To clarify the changes of esophageal motility along with age, we performed esophageal manometry on 47 healthy volunteers, and compared the values of four groups under 49 years old (n=11), 50 to 59 (n=15), 60 to 69 (n=11), and over 70 years old (n=10). Resting lower esophageal sphincter (LES) pressure in the group over 70 years old showed the tendency of decrease, but not statistically significant. Nadir LES pressure on swallow-induced relaxation was not statistically different among 4 groups. On esophageal body testing, percentage of non-conduction sequence in the group 60 to 69 and over 70 years old was statistically higher compared with that of the group under 49 years old (p<0.05) but spared in some elderly subjects. Percentage of simultaneous contractions was not statistically different among 4 groups. Peristaltic contraction amplitude in the group over 70 years old was significantly lower than that of the group under 49 years old both at the level of 5 cm above (p<0.01) and 10 cm above LES (p<0.05). We speculate that the influence of aging on esophageal motility is the reduced transmission sequence of peristalsis and contractility of esophageal body. This alteration along with age may differ from the pathological condition of scleroderma or diffuse esophageal spasm.

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We investigated the mode of relaxant effects of cytochalasin D, a capping agent of actin filaments, on contractile responses in the rat aorta and chicken gizzard smooth muscles.Cytochalasin D inhibited the contraction induced by high K⁺ or noradrenaline (10nM-1μM) without changing cytosolic Ca²⁺ level ([Ca²⁺] i) in the rat aorta. In the absence of external Ca²⁺, 12-deoxyphorbol 13-isobutylate (DPB) (1μM) induced sustained contraction without increasing in [Ca²⁺] i and cytochalasin D also inhibited this contraction. In the permeabilized chicken gizzard smooth muscle, cytochalasin D inhibited the Ca²⁺ (1-10μM)-induced contraction. Cytochalasin D also inhibited the Ca²⁺-independent contraction in the muscle which had been thiophosphorylated by ATP_γS. Cytochalasin D decreased the velocity of superprecipitation in the chicken gizzard native actomyosin (myosin B) affecting neither the level of MLC phosphorylation nor Mg²⁺-ATPase activity. These results suggest that cytochalasin D inhibits smooth muscle contractions without any effect on the Ca²⁺-dependent MLC phosphorylation or subsequent activation of myosin ATPase activity. Based on these evidences, it is concluded that cytochalasin D may inhibit smooth muscle contraction possiblly through uncoupling of the force generation from the activated actomyosin Mg²⁺-ATPase.

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Lactate liberation from thoracic aortas and intestinal smooth muscles of the guinea pig, rabbit and rat, as well as coronary arteries of the dog were determined under aerobic and hypoxic conditions (95% N₂ instead of O₂). In all smooth muscles tested, the lactate liberation was inhibited in the presence of oxygen, being known as the Pasteur effect. The rates of lactate release from guinea pig aortas and taenia caeci under hypoxia were approximately 10 times greater than those under aerobic conditions. The rate of lactate release from other smooth muscles tested were 3-4 times greater under hypoxic than aerobic conditions. The extent of Pasteur effect was not affected by a removal of adventitial layer from the rabbit aorta nor by the different size of the dog coronary arteries. These results suggest that taenia caeci and aortas of the guinea pig intrinsically possess a strong regulatory system in the glycolytic activity, being highly sensitive to the presence of oxygen.

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