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the natural mitotic microtubule remodeling that was also accompanied by SOCE inhibition. Short exposure to paclitaxel, a microtubule-stabilizing drug, bolstered SOCE, whereas long exposure resulted in microtubule disruption and SOCE inhibition. Actin-modifying drugs did not affect SOCE. These findings indicate that mitotic microtubule remodeling plays a significant role in the inhibition of SOCE during mitosis.

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ABSTRACT. Stress-induced hyperthermia is observed in animals exposed to stressful conditions. In our previous study, plant-derived fragrances such as green odor and alpha-pinene were shown to suppress this stress response in rats. In the present study, we examined the concentration-dependence of the alpha-pinene effects on stress-induced hyperthermia. Male rats carrying telemetry transmitters were transferred individually to a new cage containing bedding that had been sprayed with 0.3, 0.03, and 0.003% concentrations of alphapinene or control solvent. Following transfer to the novel environment, the body temperature increased significantly, and this response was clearly suppressed when the cage was scattered with 0.03% alpha-pinene only. These results suggest that the effect of alpha -pinene on stress-induced hyperthermia can be observed only at a certain concentration. KEY WORDS: alpha-pinene, concentration effect, hyperthermia.J. Vet. Med. Sci. 65(9): 1023-1025, 2003 When an animal is exposed to stressful situations, autonomic responses including a temporary increase of body temperature, namely stress-induced hyperthermia or emotional fever, have been observed in several species [3,4,[6][7][8][9][24][25][26]. Recent studies have suggested that in phylogeny this stress response involving body temperature has emerged between amphibians and reptiles [5]. In our previous study, it was revealed that an external olfactory stimulation could affect this autonomic stress response. Namely, plant-derived fragrances such as green odor and alphapinene showed ameliorative effects on stress-induced hyperthermia [1]. In addition, by using this model Kikusui et al. could also show an opposite effect in which exposure to alarm pheromones resulted in an aggravation of this hyperthermia [13]. When the odorant concentration was changed, the impression or the effects accompanying that odor to the physiological response and behavior in vivo could be different. For example, the event-related potential P300 was altered its amplitude by emotional change, and the experiment using components of the green odor induced different amplitudes of P300 depending on its concentration [20]. Feeding behavior of goats was suppressed by only higher concentration of trans-2-hexenal [11]. These results suggest that each odorant has a certain concentration at which it is most effective. In the present study we therefore examined concentration-dependence of the effect of alphapinene on stress-induced hyperthermia by preparing both lower (0.003%) and higher (0.3%) concentrations in addition to the concentration (0.03%) that in our previous study was confirmed to be effective.The basic experimental procedures and animals were as described previously [1]. Briefly, male Wistar rats (9 weeks old: Clea Japan, Inc., Tokyo, Japan) weighing approximately 230-300 g were housed in groups of 4 animals per cage with wood shavings (Soft chip: Japan SLC, Inc

In order to define the role of angiotensin II (AngII) receptor subtypes, AT1 and AT2, in platelet activation, we examined the effects of AngII and receptor antagonists on both aggregability and phosphorylation status of protein kinase C (PKC) isoforms in human platelets obtained from 56 healthy volunteers. AngII promoted both spontaneous and agonist (collagen and ADP) stimulated platelet aggregation at concentrations of 10 nM or less, but the promotion effects were lost at 100 nM. Antagonism of AT1 receptor inhibited the promotion effects of AngII at 10 nM or less. On the other hand, antagonism of AT2 receptor enhanced platelet aggregability modestly with AngII at 10 nM or less, and markedly with 100 nM AngII. Furthermore, with 10 nM AngII, phospho-PKCalpha/betaII expression in platelets was increased after collagen stimulation and was inhibited by antagonism of AT1 receptor. With 100 nM AngII, expression levels of phospho-PKCalpha/ betaII remained low even after collagen stimulation but were markedly enhanced by antagonism of AT2 receptor. These findings suggest that at 10 nM or below, AngII promotes aggregability and PKC phosphorylation in human platelets through the AT1 receptor, which can be inhibited by AT1 receptor antagonists, but at higher concentrations, the promotion effects were lost through the opposing action of the AT2 receptor. The present study may provide an additional mechanism for AT1 receptor antagonism, which would provide clinical benefit to patients with stroke or cardiovascular disease accompanied by hypertension.