cerebral arteries exposed to subarachnoid blood exhibit altered electrical and mechanical properties which predispose them to spasm; a phenomenon related to a reduced gk. Arterial muscle from hypertensive animals exhibit membrane electrical properties which may contribute to an elevated peripheral vascular resistance, namely, an elevated PNa/Pk ratio and altered electrogenic ion transport. Upon exposure to elevated transmural pressures, isolated cerebral arterial muscle cells depolarize and generate spontaneous "pacemaker-like" action potentials, processes which appear to be Ca2+ dependent. Cerebral arteries from spontaneously hypertensive rats depolarize more to elevated transmural pressures when compared to WKY. This increased membrane depolarization to pressure may be the result of an elevated Ca2+ permeability and/or an alteration in gk at the SHR arterial muscle cell membrane. Thus, abnormal activation of arterial muscle can be mediated by factors controlling transmembrane electrical gradients and ionic conductance systems.
D000818:Animals; D002536:Cerebral Arteries / Q000503:physiopathology; D006973:Hypertension / Q000503:physiopathology*; D002546:Ischemic Attack, Transient / Q000503:physiopathology*; D009131:Muscle, Smooth, Vascular / Q000503:physiopathology*