title: Electrophysiological properties of the rat middle cerebral artery at different levels of passive wall tension.
abstract: 1. Simultaneous measurements of intracellular membrane potential and myogenic tone of proximal segments of the rat middle cerebral artery, mounted in a small vessel myograph, were made at two levels of passive wall tension. 2. At low levels of passive tension (less than 0.25 mN/mm) vessels had a resting membrane potential of approximately -65 mV. Addition of KCl (5-60 mmol/L), BaCl2 (0.01-3 mmol/L) or tetraethylammonium (TEA; 0.1-3 mmol/L) resulted in a concentration-dependent depolarization, to approximately -40 mV, generally associated with a contractile response. After the application of high levels of passive tension (to approximately 2 mN/mm maximum) the resting membrane potential of the smooth muscle cells was -40 to -45 mV. This more positive membrane potential was generally associated with an increase in myogenic tone of the vessel. Under these conditions, addition of 5-20 mmol/L KCl resulted in a strong hyperpolarization of the cell along with a concomitant decrease in myogenic tone of the artery. The hyperpolarization and vasorelaxation induced by KCl (5-20 mmol/L) were blocked by BaCl2 (0.5-1 mmol/L). 3. While the addition of ryanodine (10 mumol/L) to vessels under low tension had no effect, when added to a vessel under high tension, this agent caused a rhythmic oscillation in membrane potential. This oscillation was augmented by BaCl2 (1 mmol/L) and inhibited by nifedipine (10 nmol/L) and 4-aminopyridine (1 mmol/L). 4. This study suggests that the electrophysiological and mechanical properties of the isolated rat middle cerebral artery depend on the passive resting conditions under which the vessel is studied. The depolarization of membrane potential observed with increased passive tension appears to result from the closure of an inward rectifying K+ channel. These results indicate that the inward rectifying K+ channel plays an important role in regulating vascular reactivity due to its functional dependence on the mechanical status of the blood vessel.
authors.affiliation: Baker Medical Research Institute, Prahran, Victoria, Australia.
authors.forename: G A
authors.initials: GA
authors.lastname: McPherson
authors.forename: S G
authors.initials: SG
authors.lastname: Keily
mesh_terms: D000818:Animals; D002536:Cerebral Arteries / Q000187:drug effects / Q000502:physiology*; D004305:Dose-Response Relationship, Drug; D004594:Electrophysiology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology; D009126:Muscle Relaxation / Q000187:drug effects / Q000502:physiology; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology*; D009213:Myography; D015221:Potassium Channels / Q000187:drug effects / Q000502:physiology; D011189:Potassium Chloride / Q000494:pharmacology; D051381:Rats; D011921:Rats, Inbred WKY; D014665:Vasodilator Agents / Q000494:pharmacology*
chemical_list: D004791:Enzyme Inhibitors; D015221:Potassium Channels; D014665:Vasodilator Agents; D011189:Potassium Chloride