Effects of endothelin on in vitro renin secretion

O. Moe, A. Tejedor, W. B. Campbell, R. J. Alpern, William L Henrich

Research output: Contribution to journalArticle

53 Citations (Scopus)

Abstract

Original languageEnglish
JournalAmerican Journal of Physiology - Endocrinology and Metabolism
Volume260
Issue number4 23-4
StatePublished - 1991
Externally publishedYes

Fingerprint

Endothelins
Renin
Endothelin-1
Isoproterenol
In Vitro Techniques
Kidney
Rats
Calcium

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology
  • Physiology

Cite this

Effects of endothelin on in vitro renin secretion. / Moe, O.; Tejedor, A.; Campbell, W. B.; Alpern, R. J.; Henrich, William L.

In: American Journal of Physiology - Endocrinology and Metabolism, Vol. 260, No. 4 23-4, 1991.

Research output: Contribution to journalArticle

Moe, O. ; Tejedor, A. ; Campbell, W. B. ; Alpern, R. J. ; Henrich, William L. / Effects of endothelin on in vitro renin secretion. In: American Journal of Physiology - Endocrinology and Metabolism. 1991 ; Vol. 260, No. 4 23-4.
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title = "Effects of endothelin on in vitro renin secretion",
abstract = "The ability of endothelin-1 (ET-1) to directly inhibit renal renin secretion in the presence of a renin stimulator is unknown, as is the mechanism of action of any renin inhibition. Thus direct effects of ET-1 on renin secretion were investigated in two distinct preparations: rat kidney cortical slices and isolated juxtaglomerular cells (JGC). In rat kidney cortical slices, ET-1 reduced basal renin release by 20 (P < 0.05) and 44{\%} (P < 0.005) at 10-9 and 10-8 M, respectively. To test the efficacy of ET-1 as a renin inhibitor, experiments were performed in the presence of the renin stimulator isoproterenol (10-5 M). Addition of isoproterenol to cortical slices increased renin release by 97{\%} (P < 0.001); ET-1 (10-8 M) limited this increase in renin release by isoproterenol by 80{\%} (P < 0.05). Similar effects were observed in JGC as ET-1 (10-8 M) significantly reduced basal renin secretion by 26{\%} (P < 0.05). In isolated JGC, isoproterenol increased renin secretion by 151{\%} (P < 0.001); ET-1 (10-8 M) significantly reduced this stimulated increase in renin secretion by 68{\%}. The mechanism of renin inhibition was examined by testing the effects of the intracellular calcium buffer 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA; 10-6 M) in JGC. BAPTA alone increased renin secretion in JGC by 116{\%} (P < 0.01); when the combination of (10-6 M) BAPTA and ET-1 (10-8 M) were tested in the JGC, renin secretion still increased significantly (by 78{\%}, P < 0.05). In summary, ET-1 directly inhibited basal and isoproterenol-stimulated renin release in both cortical slices and in isolated JGC; the mechanism of this potent inhibition may depend on an increase in intracellular calcium.",
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T1 - Effects of endothelin on in vitro renin secretion

AU - Moe, O.

AU - Tejedor, A.

AU - Campbell, W. B.

AU - Alpern, R. J.

AU - Henrich, William L

PY - 1991

Y1 - 1991

N2 - The ability of endothelin-1 (ET-1) to directly inhibit renal renin secretion in the presence of a renin stimulator is unknown, as is the mechanism of action of any renin inhibition. Thus direct effects of ET-1 on renin secretion were investigated in two distinct preparations: rat kidney cortical slices and isolated juxtaglomerular cells (JGC). In rat kidney cortical slices, ET-1 reduced basal renin release by 20 (P < 0.05) and 44% (P < 0.005) at 10-9 and 10-8 M, respectively. To test the efficacy of ET-1 as a renin inhibitor, experiments were performed in the presence of the renin stimulator isoproterenol (10-5 M). Addition of isoproterenol to cortical slices increased renin release by 97% (P < 0.001); ET-1 (10-8 M) limited this increase in renin release by isoproterenol by 80% (P < 0.05). Similar effects were observed in JGC as ET-1 (10-8 M) significantly reduced basal renin secretion by 26% (P < 0.05). In isolated JGC, isoproterenol increased renin secretion by 151% (P < 0.001); ET-1 (10-8 M) significantly reduced this stimulated increase in renin secretion by 68%. The mechanism of renin inhibition was examined by testing the effects of the intracellular calcium buffer 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA; 10-6 M) in JGC. BAPTA alone increased renin secretion in JGC by 116% (P < 0.01); when the combination of (10-6 M) BAPTA and ET-1 (10-8 M) were tested in the JGC, renin secretion still increased significantly (by 78%, P < 0.05). In summary, ET-1 directly inhibited basal and isoproterenol-stimulated renin release in both cortical slices and in isolated JGC; the mechanism of this potent inhibition may depend on an increase in intracellular calcium.

AB - The ability of endothelin-1 (ET-1) to directly inhibit renal renin secretion in the presence of a renin stimulator is unknown, as is the mechanism of action of any renin inhibition. Thus direct effects of ET-1 on renin secretion were investigated in two distinct preparations: rat kidney cortical slices and isolated juxtaglomerular cells (JGC). In rat kidney cortical slices, ET-1 reduced basal renin release by 20 (P < 0.05) and 44% (P < 0.005) at 10-9 and 10-8 M, respectively. To test the efficacy of ET-1 as a renin inhibitor, experiments were performed in the presence of the renin stimulator isoproterenol (10-5 M). Addition of isoproterenol to cortical slices increased renin release by 97% (P < 0.001); ET-1 (10-8 M) limited this increase in renin release by isoproterenol by 80% (P < 0.05). Similar effects were observed in JGC as ET-1 (10-8 M) significantly reduced basal renin secretion by 26% (P < 0.05). In isolated JGC, isoproterenol increased renin secretion by 151% (P < 0.001); ET-1 (10-8 M) significantly reduced this stimulated increase in renin secretion by 68%. The mechanism of renin inhibition was examined by testing the effects of the intracellular calcium buffer 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA; 10-6 M) in JGC. BAPTA alone increased renin secretion in JGC by 116% (P < 0.01); when the combination of (10-6 M) BAPTA and ET-1 (10-8 M) were tested in the JGC, renin secretion still increased significantly (by 78%, P < 0.05). In summary, ET-1 directly inhibited basal and isoproterenol-stimulated renin release in both cortical slices and in isolated JGC; the mechanism of this potent inhibition may depend on an increase in intracellular calcium.

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