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We carried out electrophysiological experiments on guinea‐pig mesenteric arteries in an attempt to clarify the modification of noradrenaline (NA) release from noradrenergic nerve terminals by the action of prejunctional adrenoceptors. NA (10(‐7)‐10(‐5) M) suppressed the amplitude of the first excitatory junction potential (e.j.p.(f], the facilitation process, and the e.j.p. after facilitation was completed (e.j.p.(s]with no change in the post‐junctional membrane properties of smooth muscles. These actions of NA on e.j.p.s were antagonized by high concentrations of extracellular Ca, [Ca]o, but not in a simple competitive manner. NA (10(‐7) M) suppressed the appearance but not the amplitude of the miniature e.j.p.s. These effects of NA on transmission indicate that NA acts on prejunctional nerve terminals and suppresses the release of NA from nerve terminals rather than producing a desensitization of post‐junctional adrenoceptors. Prazosin and phentolamine (10(‐6) M) did suppress the NA‐induced contraction (greater than 10(‐6) M) but did not suppress the contraction evoked by perivascular nerve stimulation, below a frequency of 1.0 Hz. At a dose of 10(‐7) M, yohimbine, clonidine, prazosin and phentolamine had no effect on the muscle membrane potential and resistance. Yet on the e.j.p.(f), yohimbine and clonidine caused suppression, phentolamine enhancement and prazosin had no effect. On the e.j.p.(s), yohimbine and phentolamine caused enhancement, clonidine suppression and prazosin had no effect. These results indicate that at least three different adrenoceptors are distributed on the neuromuscular junction in this tissue, i.e. alpha 1‐extrajunctional, alpha 2‐prejunctional, and an unknown subtype of intrajunctional adrenoceptors. Furthermore, the feedback mechanism on NA release is mediated by suppression of the influx of Ca. Nonselective and non‐specific actions of alpha‐adrenoceptor agonists and antagonists were also elucidated.

Prejunctional control mechanisms of neuromuscular transmission in mesenteric arteries of the guinea‐pig and rabbit were compared by examining excitatory junction potentials (e.j.p.s). The various agents used did not modify the membrane potential or resistance of smooth muscle cells of either tissue at the concentrations used in the present experiments. In the rabbit mesenteric artery, 10(‐7) M‐phentolamine and yohimbine had almost no effect on the amplitude of e.j.p.s or on facilitation. In the guinea‐pig mesenteric artery, phentolamine enlarged and yohimbine reduced the amplitude of the first e.j.p. but both agents markedly enlarged the amplitude of e.j.p.s evoked by repetitive perivascular nerve stimulation at frequencies over 0.1 Hz. In the rabbit mesenteric artery, isoprenaline and dibutyryl cyclic AMP inhibited the e.j.p.s and the facilitation evoked by repetitive stimulation, while in the guniea‐pig mesenteric artery, isoprenaline enhanced the amplitude of e.j.p.s and the facilitation process. In the rabbit mesenteric artery, ATP inhibited the amplitude of e.j.p.s with no change in facilitation and adenosine inhibited mainly the facilitation process evoked by repetitive perivascular nerve stimulation. In the guinea‐pig mesenteric artery, these agents had no effect on e.j.p.s or facilitation. In both the rabbit and guinea‐pig, indomethacin enlarged the amplitude and prolonged the duration of e.j.p.s. Prostaglandin E2 and F2 alpha inhibited the amplitude of e.j.p.s. Enlarged amplitudes of the e.j.p.s following pre‐treatment with indomethacin were inhibited by treatment with PGE2 or ATP. In the rabbit mesenteric artery, 8‐phenyltheophylline (an antagonist of P1 subtype of purinergic receptor) had no effect on the e.j.p.s, but these agents did reverse the inhibitory action of 2‐chloroadenosine (an agonist of P1 subtype of purinergic receptor) or adenosine on facilitation of e.j.p.s. Theophylline did not have any direct effect on e.j.p.s nor did it reverse the effects of adenosine or 2‐chloroadenosine. In the rabbit mesenteric artery, ATP and adenyl‐imidophosphate showed much the same potency in inhibiting the amplitude of e.j.p.s. Therefore, the ATP action on nerve terminals is not due to a high energy requiring mechanism. From these results we conclude that the control mechanisms related to noradrenaline (NA) release in nerve terminals differ in the guinea‐pig and rabbit mesenteric arteries.(ABSTRACT TRUNCATED AT 400 WORDS)

The pyroelectric charge of NH4Al(SO4)2·12H2O was measured after poling the crystal. It was found that the crystal becomes ferroelectric below the Curie temperature of Tc = -197°C on warming and has spontaneous polarization of 0.10μ C/cm2 at-240°C. The complex dielectric constant was measured at various frequencies in a frequency range between 330 Hz and 1 × 106 Hz. The observed temperature and frequency dependences of the complex dielectric constant can be approximated in terms of single relaxation time τ(T) of the Debye-type. Above the Curie temperature, τ(T) is described well by the relation τ(T) =(h/kB)·(T-To)-1·exp(ΔF/kbT) with the activation free energy ΔF =ΔFo[1 -α (T - Tc)]. The values of ΔFo and a are estimated to be 1.49 × 10-20 J and 0.0028 deg-1, respectively.

The structures of CuInSe 2 (CIS) grown on GaAs(001) by molecular beam epitaxy (MBE) were characterized by extended X-ray adsorption fine structure (EXAFS) for the local structure, changing the Cu/In ratio systematically. Radial distributions around Cu and Se atoms change drastically as a function of the Cu/In ratio. The results show that the ordered chalcopyrite phase is grown within a narrow composition range near the ideal stoichiometry. It is found that deviations from the stoichiometry in either direction cause a significant change in the local structure which results from the structural disorder and/or the phase separation. The temperature dependence of mean square relative displacement indicates the coexistence of Cu 2 Se in the Cu-rich region.

CuInSe 2 (CIS) films with Cu/In ratios of γ = 0.81-1.81 have been grown on (001)-oriented GaAs substrates by molecular beam epitaxy at substrate temperatures of T s = 350-550°C . Film properties were found to be substantially different for Cu- and In-rich regions. Cu-rich films were p-type, and streaky reflection high-energy electron diffraction (RHEED) patterns and sharp photoluminescence (PL) emissions were observed, suggesting high quality epitaxial films. In-rich films were highly resistive, and contained a large number of twins formed on {112} planes. A broad and strong PL emission, a donor-acceptor pair emission, was observed, which blue-shifted with increasing excitation power, indicating heavy compensation.

A thin layer electrode of birnessite-type manganese oxide was prepared by brushing a mixed solution of KOCOCH3 and Mn(OCOCH3)2 on a platinum substrate, followed by heating at 1073 K. The chemical composition of the electrode was KxMnOy (x = 0.33 and y ~ 2) with an interlayer spacing of c0 = 0.697 nm. The positive-potential going sweep on the electrode in an aqueous phase caused the deintercalation of K⁺ with an increase in c0. The quasi-reversible intercalation of K⁺ occurred with a subsequent negative-potential going sweep in a 0.2 mol/dm³ KCl solution. The electrochemical measurements suggested that K⁺ is not electrochemically active in the deintercalation/intercalation reaction but H⁺ is. The reaction proceeds based on a mechanism consisting of an electrochemical reaction (the redox reaction between Mn³⁺ and Mn⁴⁺) and an ion-exchange reaction between K⁺ and H⁺. The intercalation experiments in various alkali-metal chloride solutions showed the intercalation capacity to be in the order of Na ~ K > Li > Rb > Cs.