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T Onaka

Publications and source records attributed to T Onaka.

68 records · Page 4Linked to original sources

Bimodal effects of noxious stimuli on vasopressin secretion in rats.

Effects of electric foot shocks (FSs) on plasma immunoreactive vasopressin (ir-VP) were studied in relation to FS frequency in conscious and anesthetized rats under a hypertonic condition. The plasma ir-VP level was significantly lower after low-frequency FSs (0.05-0.2 Hz) but significantly higher after high-frequency FSs (5 Hz) in conscious rats. Plasma ir-VP was significantly higher in anesthetized rats after FSs at frequencies of either 0.2 or 50 Hz compared to unshocked control rats. These data support the hypothesis that FSs activate two distinct neural mechanisms: one potentiates and the other suppresses VP secretion.

Anesthesia↗

Plasma vasopressin is not involved in footshock-induced analgesia in rats.

Whether plasma vasopressin (VP) mediates footshock-induced analgesia was examined in conscious rats. Footshocks significantly increased threshold temperature of tail flick and plasma VP as reported previously. Intravenous VP increased the threshold only in doses that are considered to elevate plasma VP to a level more than 500 times higher than that after footshocks. In addition, posterior pituitary stimulation increased plasma VP to a level ten times higher than that after footshocks but did not significantly change the threshold. It is therefore highly likely that plasma VP is not involved in footshock-induced analgesia.

Analgesia↗

Synergistic interactions between footshocks and non-osmotic hypovolemia on vasopressin secretion in rats.

The effects of i.p. injected hypertonic NaCl and polyethylene glycol on the magnitude of increase in plasma vasopressin after footshocks were studied in male rats, to determine whether hypovolemia and body fluid osmolality interact with noxious stimuli on vasopressin secretion. Present data have demonstrated that non-osmotic hypovolemia but not body fluid hyperosmolarity interact significantly and synergistically with footshocks to potentiate vasopressin secretion.

Animals↗

Purification and characterization of high Ca2+-requiring neutral proteases from porcine and bovine brains.

Porcine and bovine brain high Ca2+-requiring neutral proteases were purified to homogeneity by the same isolation procedures, and their properties were compared. A high degree of similarity existed between the two proteases. The purification procedures included ion-exchange chromatography on DEAE-cellulose, hydrophobic chromatography on phenyl-Sepharose CL-4B, second DEAE-cellulose chromatography, second phenyl-Sepharose CL-4B chromatography, and gel filtration on Ultrogel AcA 34. Both purified enzymes were composed of Mr 75,000 and 29,000 subunits, as shown by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Both enzymes required 250 microM Ca2+ for half-maximal activity and 700 microM Ca2+ for maximal activity. Sr2+ and Ba2+, but not Mg2+ or Mn2+, also activated both enzymes but not as effectively as Ca2+. Both enzymes displayed maximum activity at pH 7.5-8.0. Leupeptin, antipain, and trans-epoxysuccinyl-L-leucylagmatine inhibited both enzymes. Neurofilament triplet proteins and microtubule-associated proteins were extensively hydrolyzed by both proteases, but tubulin and actin were not hydrolyzed. The amino acid compositions of the two proteases were very similar. Antisera against bovine brain protease cross-reacted with porcine brain protease when examined by immunoelectrotransfer blot techniques.

Amino Acids↗

Potentiation of vasopressin secretion by footshocks in rats.

Effects of footshocks (FS) on antidiuretic hormone (vasopressin, VP) in the plasma were studied in rats. Continuously applied FS of 60 s period with 5 ms pulses at 50 Hz frequency significantly increased VP as well as adrenocorticotrophic hormone (ACTH) in the plasma in a time- and shock intensity-dependent manner. Contrarily, the 50 Hz FS of 2 s period as repeated intermittently at every 15 s for over the period of 2, 10, and 30 min were much less effective for increasing plasma VP, whereas these intermittent FS increased plasma ACTH to an extremely high level. During the inter-shock intervals of 13 s between successive two shock periods rats exhibited a "freezing" behavior. Hypertonic saline or urethane injected I.P. immediately after termination of the intermittent FS significantly increased VP as well as ACTH in the plasma. These data clearly indicate that FS potentiate VP secretion and suggest the possibility that emotional stress may suppress the noxious stimuli-induced VP secretion.

Adrenocorticotropic Hormone↗

Suppression of vasopressin secretion by classically conditioned stimuli in rats.

The possibility that emotional stress suppresses footshock-induced secretion of antidiuretic hormone (VP) was tested in rats by a classical conditioning paradigm. As a training trial, rats received a flash and a brief sound (2 kHz, 0.5 s) as conditioned stimuli (CS) followed by footshocks (FS, 5 ms pulses of 3 mA intensity, 50 Hz) for 1 s period as unconditioned stimuli. Rats were trained by 100 trials repeated at an interval of 6 s. A various length of time after the training, rats were tested by CS repeated at an interval of 15 s for the period of 120 s and FS of 60 s period, which started 60 s after the CS onset. Testing CS further augmented FS-induced increase in plasma adrenocorticotrophic hormone (ACTH) but suppressed FS-induced increase in plasma VP in a time-dependent manner. The CS also increased the degree of an inhibition of motor behavior known as "freezing" behavior. Augmentation of ACTH response and suppression of VP response to testing FS were dependent on the training shock intensity. These data are consistent with the hypothesis that VP secretion is potentiated by physical but suppressed by emotional stress.

Animals↗

Parvocellular neurosecretory neurons: converging inputs after saphenous nerve and hypovolemic stimulations in the rat.

Effects of saphenous nerve stimulation and hemorrhage on discharge activity of parvocellular neurosecretory (PC) cells of the paraventricular hypothalamic nucleus (PVN) were studied in anesthetized rats. The PC cells were identified in the PVN with the criteria that units recorded in the PVN showed an antidromically conducted spike after median eminence but not after posterior pituitary stimulation of 0.45 mA intensity and were demonstrated histologically to be located in the parvocellular regions of the PVN. Saphenous nerve stimulation at 4 Hz repetition and of 3 mA intensity increased the discharge rate of 13 of the 52 PC cells tested. These excited cells exhibited a synaptically mediated excitation during post-stimulus period on peristimulus time histograms constructed during 1 Hz stimulation. Hemorrhage (4 ml/kg b.w.) activated 7 of the 10 PC cells tested which had been excited by saphenous nerve stimulation. Both saphenous nerve stimulation and hemorrhage increased immunoreactive adrenocorticotropic hormone (ACTH) in the plasma in the anesthetized rats. These data support the view that synergistic potentiation of ACTH secretion reported to occur after noxious and hypovolemic stimuli depends at least in part on the interaction between afferent neural signals originating from noxious and cardiovascular receptors on their way up to corticotropin-releasing factor (CRF)-secreting PVN neurons.

Adrenocorticotropic Hormone↗

Microbiological degradation of bile acids. Nitrogenous hexahydroindane derivatives formed from cholic acid by Streptomyces rubescens.

The metabolism of cholic acid (I) by Streptomyces rubescens was investigated. This organism effected ring A cleavage, side-chain shortening and amide bond formation and gave the following metabolites: (4R)-4-[4alpha-(2-carboxyethyl)-3aalpha-hexahydro-7abeta-methyl-5-oxoindan-1 beta-yl]valeric acid (IIa) and its mono-amide (valeramide) (IIb); and 2,3,4,6, 6abeta,7,8,9,9aalpha,9bbeta-decahydro-6abeta-methyl-1H-cyclopenta[f]quinoline-3,7-dione(IIIe)and its homologues with the beta-oriented side chains, valeric acid, valeramide, butanone and propionic acid, in the place of the oxo group at C-7, i.e.compounds (IIIa), (IIIb), (IIIc) and (IIId) respectively. All the nitrogenous metabolites were new compounds, and their structures were established by partial synthesis except for the metabolite (IIIc). The mechanism of formation of these metabolites is considered. A degradative pathway of cholic acid (I) into the metabolites is also tentatively proposed.

Cholic Acids↗