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Biomedical subjects

M Ariyoshi

Publications and source records attributed to M Ariyoshi.

47 records · Page 3Linked to original sources

Mianserin blocks alpha 2 adrenoceptors in submucous neurones of the guinea-pig caecum.

Intracellular recordings were made from submucous plexus neurones of the guinea-pig caecum in vitro. The peak amplitude of the adrenergic inhibitory postsynaptic potential (IPSP) was depressed by mianserin in a dose-dependent manner (300 nM-100 microM). This was due to a direct blockade of postsynaptic alpha 2 adrenoceptors. The nicotinic excitatory postsynaptic potential (EPSP) and the non-cholinergic EPSP were not affected by mianserin (100 microM). The presynaptic inhibition of the release of acetylcholine, mediated by presynaptic alpha 2 receptors, was also blocked by mianserin (30 microM). The results suggest that mianserin antagonizes both pre- and post-synaptic alpha 2 adrenoceptors in enteric plexus neurones.

Adrenergic alpha-Antagonists↗

Presynaptic effects of cholecystokinin octapeptide on neuromuscular transmission in the frog.

Intracellular recordings were obtained from the frog sartorius muscle end-plate to investigate the effects of cholecystokinin octapeptide (CCK-8) on cholinergic transmission at the neuromuscular junction. A brief bath-application of CCK-8 (1 microM) produced a depression, followed by a long-lasting facilitation, of the amplitude and the quantal content of the end-plate potential (epp). CCK-8 had a biphasic effect, an initial depression followed by an augmentation of the frequency of the miniature epps. CCK-8 did not affect the sensitivity of the nicotinic receptor at the end-plate. These results suggest a significant role for CCK-8 in cholinergic transmission, possibly as a modulator of the evoked release of acetylcholine from motor nerve terminals.

Animals↗

Glucocorticoid modulates the sensitivity of the GABAA receptor on primary afferent neurons of bullfrogs.

With intracellular and voltage-clamp recording techniques, we have demonstrated that the glucocorticoids, prednisolone and hydrocortisone at a concentration of 5 microM to 1 mM, reversibly depressed gamma-aminobutyric acid (GABA)-induced responses on primary afferent neurons of bullfrogs. An analysis with dose-response curves revealed that the glucocorticoids decreased the sensitivity of the GABAA receptor in a non-competitive manner. We suggest that glucocorticoids act as an antagonist of the GABAA receptor on primary afferent neurons, probably by reducing the number of functional GABAA receptor ionic channel complexes.

Animals↗

Histamine is an antagonist of the acetylcholine receptor at the frog endplate.

The effects of histamine on the acetylcholine (ACh) receptor-channel complex were examined by means of voltage-clamp at the frog endplate. ACh was ionophoretically applied to the endplate. Histamine was added to the perfusate. Histamine (100 nM - 1 mM) reversibly depressed the peak amplitude of the ACh-induced inward current in a dose-dependent manner. The double reciprocal plot of the dose-response relationship between the peak ACh current and the amount of ACh applied suggested that histamine (100 microM) depressed the ACh-induced current in a competitive manner. Histamine prevented the specific ACh binding site within the receptor-channel complex from binding erabutoxin, a sea-snake venom, which binds irreversibly to the specific ACh binding site. Histamine had no detectable effects on the equilibrium potential of the endplate current but shortened the half-decay time of the endplate current in a voltage-dependent manner. It was therefore concluded that histamine blocks not only the specific ACh binding site but also interacts with the ACh-channel site. The present experiments strongly suggest that histamine can act as an antagonist to modulate nicotinic cholinergic transmission.

Acetylcholine↗

Histamine as an endogenous antagonist of nicotinic ACh-receptor.

The mechanism of an inhibitory effect of histamine on the sensitivity of frog skeletal muscle endplate was analyzed by studying the dose-response relation between the quantity of ACh applied iontophoretically and the ACh-induced postsynaptic current (ACh current), and also the interaction between histamine and erabutoxin-b (ETX-b). The results obtained show that histamine, like curare, decreased the sensitivity of ACh-receptor in a competitive manner.

Animals↗

Influence of running pace upon performance: effects upon treadmill endurance time and oxygen cost.

Three possible patterns of pacing (type 1, fast/slow; type 2, slow/fast; and type 3, steady rate) were compared over a 1400 m, 4 min run. The subsequent running time to exhaustion at 370 m . min-1 was significantly longer with a type 1 than with a type 2 protocol (P less than 0.05). The steady rate pattern gave results intermediate between type 1 and type 2 pacing. Data for oxygen debt and recovery heart rate confirmed the superiority of type 1 pacing. Possible explanations included (1) a reduction of inefficient anaerobic work, and (2) a greater mechanical efficiency associated with the better matching of required effort to a tapering physiological power. Runners should aim at a steady physiological rather than a steady physical load.

Adult↗

Influence of running pace upon performance: effects upon oxygen intake, blood lactate, and rating of perceived exertion.

Three different techniques of middle distance running (fast/slow, slow/fast, and steady pace) have been compared in terms of oxygen intake, blood lactate and ratings of perceived exertion (RPE). The subjects (10 middle distance and long distance male runners) carried out the three patterns of running on the laboratory threadmill according to a randomly ordered sequence, on each occasion covering 1400 m in 4 min. The fast/slow protocol resulted in a rapid and sustained on-transient of oxygen intake, less lactate accumulation, and a lower rating of perceived exertion during the final 2 min of th4 min run. Physiological data thus support coaching impressions of the superiority of the fast/slow protocol.

Adult↗