Electrical properties of smooth muscle cell membrane and neuromuscular transmission in the guinea-pig basilar artery.
1 The membrane properties of smooth muscle cells and neuromuscular transmission in the guinea-pig basilar artery were investigated by use of microelectrodes.2 The membrane potential was -47.0 mV and the muscle tissue possessed cable-like properties as determined by the current-voltage relationships. The mean value of the spacè constant was 0.78 mm.3 An outward current produced a graded response and, in some cases, spike generation. This membrane response was enhanced in the presence of tetraethylammonium (TEA, 5 mM), and an increased concentration of TEA (10 mM) generated spontaneous spikes in most of the cells. Action potentials induced by TEA were abolished in the presence of MnCl(2) (5 mM) but not by isoprenaline (4 x 10(-6) M).4 Acetylcholine (ACh), over 10(-7) M, hyperpolarized the membrane and decreased the membrane resistance. This hyperpolarization increased in the presence of low [K](o) (below 5.9 mM), but decreased in [K](o) concentrations over 17.8 mM. Pretreatment with atropine (10(-6) M) suppressed the ACh-induced hyperpolarization. Therefore, this action of ACh is due to an increase in the K-conductance of the membrane produced by activation of the muscarinic receptors.5 Noradrenaline in concentrations up to 10(-4) M did not modify the membrane potential and resistance, while 10(-5) M, histamine, 5-hydroxytryptamine and adenosine triphosphate (ATP) depolarized the membrane. The depolarization induced by histamine or ATP was suppressed by reducing [Na](o). The histamine-induced depolarization was accompanied by an increase and the ATP-induced one by a decrease in the membrane resistance. The action of histamine was suppressed by treatment with H(1)- but not H(2)-receptor blocking agents (dephenhydramine and cimetidine, respectively).6 Perivascular nerve stimulation (0.2 ms pulse duration) evoked excitatory junction potentials (e.j.ps). An increase in the number and frequency of stimuli enhanced the e.j.p. amplitude. In the presence of 1 mM TEA, a spike was evoked on the e.j.ps. A very high concentration of phentolamine (3.6 x 10(-4) M) or the usual concentration of tetrodotoxin (10(-7) M) abolished the generation of e.j.ps. Spontaneously generated miniature e.j.ps were never recorded from the resting membrane.7 The results are discussed in relation to regional specificities of smooth muscle cells of cerebral arteries in the guinea-pig.
D000109:Acetylcholine / Q000494:pharmacology; D000255:Adenosine Triphosphate / Q000494:pharmacology; D000818:Animals; D001488:Basilar Artery / Q000294:innervation / Q000502:physiology*; D005260:Female; D006168:Guinea Pigs; D008297:Male; D008564:Membrane Potentials; D009131:Muscle, Smooth, Vascular / Q000502:physiology*; D009469:Neuromuscular Junction / Q000502:physiology*; D009638:Norepinephrine / Q000494:pharmacology; D011188:Potassium / Q000494:pharmacology; D009435:Synaptic Transmission; D013757:Tetraethylammonium Compounds / Q000494:pharmacology
D013757:Tetraethylammonium Compounds; D000255:Adenosine Triphosphate; D000109:Acetylcholine; D011188:Potassium; D009638:Norepinephrine