COEXISTENCE OF PARAELECTRIC/PROTON-GLASS AND FERROELECTRIC (ANTIFERROELECTRIC) ORDERS IN Rb_{1-x}(NH_{4})_{x}H_{2}AsO_{4} CRYSTALS
This paper reviews the results of dielectric studies of the proton glass state in a mixed crystal Rubidium Ammonium Dihydrogen Arsenate (RADA) The coexistence of paraelectric/proton glass and ferroelectric or antiferroelectric orders, confirmed by other studies, has been discussed in detail. The phase diagram of RADA is asymmetric. The proton glass state exists for ammonium concentration in the range of 0.1 < x < 0.5 . The phase diagram of deuterated DRADA is presented. The proton glass state region in DRADA, 0.2 < x < 0.35 is narrower than that for non-deuterated RADA. The effects of hydrostatic pressure on the dielectric properties in the proton glass state are presented. The glass temperature Tg decreases with pressure and is expected to vanish at 5 kbar. Low temperature behaviour is still an open question, since there is no experimental evidence of Tg(p) dependence below 4K for proton glass systems.
Proton glassy behavior in Rb1-x(NH4)xH2AsO4 mixed crystal.
Ce comportement est etudie en mesurant la constante dielectrique suivant les axes a et c, entre 30 et 200 K. La limite de la phase entre la phase ferroelectrique et l'etat de verre protonique est observe entre x=0,13 et 0,20. On observe une limite similaire avec la phase antiferroelectrique entre 0,44 et 0,49. Pour 0,23≤x≤0,44, les donnees dielectriques peuvent etre echelonnees en utilisant la loi de Vogel-Fuchler. Construction du diagramme de phase
Mechanism of the depressor response to dopamine in the rat treated with phenoxybenzamine.
Alterations of hypotensive responses to dopamine by antagonists were characterized in alpha-blocked, anaesthetized rats. Responses were not affected by d-propranolol (0.1 mg/kg) whereas d,1-propranolol (0.1 mg/kg) or haloperidol (1.0 mg/kg) attenuated them; higher doses of inhibitors (1.0 mg/kg; 5.0 mg/kg, respectively) failed to produce a higher inhibition, but combinations of low doses abolished the depressor responses. In adrenalectomized rats, hypotensive responses decreased; haloperidol always attenuated the responses while d,1-propranolol became ineffective. Dopamine produced an enhancement of plasma adrenaline and noradrenaline levels, which was decreased by d,1-propranolol and increased by haloperidol. The data suggest that in rats the depressor component of dopamine is due to activation of both dopaminergic and beta-adrenoceptors. The beta component appears to be due to the release of adrenaline. The results also support the concept of the existence in sympathetic nerve endings and adrenal glands of stimulatory beta-adrenergic and inhibitory dopaminergic prejunctional receptors.