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Biomedical subjects

T Nakadate

Publications and source records attributed to T Nakadate.

At least 109 records · Page 6Linked to original sources
PubMed1981

Acute physical dependence induced by continuous intravenous infusion of morphine or meperidine in the rat.

An intravenous infusion method is described for rapidly producing physical dependence in rats. Rats were infused with morphine or meperidine for 24 or 48 h at constant rates and the development of physical dependence was assessed by body weight loss after naloxone challenge. Naloxone challenge induced body losses that were dependent upon magnitude, rate and duration of infusion. The steady-state concentrations of morphine (4 mg/kg/h) in serum and meperidine (6 mg/kg/h) in plasma were 4 and 2.5 microgram/ml, respectively. Morphine concentration in the brain in the steady-state (40 mg/kg/h) was 0.7 micrograms 1 g and in the serum was proportional to the infusion rate. Maximum body weight loss was significantly correlated with total amount of infused morphine, but not with the steady-state concentration of the drug in the serum. These results suggest that total doses of infused morphine, not steady-state concentrations, are critical in producing body weight loss.

Animals↗
PubMed1981

[Airway response to short-term inhalation of NO2, O3 and their mixture in healthy men (author's transl)].

One hour inhalation of 0.7 ppm (1.32 mg/m3) of nitrogen dioxide (NO2), 0.7 ppm (1.4 mg/m3) of ozone (O3), and their mixture, 0.5 ppm (0.9 mg/m3) of NO2 and 0.5 ppm (1.0 mg/m3) of O3, and sham inhalation were conducted in five healthy male volunteers through mouth breathing using a multipurpose inhalation apparatus. Airway response was measured by specific airway conductance (Gaw/Vtg) and maximum expiratory flow rate at 50 and 25 percent forced vital capacity (Vmax50, Vmax25). Evaluations by analysis of variance revealed: no significant effect of inhalation of NO2 alone, slight significant transient decrease of Vmax50 in inhalation of O3 along (0.1 greater than p greater than 0.05), and slight reversible decrease of Gaw/Vtg and Vmax50 in inhalation of NO2 and O3 in combination (0.1 greater than p greater than 0.05). As their variations were within the range of normal diurnal change, these results were considered to be non-adverse effects.

Adult↗
PubMed1981

Postsynaptic alpha-2 adrenergic receptors in isolated rat islets of Langerhans: inhibition of insulin release and cyclic 3':5'-adenosine monophosphate accumulation.

Effects of various alpha adrenergic agents on insulin release and cyclic 3':5'-adenosine monophosphate (cAMP) accumulation in pancreatic islets were investigated. Clonidine, epinephrine, alpha-methylnorepinephrine and norepinephrine were most potent and methoxamine and phenylephrine least potent in inhibiting the glucose-stimulated insulin release. Yohimbine and phentolamine were the most effective and prazosin was the least effective in antagonizing the epinephrine-inhibited insulin release. Clonidine markedly inhibited the glucagon-stimulated cAMP accumulation, whereas methoxamine showed weak inhibition. Yohimbine markedly increased cAMP accumulation in the presence of epinephrine, whereas prazosin showed little effect. The effects of alpha adrenergic agents on rabbit aorta contraction were also examined for comparison with alpha adrenergic receptors in pancreatic islets. In the aorta, the order of agonist potency was norepinephrine greater than phenylephrine greater than epinephrine greater than methoxamine greater than alpha-methylnorepinephrine and that of antagonist potency was prazosin greater than WB-4101 greater than phentolamine greater than dihydroergotamine greater than phenoxybenzamine greater than yohimbine. These orders of potencies were markedly different from those in pancreatic islets. These results clearly demonstrate that the alpha adrenergic receptors in rat pancreatic islets are different from those on rabbit aorta (alpha-1) and are typical postsynaptic alpha-2 adrenergic receptors.

Adrenergic alpha-Agonists↗
PubMed1980

Regulation of plasma insulin level by alpha 2-adrenergic receptors.

Phentolamine, yohimbine or dihydroergotamine markedly increased plasma immunoreactive insulin (IRI) and inhibited epinephrine-induced hyperglycemia in fasted mice. On the other hand, phenoxybenzamine or prazosin only slightly increased plasma IRI and enhanced epinephrine-induced hyperglycemia. These results indicate that there is a distinct difference in the effects of alpha-adrenergic blockers on the plasma IRI and glucose levels, and that alpha-adrenergic receptors responsible for the plasma IRI level resemble alpha 2-adrenergic receptors more closely.

Adrenergic alpha-Agonists↗
PubMed1980

Mechanism of chlorpromazine action on plasma glucose and cyclic AMP levels.

The s.c. administration of chlorpromazine (CPZ) caused an elevation of plasma glucose and cyclic AMP levels in fed intact mice, but not in fed adrenalectomized mice. The pretreatment with reserpine partially blocked the elevation of plasma glucose and cyclic AMP. The pretreatment with 6-hydroxydopamine or alpha-methyl-p-tyrosine failed to inhibit the increase of plasma glucose and cyclic AMP induced by CPZ. These findings suggest that CPZ acts on the central nervous system and increases plasma glucose and cyclic AMP through epinephrine release from the adrenal medulla. The elevations of plasma glucose and cyclic AMP induced by epinephrine were enhanced by CPZ. CPZ increased plasma glucose and cyclic AMP significantly at high room temperatures (28 and 33 degrees C) at which CPZ did not decrease body temperature. The mechanism of CPZ action is discussed in relation to the increase in the plasma glucose and cyclic AMP levels.

Adrenal Glands↗
PubMed1980

Alpha 2-adrenoceptors modulating insulin release from isolated pancreatic islets.

Using rat isolated pancreatic islets, we investigated the effects of various alpha-adrenoceptor blocking agents on adrenaline-induced inhibition of glucose-stimulated insulin release. Yohimbine was about 100 times more potent than prazosin in antagonizing the inhibitory effect of adrenaline. At concentrations of 10 micro M, phentolamine was about as effective as an antagonist as yohimbine, whereas dihydroergotamine, WB-4101 and phenoxybenzamine were less effective and prazosin produced very little antagonism. These results strongly suggest that post-synaptic alpha 2-adrenoceptors modulate insulin release from pancreatic islets.

Animals↗
PubMed1980

Level and shape of sequences of motor behavior in inbred and hybrid mice.

Three-hundred seventy-five mice of six inbred strains and their F1 hybrid crosses were observed in a barrier apparatus. Frequencies of jumping over barriers were recorded at each of ten 30-sec intervals. Graphs plotted of mean jumps at each time point show several F1 curves with an apparently adaptive pattern: low frequencies of jumps at start, gradually rising, then leveling off. Nine out of 15 F1 curves also show evidence of heterosis: jumping frequencies of hybrids exceed those of parent strains. Lack of heterosis was peculiar to crosses in which C57BL/6 was one of the parents. A coefficient of convexity C was developed to quantify the shapes of the temporal patterns of proportions of animals engaged in jumping at a given point in the sequence. F1 curves (unlike inbred strains) were found, on the whole, to be negatively convex.

Animals↗
PubMed1980

Effects of alpha- and beta-adrenergic blockers on chlorpromazine-induced elevation of plasma glucose and cyclic AMP in fed mice.

The subcutaneous administration of chlorpromazine (CPZ) caused a dose response increase in plasma glucose and cyclic AMP levels in fed male mice. Hexamethonium abolished the elevation of both plasma glucose and cyclic AMP. Propranolol did not inhibit the elevation of plasma glucose but inhibited the increase of plasma cyclic AMP. In contrast, phentolamine and yohimbine completely suppressed the elevation of plasma glucose but not that of plasma cyclic AMP. These results indicate that the hyperglycemia due to CPZ was mediated through the stimulation of alpha-adrenoceptor and on the contrary CPZ increased plasma cyclic AMP through the stimulation of beta-adrenoceptor and that the increase in plasma glucose induced by CPZ was independent of the activation of adenylate cyclase and the increased plasma cyclic AMP. In addition, in contrast to phentolamine and yohimbine, phenoxybenzamine was ineffective to prevent the hyperglycemia induced by CPZ. Moreover, a higher dose of dihydroergotamine was required to inhibit the hyperglycemia.

Adrenergic alpha-Antagonists↗
PubMed1980

Effect of morphine on the release of thyroid-stimulating hormone stimulated by exposure to cold, thyroidectomy and the administration of thyrotrophin releasing hormone in male rats.

Morphine reduced the release of thyroid-stimulating hormone (TSH) which stimulated by exposure to cold and by thyroidectomy as well as reducing the basal level of TSH in the serum of male rats. Thi inhibitory effect of morphine was antagonized by naloxone which did not enhance the basal or cold-induced TSH release. Pretreatment with morphine did not reduce the release of TSH induced by exogenous thyrotrophin-releasing hormone (TRH) but enhanced it. This effect of morphine was also antagonized by naloxone. The above results suggested that the effect of morphine in reducing levels of serum TSH was not mediated by blocking the effect of TRH on the anterior pituitary gland, but that it was probably mediated by the inhibition of the release of TRH.

Animals↗
PubMed1980

Adrenergic regulation of blood glucose levels: possible involvement of postsynaptic alpha-2 type adrenergic receptors regulating insulin release.

We have demonstrated that while phenoxybenzamine and prazosin (10(-7)-10(-4) mol/kg i.p.) are ineffective in inhibiting the hyperglycemia induced by alpha adrenergic agonists in fed male mice, phentolamine, yohimbine and dihydroergotamine are effective. These results suggest the involvement of alpha-2 type adrenergic receptors in the regulation of the plasma glucose levels. When attempting to elucidate the mechanism of such differences, we found that the release of immunoreactive insulin induced by epinephrine was markedly stimulated by phentolamine, yohimbine and dihydroergotamine, whereas phenoxybenzamine and prazosin had little effect. The ineffectiveness of these two compounds to inhibit the hyperglycemia induced by alpha adrenergic agonists indicates that the postsynaptic alpha adrenergic receptors which suppress the secretion of immunoreactive insulin from B cells of pancreatic islets are not blocked and that the alpha adrenergic receptors which control immunoreactive insulin secretion differ from the classical postsynaptic alpha adrenergic receptors and more closely resemble presynaptic alpha-2 adrenergic receptors.

Adrenergic alpha-Antagonists↗
PubMed1980

Suppressive effect of morphine on serum gonadotropin levels in castrated rats.

A single administration of morphine reduced both serum LH and FSH levels in castrated Wistar rats. As the inhibitory effect of morphine on serum LH was antagonized by naloxone, the opiate receptors are involved. Decrease in the serum FSH levels induced by morphine was considerably less than the decrease in serum LH, and naloxone did not significantly reverse this effect of morphine on serum FSH. Increase in the serum LH induced by exogenous LHRH was slightly potentiated and not inhibited by a large dose of morphine, in both intact and castrated rats. Increase in the serum FSH in intact male rats induced by exogenous LHRH was not altered by morphine. In the castrated animals, exogenous LHRH did not further increase the serum FSH levels and the latter was not altered by a concomitant administration of morphine. These results clearly show that the decrease in serum gonadotropin levels by morphine is not due to inhibition of the stimulatory effect of LHRH on the pituitary gland. The mechanism of the differential suppression on serum LH and FSH by morphine is postulated.

Animals↗
PubMed1979

Inhibition by cholinergic agonists of the prolactin release induced by morphine.

The cholinergic agonists, pilocarpine, physostigmine and nicotine, inhibited the prolactin release induced by morphine in male rats in vivo. Pilocarpine also inhibited the release of prolactin induced by beta-endorphin or metoclopramide without affecting the basal and haloperidol-stimulated serum prolactin levels. The inhibitory effect of pilocarpine on the morphine-stimulated release of prolactin was antagonized by concurrent administration of atropine but not by atropine methylnitrate or by mecamylamine, while the inhibition by nicotine was antagonized by mecanylamine but not by atropine. The stimulation of prolactin release by morphine and its reversal by pilocarpine were observed after the administration of haloperidol or alpha-methyltyrosine. These results suggest that the central cholinergic system exertes an inhibitory influence on the prolactin release induced by morphine or beta-endorphin and the cholinergic inhibition is not mediated via catecholaminergic neurons.

Animals↗