AUTOCRINE AND PARACRINE REGULATION OF VASCULAR SMOOTH MUSCLE PROLIFERATION AND TONE BY THE BIOLOGICALLY ACTIVE PEPTIDES.

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AUTOCRINE AND PARACRINE REGULATION OF VASCULAR SMOOTH MUSCLE PROLIFERATION AND TONE BY THE BIOLOGICALLY ACTIVE PEPTIDES.

Format:
Grant
Kyushu Univ. Production Kyushu Univ. Production
Title(Other Language):
生理活性ペプチドによる血管のオートクリン-パラクリン型緊張・増殖制御機構の解明
Responsibility:
西村 淳二(九州大学・医学部・助教授)
NISIMURA Junji(九州大学・医学部・助教授)
Language:
Japanese
Project Year:
1996-1997
Latest Report:
In the present research project, the mechanisms for the action of vasoactive peptides as autocrine and paracrine transmitters were investigated, using both physiological and molecular biological techniques. The major findings were as follows : (1) We found that adrenomedullin mRNA was widely expressed in various kind of cell types, while its effects on smooth muscle tone was limited. Thus, adrenomedullin has autocrine role in some smooth muscle preparation. However, adrenomedullin must have some function other than the regulation of smooth muscle tone. (2) We investigated the autocrine role of endothelins (ETs) in the airway smooth muscle cells. The tracheal smooth muscle cells expressed prepro-ET-1, prepro-ET-3, ET converting enzyme, ET_A- and or ET_B-receptors. Tracheal epithelial cells also expressed those except ET_B receptors. These endothelin systems in the airway thought to play a physiologial role. (3) We found that ET_B-receptors in the rabbit saphenous vein is down-regulated when this vein was grafted into arterial circulation. (4) Bradykinin was found to induce contractions of the rabbit saphenous vein via B2-receptors. (5) We found that the mechanism of relaxation induced by atrial natriuretic peptide in the porcine renal artery involves reduction of Ca^<+2> sensitivity of the contractile apparatus. (6) We found that Endothelin-1 and angiotensin II act as progression but not competence growth factors in vascular smooth muscle cells. (7) We found that rhoA and rho kinase mRNAs were expressed in various smooth muscle cells. Read more
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