MEMBRANE PROPERTIES AND EXCITATORY NEUROMUSCULAR TRANSMISSION IN THE SMOOTH MUSCLE OF DOG CEREBRAL ARTERIES

Open Access
Publisher Website
Google Scholar
Abstract
1 Drug actions on electrical and mechanical properties of smooth muscle cells and neuromuscular transmission in the canine cerebral arteries were investigated by use of microelectrode and isometric tension recording methods. 2 In the basilar and middle cerebral arteries, the resting membrane potentials were — 49.4 mV and — 51.7 mV, respectively, the length constants 0.57 mm and 0.45 mm, respectively and the time constants 142 ms and 118 ms, respectively. 3 Outward current pulses did not evoke the spike in either artery but did evoke the spike under conditions of pretreatment with 10 mm tetraethylammonium (TEA). 4 The maximum slope of depolarization produced by a ten fold increase in [K]o plotted on a log scale was 40.1 mV in the basilar artery and 42.2 mV in the middle cerebral artery. 2-Nicotinamidoethyl nitrate, the K-permeability accelerator, had no effect on the membrane potential. 5 K-free or ouabain [10−5m] treatment slightly depolarized the membrane. Re-addition of K [5.9 mm] hyperpolarized the membrane by several mV. Thus, the contribution of an active Na-K pump in the membrane potential seems to be small. 6 In both arteries, acetylcholine, adenosine, noradrenaline and isoprenaline in concentrations up to 10−5 m did not modify the membrane potential and resistance, while 5-hydroxytryptamine (over 10−8 m) and ATP (over 10−5 m) depolarized the membrane, decreased the membrane resistance and produced a dose-dependent contraction. Adenosine suppressed the contraction evoked by excess [K]o(39.8 mm). 7 Perivascular nerve stimulation produced excitatory junction potentials (e.j.ps). Often e.j.ps were followed by a hyperpolarization. Repetitive stimulation produced facilitation after several stimuli and depression followed. In some cells, this depression appeared without facilitation. 8 The e.j.ps ceased with pretreatment with guanethidine (10−6 m) or tetrodotoxin (3 × 10−7 m), while phentolamine (10−7m) and yohimbine (10−7m) enhanced the amplitude of e.j.ps. ATP (10−5 m) and noradrenaline (10−6 m) supressed and prazosin had little effect on the e.j.ps. Atropine (10−6 m) also had no effect on the e.j.ps. 9 Specific features of the cerebral artery and systemic vascular beds were compared, and the features of adrenoceptors on the smooth muscle membrane were compared with findings in other vascular beds.