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.
| Original language | English |
|---|---|
| Pages (from-to) | 2791-2796 |
| Number of pages | 6 |
| Journal | Endocrinology |
| Volume | 144 |
| Issue number | 7 |
| DOIs | |
| Publication status | Published - 01-07-2003 |
| Externally published | Yes |
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All Science Journal Classification (ASJC) codes
- Endocrinology
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Centrally administered tuberoinfundibular peptide of 39 residues inhibits arginine vasopressin release in conscious rats. / Sugimura, Yoshihisa; Murase, Takashi; Ishizaki, Seiji; Tachikawa, Kazushige; Arima, Hiroshi; Miura, Yoshitaka; Usdin, Ted B.; Oiso, Yutaka.
In: Endocrinology, Vol. 144, No. 7, 01.07.2003, p. 2791-2796.Research output: Contribution to journal › Article
TY - JOUR
T1 - Centrally administered tuberoinfundibular peptide of 39 residues inhibits arginine vasopressin release in conscious rats
AU - Sugimura, Yoshihisa
AU - Murase, Takashi
AU - Ishizaki, Seiji
AU - Tachikawa, Kazushige
AU - Arima, Hiroshi
AU - Miura, Yoshitaka
AU - Usdin, Ted B.
AU - Oiso, Yutaka
PY - 2003/7/1
Y1 - 2003/7/1
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=0038336902&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0038336902&partnerID=8YFLogxK
U2 - 10.1210/en.2002-0017
DO - 10.1210/en.2002-0017
M3 - Article
C2 - 12810532
AN - SCOPUS:0038336902
VL - 144
SP - 2791
EP - 2796
JO - Endocrinology
JF - Endocrinology
SN - 0013-7227
IS - 7
ER -