scholarly journals Centrally Administered Tuberoinfundibular Peptide of 39 Residues Inhibits Arginine Vasopressin Release in Conscious Rats

Endocrinology ◽  
2003 ◽  
Vol 144 (7) ◽  
pp. 2791-2796 ◽  
Author(s):  
Yoshihisa Sugimura ◽  
Takashi Murase ◽  
Seiji Ishizaki ◽  
Kazushige Tachikawa ◽  
Hiroshi Arima ◽  
...  

Abstract Tuberoinfundibular peptide of 39 residues (TIP39) is a recently discovered neuropeptide identified on the basis of its ability to activate the PTH2 receptor, and it is thought to be the brain PTH2 receptor’s endogenous ligand. The PTH2 receptor is highly expressed in the hypothalamus, suggesting a role in the modulation of neuroendocrinological functions. PTHrP, which also belongs to the PTH-related peptides family, stimulates arginine vasopressin (AVP) release. In the present study, therefore, we investigated the effect of centrally administered TIP39 on AVP release in conscious rats. Intracerebroventricular administration of TIP39 (10–500 pmol/rat) significantly suppressed the plasma AVP concentration in dehydrated rats, and the maximum effect was obtained 5 min after administration (dehydration with 100 pmol/rat TIP39, 4.32 ± 1.17 pg/ml; vs. control, 8.21 ± 0.70 pg/ml). The plasma AVP increase in response to either hyperosmolality [ip injection of hypertonic saline (HS), 600 mosmol/kg] or hypovolemia [ip injection of polyethylene glycol (PEG)] was also significantly attenuated by an intracerebroventricular injection of TIP39 (HS with 100 pmol/rat TIP39, 2.65 ± 0.52 pg/ml; vs. HS alone, 4.69 ± 0.80 pg/ml; PEG with 100 pmol/rat TIP39, 4.10 ± 0.79 pg/ml; vs. PEG alone, 6.19 ± 0.34 pg/ml). Treatment with naloxone [1.5 mg/rat, sc injection], a nonselective opioid receptor antagonist, significantly reversed the inhibitory effects of TIP39 on AVP release. These results suggest that central TIP39 plays an inhibitory role in the osmoregulation and baroregulation of AVP release and that intrinsic opioid systems are involved in its mechanism.

1991 ◽  
Vol 128 (2) ◽  
pp. 245-248 ◽  
Author(s):  
Kunikazu Kondo ◽  
Takashi Murase ◽  
Kazuo Otake ◽  
Masafumi Ito ◽  
Yutaka Oiso

Endocrinology ◽  
2000 ◽  
Vol 141 (12) ◽  
pp. 4466-4471 ◽  
Author(s):  
Satoshi Kakiya ◽  
Takashi Murase ◽  
Hiroshi Arima ◽  
Hisashi Yokoi ◽  
Yasumasa Iwasaki ◽  
...  

1993 ◽  
Vol 265 (4) ◽  
pp. E585-E591 ◽  
Author(s):  
G. Luheshi ◽  
S. J. Hopkins ◽  
R. A. Lefeuvre ◽  
M. J. Dascombe ◽  
P. Ghiara ◽  
...  

Interleukin-1 (IL-1) acts centrally to induce fever and thermogenesis in rodents. The central actions of IL-1 alpha and IL-1 beta apparently involve different mechanisms, and the effects of IL-1 beta are not consistent with interaction with a type I (IL-1RI) 80-kDa receptor. In the present study the involvement of the type II IL-1 receptor (IL-1RII) was tested in the rat by examining the effects of central injection of a monoclonal antibody (ALVA-42), which blocks the IL-1RII. Pretreatment of rats with ALVA-42 (6 micrograms icv) inhibited the thermogenic and pyrogenic responses to intracerebroventricular injection of 5 ng (but not 50 ng) of IL-1 beta in conscious rats but did not significantly modify responses to IL-1 alpha. ALVA-42 also failed to modify the responses to peripherally administered IL-1 beta (1 microgram) but significantly attenuated the pyrogenic and thermogenic responses to peripheral (125 micrograms) or central (1 microgram) injection of endotoxin. These data indicate that IL-1RII mediates the central effects of a low dose of IL-1 beta, but not IL-1 alpha, on fever and thermogenesis in the rat. They also imply that responses to endotoxin are due, at least in part, to the activation of IL-1RII by IL-1 beta released within the brain and that effects of peripherally injected IL-1 beta involve different mechanisms, probably associated with IL-1RI.


1996 ◽  
Vol 216 (1) ◽  
pp. 65-67 ◽  
Author(s):  
Hisashi Yokoi ◽  
Hiroshi Arima ◽  
Takashi Murase ◽  
Kunikazu Kondo ◽  
Yasumasa Iwasaki ◽  
...  

1993 ◽  
Vol 57 (6) ◽  
pp. 1092-1096 ◽  
Author(s):  
Takashi Murase ◽  
Kunïkazu Kondo ◽  
Kazuo Otake ◽  
Yutaka Oiso

Endocrinology ◽  
1996 ◽  
Vol 137 (5) ◽  
pp. 1523-1529 ◽  
Author(s):  
H Arima ◽  
T Murase ◽  
K Kondo ◽  
Y Iwasaki ◽  
Y Oiso

1990 ◽  
Vol 259 (5) ◽  
pp. R1056-R1062 ◽  
Author(s):  
R. Landgraf ◽  
T. J. Malkinson ◽  
W. L. Veale ◽  
K. Lederis ◽  
Q. J. Pittman

Urethan-anesthetized rats were used to identify effective stimuli for the release of the peptides arginine vasopressin (AVP) and oxytocin into the ventral septal area (VSA) of the brain. Febrile responses to intracerebroventricular injection of prostaglandin E1 (PGE1) were observed in rats whose body temperatures were maintained at 35, 37, or 39 degrees C. Microinjection of the AVP antagonist d(CH2)5Tyr(Me)AVP into the VSA enhanced fever only when PGE1 administration was associated with a significant rise in body temperature. Passive elevation (“artificial fever”) or reduction of body temperature in the absence of a PGE1 stimulus was not affected by the antagonist. Push-pull perfusion of the VSA and the dorsal hippocampus, followed by radioimmunoassay of perfusates for AVP and oxytocin, revealed enhanced release into the VSA of AVP only when PGE1 administration was followed by a rise in body temperature. Oxytocin was released whenever body temperature was raised. Peptide concentrations in simultaneous perfusates of dorsal hippocampus did not change in response to PGE1 administration or to passive elevation of body temperature. We conclude that AVP is released into the VSA, but not the dorsal hippocampus, of the rat during a fever induced by PGE1. Oxytocin is released into the VSA, but not the hippocampus, when temperature is elevated.


2009 ◽  
Vol 21 (9) ◽  
pp. 753-759 ◽  
Author(s):  
Shintaro Iwama ◽  
Yoshihisa Sugimura ◽  
Takashi Murase ◽  
Maiko Hiroi ◽  
Motomitsu Goto ◽  
...  

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