The role of sodium pump activity in the hyperpolarization and in subsequent depolarization of smooth muscle in response to stimulation of post-synaptic alpha 1-adrenoceptors.
The electrical and mechanical activities of guinea pig taenia coli smooth muscle were measured by a "sucrose gap" technique. Under the same experimental conditions the ionic content of smooth muscle was also measured. The mean value of the resting potential was 56.9 +/- 1.1 mV (S.E.M.; n = 46). In normal Krebs solution immediately after dissection intracellular sodium amounted to 30.1, and intracellular calcium to 1.5 mmole x kg-1 wet weight. In response to adrenaline administration there was a Ca-dependent hyperpolarization (peak, 6.8 +/- 0.3 mV S.E.M.; n = 5) and an increased Na efflux with a rate constant (k) of 0.16 min-1 (60'). Removal of adrenaline was followed by so-called "postadrenaline depolarization" i.e. the decrease of the membrane potential was greater than the initial rise, an effect enhanced by ouabain (2 X 10(-5) M). Clonidine (5.3 X 10(-6) M), a selective presynaptic-adrenoceptor (alpha 2-receptor) stimulant failed to produce hyperpolarization, however, phenylephrine (5 X 10(-5) M) a pure postsynaptic alpha-adrenoceptor (alpha 1-receptor) stimulant produced a similar effect as adrenaline. In addition, yohimbine (1.4 X 10(-6) M), a typical presynaptic alpha-adrenoceptor inhibitor failed to affect the action of adrenaline or phenylephrine. These facts indicate that the alpha 1-adrenoceptors present on the smooth muscle are different from those situated presynaptically on the cholinergic nerve terminals modulating the release of acetylcholine. The effect of ouabain to lower membrane potential proved to be Ca2+-dependent. The intracellular sodium content was enhanced by ouabain from 30.1 to 90.9 +/- 4.7 mmole x kg-1 wet weight (60'). On washing out ouabain, hyperpolarization "post-ouabain hyperpolarization" was detected, i.e. the rise of membrane potential was greater than the initial fall. It is suggested that the sodium pump plays a significant role in the post-ouabain hyperpolarization. Direct calculation of sodium movements suggests that the sodium permeability is about 3.7 p-mole x cm-2 x sec-1 and the pump generates a current of 1.06 X 10(-7) A x cm-2 which, in fact, while crossing the smooth muscle membrane with a resistance of 30-60 k omega cm2 would produce a potential difference of 3.2-6.4 mV. It is suggested that the electrogenic sodium pump may contribute to the resting membrane potential about 15 mV, a value obtained from the summation of depolarization induced by ouabain and hyperpolarization produced by adrenaline.
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D003000:Clonidine / Q000494:pharmacology; D003106:Colon / Q000502:physiology*; D004837:Epinephrine / Q000494:pharmacology; D005260:Female; D006168:Guinea Pigs; D066298:In Vitro Techniques; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D009119:Muscle Contraction / Q000187:drug effects; D009130:Muscle, Smooth / Q000378:metabolism / Q000502:physiology*; D010042:Ouabain / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D011941:Receptors, Adrenergic / Q000502:physiology*; D011942:Receptors, Adrenergic, alpha / Q000502:physiology*; D012964:Sodium / Q000378:metabolism*; D015016:Yohimbine / Q000494:pharmacology
D011941:Receptors, Adrenergic; D011942:Receptors, Adrenergic, alpha; D010656:Phenylephrine; D015016:Yohimbine; D010042:Ouabain; D012964:Sodium; D003000:Clonidine; D002118:Calcium; D004837:Epinephrine