Abstract
Ghrelin is an orexigenic peptide originally isolated from the stomach. Intracerebroventricular administration of ghrelin has been shown to elicit decreases in arterial pressure and renal sympathetic nerve activity in conscious rabbits. The aim of the present study was to determine the role of ghrelin in the brain stem in cardiovascular responses in rats. Unilateral microinjection of ghrelin into the nucleus of the solitary tract significantly decreased the mean arterial pressure and heart rate (- 17.3±0.8 mm Hg and -13.6±3.5 bpm by 20 pmol). The microinjection of ghrelin into the nucleus of the solitary tract also suppressed the renal sympathetic nerve activity (-29.5±3.4%; P<0.0001). Pretreatment with intravenous injection of pentolinium (5 mg/kg), a ganglion-blocking agent, eliminated these cardiovascular responses induced by the microinjection of ghrelin (20 pmol) into the nucleus of the solitary tract; however, pretreatment with intravenous injection of atropine sulfate (0.1 mg/kg), an antagonist of muscarinic acetylcholine receptors, failed to prevent them. In contrast, unilateral microinjection of ghrelin into the area postrema, rostral, and caudal ventrolateral medulla caused no significant changes in the mean arterial pressure and heart rate. On the other hand, immunohistochemical study revealed that the receptor for ghrelin, the growth hormone secretagogue receptor, was expressed in the neuronal cells of the nucleus of the solitary tract and the dorsal motor nucleus of the vagus, but not in the cells of the area postrema. These results suggest that ghrelin acts at the nucleus of the solitary tract to suppress sympathetic activity and to decrease arterial pressure in rats.
| Original language | English |
|---|---|
| Pages (from-to) | 977-982 |
| Number of pages | 6 |
| Journal | Hypertension |
| Volume | 43 |
| Issue number | 5 |
| DOIs | |
| Publication status | Published - May 1 2004 |
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All Science Journal Classification (ASJC) codes
- Internal Medicine
Cite this
Ghrelin Acts at the Nucleus of the Solitary Tract to Decrease Arterial Pressure in Rats. / Lin, Yingzi; Matsumura, Kiyoshi; Fukuhara, Masayo; Kagiyama, Shuntaro; Fujii, Koji; Iida, Mitsuo.
In: Hypertension, Vol. 43, No. 5, 01.05.2004, p. 977-982.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Ghrelin Acts at the Nucleus of the Solitary Tract to Decrease Arterial Pressure in Rats
AU - Lin, Yingzi
AU - Matsumura, Kiyoshi
AU - Fukuhara, Masayo
AU - Kagiyama, Shuntaro
AU - Fujii, Koji
AU - Iida, Mitsuo
PY - 2004/5/1
Y1 - 2004/5/1
N2 - Ghrelin is an orexigenic peptide originally isolated from the stomach. Intracerebroventricular administration of ghrelin has been shown to elicit decreases in arterial pressure and renal sympathetic nerve activity in conscious rabbits. The aim of the present study was to determine the role of ghrelin in the brain stem in cardiovascular responses in rats. Unilateral microinjection of ghrelin into the nucleus of the solitary tract significantly decreased the mean arterial pressure and heart rate (- 17.3±0.8 mm Hg and -13.6±3.5 bpm by 20 pmol). The microinjection of ghrelin into the nucleus of the solitary tract also suppressed the renal sympathetic nerve activity (-29.5±3.4%; P<0.0001). Pretreatment with intravenous injection of pentolinium (5 mg/kg), a ganglion-blocking agent, eliminated these cardiovascular responses induced by the microinjection of ghrelin (20 pmol) into the nucleus of the solitary tract; however, pretreatment with intravenous injection of atropine sulfate (0.1 mg/kg), an antagonist of muscarinic acetylcholine receptors, failed to prevent them. In contrast, unilateral microinjection of ghrelin into the area postrema, rostral, and caudal ventrolateral medulla caused no significant changes in the mean arterial pressure and heart rate. On the other hand, immunohistochemical study revealed that the receptor for ghrelin, the growth hormone secretagogue receptor, was expressed in the neuronal cells of the nucleus of the solitary tract and the dorsal motor nucleus of the vagus, but not in the cells of the area postrema. These results suggest that ghrelin acts at the nucleus of the solitary tract to suppress sympathetic activity and to decrease arterial pressure in rats.
AB - Ghrelin is an orexigenic peptide originally isolated from the stomach. Intracerebroventricular administration of ghrelin has been shown to elicit decreases in arterial pressure and renal sympathetic nerve activity in conscious rabbits. The aim of the present study was to determine the role of ghrelin in the brain stem in cardiovascular responses in rats. Unilateral microinjection of ghrelin into the nucleus of the solitary tract significantly decreased the mean arterial pressure and heart rate (- 17.3±0.8 mm Hg and -13.6±3.5 bpm by 20 pmol). The microinjection of ghrelin into the nucleus of the solitary tract also suppressed the renal sympathetic nerve activity (-29.5±3.4%; P<0.0001). Pretreatment with intravenous injection of pentolinium (5 mg/kg), a ganglion-blocking agent, eliminated these cardiovascular responses induced by the microinjection of ghrelin (20 pmol) into the nucleus of the solitary tract; however, pretreatment with intravenous injection of atropine sulfate (0.1 mg/kg), an antagonist of muscarinic acetylcholine receptors, failed to prevent them. In contrast, unilateral microinjection of ghrelin into the area postrema, rostral, and caudal ventrolateral medulla caused no significant changes in the mean arterial pressure and heart rate. On the other hand, immunohistochemical study revealed that the receptor for ghrelin, the growth hormone secretagogue receptor, was expressed in the neuronal cells of the nucleus of the solitary tract and the dorsal motor nucleus of the vagus, but not in the cells of the area postrema. These results suggest that ghrelin acts at the nucleus of the solitary tract to suppress sympathetic activity and to decrease arterial pressure in rats.
UR - http://www.scopus.com/inward/record.url?scp=2342620868&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=2342620868&partnerID=8YFLogxK
U2 - 10.1161/01.HYP.0000122803.91559.55
DO - 10.1161/01.HYP.0000122803.91559.55
M3 - Article
C2 - 14993197
AN - SCOPUS:2342620868
VL - 43
SP - 977
EP - 982
JO - Hypertension
JF - Hypertension
SN - 0194-911X
IS - 5
ER -