| Project/Area Number |
02660312
|
|---|
| Research Category |
Grant-in-Aid for General Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
基礎獣医学
|
|---|
| Research Institution | Miyazaki University |
|---|
Principal Investigator |
ITO Katsuaki Fac. Agriculture Dept. Veterinary Pharmacology Professor, 農学部, 教授 (70136795)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
MURAKAMI Kazuyasu Fac. Agriculture Dept. Veterinary Pharmacology Associate professor, 農学部, 助教授 (00190877)
|
|---|
| Project Period (FY) |
1990 – 1991
|
| Project Status |
Completed (Fiscal Year 1991)
|
| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1991: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1990: ¥1,100,000 (Direct Cost: ¥1,100,000)
|
|---|
| Keywords | Resistance vessels / Calcium / Sarcoplasmic reticulum / Calcium channel / Vascular smooth muscle / Calcium release / alpha_1-Adrenoceptor / Protein kinase C / α_1受容体 |
|---|
| Research Abstract |
We investigated the cellular Ca^<2+> Movement and its role in regulation of contractions and relaxations in vascular smooth muscles of resistance vessels. Major aidings are as follows.
1. Relation of transmembrane Ca^<2+> influx to intracellular Ca^<2+> release. Based on the sensitivity to ryanodine of Ca^<2+>-induced contraction of rat mesenteric resistance vessels which had been depolarized by 40mMK^+, Ca^<2+>-free medium, it has been shown that Ca^<2+> influx through Ca^<2+> Channels triggers that Ca^<2+> release from sarcoplasmic reticulum. This mechanism may be physiologically important since it amplifies the threshold level of contraction to half maximal one. On the other hand, in resting state, the sarcoplasmic reticulum plays a role as a sink to buffer cytoplasmic Ca^<2+>. Removal of this function by ryanodine induced a tension development. 2. Increased level of cytoplasmic Ca^<2+> at resting state in hypertensive vessels and activation of Ca^<2+>-dependent K^+ channel. Femoral
… More
and carotid arterie s from spontaneously hypertensive rats(SHR)showed a greater decrease in tension in response to Ca^<2+>-removal from bathing solution or Ca^<2+> channel blockers and greater contractile responses to charybdotoxin and TEA, Ca^<2+>-activated K^+ channel blockers, than those from normotensive rats. Measurement of cytoplasmic Ca^<2+> with fura-2 revealed that the resting level of cytoplasmic Ca^<2+> was higher in SHR vessels. Resting membrane potential did not differ between hypertensive and normotensive vessels. It is suggested that Ca^<2+> easily enters cells in SHR vessels at resting state, thereby produces the active tension and activates Ca^<2+>-activated K^+ channels.
3. The nature of tonic contraction induced by alpha-adrenoceptor activation. We analyzed the tonic contraction induced by phenylephrine, alpha1 receptor agonist, and found that the contraction was composed of two components, one is related to activation of protein kinase C and the other depends on Ca^<2+> influx through L-type Ca^<2+> channels. The former may cause an increase in the sensitivity to Ca^<2+> of contractile systems. It is under investigation whether the same mechanism underlies the alpha1-adrenoceptor mediated contraction of resistance vessels. Less
|
