TY - JOUR
T1 - Effect of morphine on electrophysiological properties of circular and longitudinal muscles
AU - Gilbert, R. J.
AU - Sarna, S. K.
AU - Harder, D. R.
PY - 1987
Y1 - 1987
N2 - We have measured the effects of morphine on the intracellular electrophysiological properties of smooth muscle cells from the circular and longitudinal muscle layers of the canine jejunum. Morphine hyperpolarized the circular muscle membrane by ~12 mV and increased the electrical control activity (ECA) amplitude and dV/dt. Morphine had no significant effect on the electrical properties of the longitudinal muscle cells. The morphine-induced hyperpolarization of the circular muscle membrane was blocked by tetrodotoxin (TTX) and naloxone, but not by atropine and hexamethonium, propranolol, or phentolamine. Morphine significantly increased the slope of the resting membrane potential vs. the log of the potassium concentration in bathing medium from 38 to 50 mV/decade. The sodium permeability to potassium permeability ratio, calculated from the Goldman constant field equation, was reduced by morphine from 0.13 to 0.07 at 4 mM of K+. The above results suggest that when measured by intracellular techniques, morphine hyperpolarizes the circular muscle membrane by release of a nonadrenergic, noncholinergic neurotransmitter. The mechanism of this hyperpolarization is consistent with an increase in potassium conductance.
AB - We have measured the effects of morphine on the intracellular electrophysiological properties of smooth muscle cells from the circular and longitudinal muscle layers of the canine jejunum. Morphine hyperpolarized the circular muscle membrane by ~12 mV and increased the electrical control activity (ECA) amplitude and dV/dt. Morphine had no significant effect on the electrical properties of the longitudinal muscle cells. The morphine-induced hyperpolarization of the circular muscle membrane was blocked by tetrodotoxin (TTX) and naloxone, but not by atropine and hexamethonium, propranolol, or phentolamine. Morphine significantly increased the slope of the resting membrane potential vs. the log of the potassium concentration in bathing medium from 38 to 50 mV/decade. The sodium permeability to potassium permeability ratio, calculated from the Goldman constant field equation, was reduced by morphine from 0.13 to 0.07 at 4 mM of K+. The above results suggest that when measured by intracellular techniques, morphine hyperpolarizes the circular muscle membrane by release of a nonadrenergic, noncholinergic neurotransmitter. The mechanism of this hyperpolarization is consistent with an increase in potassium conductance.
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U2 - 10.1152/ajpgi.1987.252.3.g333
DO - 10.1152/ajpgi.1987.252.3.g333
M3 - Article
C2 - 3826373
AN - SCOPUS:0023274281
SN - 0193-1857
VL - 252
SP - G333-G338
JO - American Journal of Physiology - Gastrointestinal and Liver Physiology
JF - American Journal of Physiology - Gastrointestinal and Liver Physiology
IS - 3 (15/3)
ER -