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&middot;h<SUP>-1</SUP>&middot;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&plusmn;0.14ngAI&middot;h<SUP>-1</SUP>&middot;Af<SUP>-1</SUP>/h (X&plusmn;SEM, n=23) and remained stable throughout the incubations. Basal renin release rate from Af+MD was 0.33&plusmn;0.04ngAI&middot;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&plusmn;0.05 to 1.59&plusmn;0.15ngAI&middot;h<SUP>-1</SUP>&middot;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&plusmn;0.02 to 0.56&plusmn;0.09 ng AI&middot;h<SUP>-1</SUP>&middot;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 &mu;M), renin release rate from Af increased from 0.45&plusmn;0.14 to 1.49&plusmn;0.53 ng AI&middot;h<SUP>-1</SUP>&middot;AN/h (n=9, p<0.05), and further increased to 4.50&plusmn;1.24 ng AI&middot;h<SUP>-1</SUP>&middot;Af<SUP>-1</SUP>/h (p<0.02) after removal from PGI<SUB>2</SUB>. When PGE<SUB>2</SUB> (10 &mu;M) was added to Af+MD, renin release rate increased from 0.54&plusmn;0.09 to 1.26&plusmn;0.24ng AI&middot;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.
著者
矢尾板 啓 伊藤 修 有馬 秀二 遠藤 好美 竹内 和久 尾股 健 伊藤 貞嘉
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.41, no.7, pp.697-703, 1999

We investigated the direct effect of adenosine on afferent arterioles (Af-Arts) and the receptor subtype that mediates the constrictor or dilator action of adenosine . Af-Arts were isolated from the superficial cortex of rabbit kidney and perfused in vitro. Adenosine added to either the lumen or bath constricted the Af-Arts in a dose dependent manner. This constriction was blocked by the A1 receptor antagonist, 6-oxo-3- (2-phenylpyrazole (1, 5-a) pyridin-3-yl) -1(6H) -pyridazinebutyric acid (FK838) or 8-cyclopentyl-1, 3 - dipropylxanthine (DPCPX). We also examined the effect of adenosine on preconstricted Af-Arts with norepinephrine. Adenosine added to either the lumen or bath further constricted the preconstricted Af-Arts. In the presence of FK838, adenosine added to either the lumen or bath dilated the preconstricted Af-Arts, but in a different dose dependent manner. Adenosine induced dilation was inhibited by the A<SUB>2</SUB> receptor antagonist, 3, 7-dimetyl-1- propargylxanthine (DMPX). These data indicate that adenosine constricts Af-Arts via A<SUB>1</SUB> receptors and that adenosine dilates preconstricted Af-Arts via A<SUB>2</SUB> receptors when A<SUB>1</SUB> receptors are blocked.