1 0 0 0 レニン分泌の密集斑機構とプロスタグランジン
- 著者
- 伊藤 貞嘉 阿部 圭志 尾股 健 保嶋 実 吉永 馨
- 出版者
- 社団法人 日本腎臓学会
- 雑誌
- 日本腎臓学会誌 (ISSN:03852385)
- 巻号頁・発行日
- vol.30, no.1, pp.85-90, 1988
To examine the role of prostaglandins (PGs) in the macula densa mechanism of renin release, rabbit afferent arteriole (Af) alone and afferent arteriole with macula densa attached (Af+MD) were microdissected and incubated consecutively. Hourly renin release rate from a single Af (or Af+MD) was calculated and expressed as ngAI·h<SUP>-1</SUP>·Af<SUP>-1</SUP> (or Af+MD<SUP>-1</SUP>)/h (where AI is angiotensin I). Basal renin release rate from Af was 0.84±0.14ngAI·h<SUP>-1</SUP>·Af<SUP>-1</SUP>/h (X±SEM, n=23) and remained stable throughout the incubations. Basal renin release rate from Af+MD was 0.33±0.04ngAI·h<SUP>-1</SUP>Af+MD<SUP>-1</SUP>/h (n=17), which was significantly lower (p<0.01) than that from Af. When furosemide (1.5 mM) was added to Af, no significant change in renin release rate was observed. However, when furosemide was added to Af+MD, renin release rate increased from 0.40±0.05 to 1.59±0.15ngAI·h<SUP>-1</SUP>·Af+MD<SUP>-1</SUP>/h (n=10, p<0.01). After the pretreatment with indomethacin, a cyclooxygenase inhibitor, furosemide still increased renin release rate from 0.17±0.02 to 0.56±0.09 ng AI·h<SUP>-1</SUP>·Af+MD<SUP>-1</SUP>/h (n=5, p<0.05) ; however, indomethacin pretreatment reduced both basal and furosemide-stimulated renin release rate (p<0.05). In the presence of PGI<SUB>2</SUB> (10 μM), renin release rate from Af increased from 0.45±0.14 to 1.49±0.53 ng AI·h<SUP>-1</SUP>·AN/h (n=9, p<0.05), and further increased to 4.50±1.24 ng AI·h<SUP>-1</SUP>·Af<SUP>-1</SUP>/h (p<0.02) after removal from PGI<SUB>2</SUB>. When PGE<SUB>2</SUB> (10 μM) was added to Af+MD, renin release rate increased from 0.54±0.09 to 1.26±0.24ng AI·h<SUP>-1</SUP>Af+MD<SUP>-1</SUP>/h (n=8, p< 0.05). However PGE<SUB>2</SUB> had no effect on renin release rate from Af alone. We concluded that (1) the prostaglandin system may be a modulating factor of response in the macula densa mechanism of renin release, (2) PGI<SUB>2</SUB> has direct action on renin release from affer-ent arteriole, and (3) PGE<SUB>2</SUB> may participate in the control of renin release through the action on the macula densa.
1 0 0 0 白ウサギ腎表層,中皮質,傍髄質輸入細動脈のレニン含量
- 著者
- 主代 昇 阿部 圭志 伊藤 貞嘉 三沢 誠一 吉永 馨
- 出版者
- 社団法人 日本腎臓学会
- 雑誌
- 日本腎臓学会誌 (ISSN:03852385)
- 巻号頁・発行日
- vol.34, no.10, pp.1107-1111, 1992
Tissue renin content within the kidney decreases from outer to inner cortex. However, it is not known whether this gradient is due to a decrease in the number of afferent arterioles from the outer to inner cortex or the decrease in renin content per afferent arteriole. Furthermore, it is still controversial whether sodium depletion increases or decreases this gradient. According to Taugner et al., sodium depletion induces the extension of renin positive part of afferent arterioles from vascular pole toward interlobular artery. Since the length of extension may differ among superficial, midcortical, and juxtamedullary afferent arterioles, the observed gradient may vary depending on whether the entire afferent arteriole or only the vascular pole is examined. In the present study, we microdissected the entire afferent arterioles from superficial, middle, and juxtamedullary cortex of rabbit kidney, and examined tissue renin content. We studied: 1. whether tissue renin content per afferent arteriole decreases from the outer to inner cortex. 2. whether sodium depletion affects the gradient of tissue renin content within the cortex. In result, we reached the conclusions, as follows: 1. Tissue renin content per afferent arteriole decreases steeply from superficial to midcortical to juxtamedullary afferent arterioles. 2. The absolute difference in renin content among the three types of afferent arterioles becomes greater during sodium depletion. The internephron heterogeneity of tissue renin content may contribute to functional heterogeneity.
1 0 0 0 OA 血圧調節ホルモンの分泌と細胞性作用機序
- 著者
- 阿部 高明 阿部 圭志
- 出版者
- 一般社団法人 日本内分泌学会
- 雑誌
- 日本内分泌学会雑誌 (ISSN:00290661)
- 巻号頁・発行日
- vol.68, no.12, pp.1240-1248, 1992-12-20 (Released:2012-09-24)
- 参考文献数
- 23
Renin-angiotensin (RA) system plays an important role in cardiovascular homeostasis. Here, we have described the recent progress in our study of renin release as well as the cellular action of angiotensin II.(1) Microdissection of an isolated afferent artery with or without macula densa (MD) has revealed that renin release is regulated by NaCl exposure to MD. Furosemide, prostaglandins (PGE2 and PGI2) and adenosine modulate its function.(2) Angiotensin (ang) II increases cytosolic free calcium and induces the formation of inositolphosphates in vascular smooth muscle cells. Deduced protein structure of ang II receptor (AT1-R) cDNA has indicated the presumed link of AT1-R with phospholipase C. Through the cellular action, ang II has been reported to regulate gene expression.