Masahiro Kamouchi
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Masahiro Kamouchi has a total of 10 co-authors. Here are the top co-authors by number of shared publications:
Setsuro Ibayashi
Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan
2 shared publications- Hiroaki Ooboshi
Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan
1 shared publication Junichi Takada
Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan
1 shared publicationKensuke Egashira
Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan
1 shared publicationMasatoshi Fujishima
Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan
1 shared publicationMitsuo Iida
Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan
1 shared publication
Latest Publications
- 1 December 2004
- Published by SAGE Publications in Journal of Cerebral Blood Flow & Metabolism
- Vol. 24 (12) , 1359-1368
Anti-Monocyte Chemoattractant Protein-1 Gene Therapy Protects Against Focal Brain Ischemia in Hypertensive Rats
Journal of Cerebral Blood Flow & Metabolism stands at the interface between basic and clinical neurovascular research, and features research on experimental, theoretical, and clinical aspects of brain circulation, metabolism and imaging. The journal is relevant to any physician or scientist with an interest in brain function, cerebrovascular disease, cerebral vascular regulation and brain metabolism, including neurologists, neurochemists, physiologists, pharmacologists, anesthesiologists, neuroradiologists, neurosurgeons, neuropathologists and neuroscientists.
- 1 December 2004
- Published by SAGE Publications in Journal of Cerebral Blood Flow & Metabolism
- Vol. 24 (12) , 1359-1368
Anti-Monocyte Chemoattractant Protein-1 Gene Therapy Protects Against Focal Brain Ischemia in Hypertensive Rats
Journal of Cerebral Blood Flow & Metabolism stands at the interface between basic and clinical neurovascular research, and features research on experimental, theoretical, and clinical aspects of brain circulation, metabolism and imaging. The journal is relevant to any physician or scientist with an interest in brain function, cerebrovascular disease, cerebral vascular regulation and brain metabolism, including neurologists, neurochemists, physiologists, pharmacologists, anesthesiologists, neuroradiologists, neurosurgeons, neuropathologists and neuroscientists.
- 7 June 2002
- Published by Wiley in Clinical and Experimental Pharmacology and Physiology
- Vol. 29 (7) , 575-581
Role Of CA2+‐Activated K+ Channels In The Regulation Of Basilar Arterial Tone In Spontaneously Hypertensive Rats
SUMMARY: 1. Ionic channels appear to play an important role in contractile responses of the cerebral arteries and, thereby, contribute to the regulation of cerebral circulation. In the present study, we investigated the role of large‐conductance Ca2+‐activated K+ (BKCa) channels in the regulation of cerebral arterial tone during chronic hypertension.2. Ring segments of the basilar artery from spontaneously hypertensive rats (SHR) and normotensive Wistar‐Kyoto (WKY) rats were placed in bath chambers and the isometric tension of each ring was measured.3. Application of inhibitors of BKCa channels, namely tetraethylammonium (TEA; ≥ 0.1 mmol/L) and charybdotoxin (CTX; ≥ 0.1 nmol/L), produced spontaneous contraction with rhythmic oscillation in the basilar artery from SHR.4. The oscillatory contraction was not induced by 5‐hydroxytryptamine (0.01–10 μmol/L) or depolarization by external high K+ (20–60 mmol/L).5. The rhythmic contraction was completely abolished by either the removal of external Ca2+ or the application of nicardipine (10 nmol/L).6. The oscillation was not affected by the substitution of external Cl– by various equimolar anions (i.e. acetate, benezenesulphonate, bromide and isethianate).7. The amplitude of the oscillation was dose‐dependently increased by the vasodilators forskolin and sodium nitroprusside, as well as by stimulation of the endothelium with histamine and acetylcholine, whereas the frequency was decreased.8. In contrast, the oscillation was eliminated by depletion of Ca2+ stores by caffeine. Neither TEA (10 mmol/L) nor CTX (10 nmol/L) produced any significant contraction of the basilar artery in WKY rats.9. These results suggest that BKCa channels may play an important role in regulating the resting tone of the cerebral artery in SHR.
- 7 June 2002
- Published by Wiley in Clinical and Experimental Pharmacology and Physiology
- Vol. 29 (7) , 575-581
Role Of CA2+‐Activated K+ Channels In The Regulation Of Basilar Arterial Tone In Spontaneously Hypertensive Rats
SUMMARY: 1. Ionic channels appear to play an important role in contractile responses of the cerebral arteries and, thereby, contribute to the regulation of cerebral circulation. In the present study, we investigated the role of large‐conductance Ca2+‐activated K+ (BKCa) channels in the regulation of cerebral arterial tone during chronic hypertension.2. Ring segments of the basilar artery from spontaneously hypertensive rats (SHR) and normotensive Wistar‐Kyoto (WKY) rats were placed in bath chambers and the isometric tension of each ring was measured.3. Application of inhibitors of BKCa channels, namely tetraethylammonium (TEA; ≥ 0.1 mmol/L) and charybdotoxin (CTX; ≥ 0.1 nmol/L), produced spontaneous contraction with rhythmic oscillation in the basilar artery from SHR.4. The oscillatory contraction was not induced by 5‐hydroxytryptamine (0.01–10 μmol/L) or depolarization by external high K+ (20–60 mmol/L).5. The rhythmic contraction was completely abolished by either the removal of external Ca2+ or the application of nicardipine (10 nmol/L).6. The oscillation was not affected by the substitution of external Cl– by various equimolar anions (i.e. acetate, benezenesulphonate, bromide and isethianate).7. The amplitude of the oscillation was dose‐dependently increased by the vasodilators forskolin and sodium nitroprusside, as well as by stimulation of the endothelium with histamine and acetylcholine, whereas the frequency was decreased.8. In contrast, the oscillation was eliminated by depletion of Ca2+ stores by caffeine. Neither TEA (10 mmol/L) nor CTX (10 nmol/L) produced any significant contraction of the basilar artery in WKY rats.9. These results suggest that BKCa channels may play an important role in regulating the resting tone of the cerebral artery in SHR.