Stimulatory action of parathyroid hormone on renin secretion in vitro: a study using isolated rat kidney, isolated rabbit glomeruli and superfused dispersed rat juxtaglomerular cells

1993 ◽  
Vol 84 (1) ◽  
pp. 11-19 ◽  
Author(s):  
Christian Saussine ◽  
C. Judes ◽  
T. Massfelder ◽  
M.-J. Musso ◽  
U. Simeoni ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Rat Kidney ◽  
Renin Secretion ◽  
Renin Release ◽  
Juxtaglomerular Cells ◽  
Isolated Kidney ◽  
Stimulatory Action ◽  
Isolated Rat Kidney ◽  
Isolated Rat

1. We have previously reported that pharmacological concentrations (125 nmol/l) of parathyroid hormone may stimulate renin release in the stable recirculating and non-filtering isolated rat kidney. 2. In the present study we have attempted to extend these initial observations by examining the concentration-related response of renin release to parathyroid hormone, using the same model of isolated kidney, and determining whether the effect of parathyroid hormone on renin release can be demonstrated by more direct approaches. Thus, the effects of parathyroid hormone on renin secretion were investigated in two other renal preparations: isolated rabbit glomeruli and isolated rat juxtaglomerular cells. 3. In the isolated kidney, rat parathyroid hormone significantly stimulated renin accumulation in the perfusate in a concentration-related manner with a threshold of 1 nmol/l. 4. In both glomeruli and juxtaglomerular cells bovine [Nle8,18,Tyr34]parathyroid hormone-(1–34)amide effectively and repeatedly stimulated renin release. These results imply that there is a direct stimulatory effect of parathyroid hormone on renin release. 5. We also examined the effect of [Nle8,18, Tyr34]parathyroid hormone-(l-34)amide during extracellular calcium buffering in the glomeruli. [Nle8,18,Tyr34]parathyroid hormone-(1–34)amide was uneffective in calcium-free medium. Increasing the extracellular ionized calcium concentration to 2.5 mmol/l increased the extent of stimulation in accordance with the reported ability of parathyroid hormone to block calcium channels and relax vascular smooth muscle cells. 6. These results provide further support for the role of parathyroid hormone as a direct mediator of renin secretion; moreover, the renin-stimulating action of parathyroid hormone may be mediated through the inhibition of calcium influx.s

Effects of endothelin on in vitro renin secretion

1991 ◽  
Vol 260 (4) ◽  
pp. E521-E525 ◽  
Author(s):  
O. Moe ◽  
A. Tejedor ◽  
W. B. Campbell ◽  
R. J. Alpern ◽  
W. L. Henrich
Keyword(s):  
Rat Kidney ◽  
Renin Secretion ◽  
Renin Release ◽  
Juxtaglomerular Cells ◽  
Tetraacetic Acid ◽  
Direct Effects ◽  
Calcium Buffer ◽  
Renin Inhibition ◽  
Cortical Slices

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 less than 0.05) and 44% (P less than 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 less than 0.001); ET-1 (10(-8) M) limited this increase in renin release by isoproterenol by 80% (P less than 0.05). Similar effects were observed in JGC as ET-1 (10(-8) M) significantly reduced basal renin secretion by 26% (P less than 0.05). In isolated JGC, isoproterenol increased renin secretion by 151% (P less than 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 less than 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 less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Calcium in the control of renin secretion: Ca2+ influx as an inhibitory signal

1981 ◽  
Vol 240 (1) ◽  
pp. F70-F74 ◽  
Author(s):  
C. S. Park ◽  
D. S. Han ◽  
J. C. Fray
Keyword(s):  
Incubation Temperature ◽  
Inhibitory Effect ◽  
Renin Secretion ◽  
Juxtaglomerular Cells ◽  
Stimulatory Action ◽  
Inhibitory Signal ◽  
Ca Antagonist ◽  
K Concentration ◽  
Energy Dependent

The mechanism for the inhibition of renin secretion in vitro from renal cortical slices by angiotensin II, antidiuretic hormone, ouabain, and high K+ concentration was studied. The inhibitory effect of these agents was blocked by a Ca antagonist, verapamil. In addition, epinephrine stimulated renin secretion and its stimulatory action was blocked by ouabain. These results support the hypothesis that Ca2+ influx into juxtaglomerular cells plays a role as an inhibitory signal whereas Ca2+ efflux is a stimulatory signal for renin secretion. Renin secretion was greatly stimulated by lowering incubation temperature, indicating that renin secretion is not energy dependent. The possibility is discussed that Ca2+ of juxtaglomerular cells might activate an enzyme(s) that then modulates some sequential steps of renin secretory processes, thereby controlling the rate of renin secretion.

Failure of α-adrenergic stimulation by phenylephrine to enhance renin secretion in the isolated rat kidney

1977 ◽  
Vol 45 (2) ◽  
pp. 141-144 ◽  
Author(s):  
Karel D. Strang ◽  
Robert Vandongen ◽  
Marianne H. Poessé ◽  
Willem H. Birkenhäger
Keyword(s):  
Rat Kidney ◽  
Renin Secretion ◽  
Adrenergic Stimulation ◽  
Isolated Rat Kidney ◽  
Isolated Rat

Do osmotic forces play a role in renin secretion?

1988 ◽  
Vol 255 (1) ◽  
pp. F1-F10 ◽  
Author(s):  
O. Skott
Keyword(s):  
Secretory Granules ◽  
Proton Gradient ◽  
Renin Secretion ◽  
Renin Release ◽  
Juxtaglomerular Cells ◽  
Proton Gradients ◽  
Low Calcium ◽  
Release In Vitro

Secretory granules swell during exocytosis. Swelling may follow fusion and assist in extrusion of the granular content, or swelling may cause granular fusion with the plasmalemma. A granular proton gradient has been suggested to be involved in such preexocytic granular swelling. Exocytosis of renin from juxtaglomerular cells of isolated preparations is very sensitive to changes in the extracellular osmolality. Extracellular hyposmolality causes swelling of secretory granules, fusions between peripherally located granules and plasmalemma, and an increased number of release episodes. Induction of granule swelling at constant extracellular osmolality also stimulates renin release. Newly recruited renin granules are osmosensitive, and a high extracellular osmolality blocks secretion induced by other means (low calcium). Dissipation of granular proton gradients inhibits renin release without affecting the osmosensitivity. Thus, in renin release in vitro, a granular swelling precedes fusion and exocytosis, and a granular proton gradient may contribute to preexocytic swelling when extracellular osmolality is constant. The osmosensitivity may be important for macula densamediated renin release.

RENIN SECRETION IN VITRO FROM RAT KIDNEY CORTEX SLICES

1969 ◽  
Vol 60 (3) ◽  
pp. 550-554 ◽  
Author(s):  
Lj. Božović ◽  
S. Efendić
Keyword(s):  
Rat Kidney ◽  
Renin Secretion ◽  
Renin Release ◽  
Kidney Cortex ◽  
Rat Kidney Cortex ◽  
Active Mechanism ◽  
Cortex Slices ◽  
Kidney Cortex Slices

ABSTRACT A method for in vitro studies of renin release is described. Kidney cortex slices taken from control rats and rats stimulated to release renin were incubated with and without glucose. Renin release from the slices to a large extent was glucose-dependent. This result supports the hypothesis of an active mechanism of renin secretion.

Corticosteroid metabolism in isolated rat kidney in vitro

1984 ◽  
Vol 400 (4) ◽  
pp. 377-380 ◽  
Author(s):  
G. -A. Hoyer ◽  
D. Tsiakiras ◽  
H. Siebe ◽  
K. Hierholzer
Keyword(s):  
Rat Kidney ◽  
Isolated Rat Kidney ◽  
Isolated Rat

Inhibition of Renin Secretion in the Isolated Rat Kidney by Antidiuretic Hormone

1975 ◽  
Vol 49 (1) ◽  
pp. 73-76 ◽  
Author(s):  
R. Vandongen
Keyword(s):  
Antidiuretic Hormone ◽  
Calcium Ions ◽  
Perfusion Pressure ◽  
Direct Action ◽  
Rat Kidney ◽  
Renal Perfusion ◽  
Renin Secretion ◽  
Renal Perfusion Pressure ◽  
Isolated Rat Kidney ◽  
Isolated Rat

1. The effect of antidiuretic hormone (ADH) on isoprenaline-stimulated renin secretion was examined in the isolated rat kidney perfused with modified Krebs-Ringer saline. 2. Intrarenal infusion of ADH effectively prevented stimulation of renin secretion by isoprenaline whilst increasing renal perfusion pressure. 3. The exclusion of calcium ions from the perfusion medium abolished the vasoconstrictor effect of ADH and attenuated the inhibitory effect of ADH on isoprenaline-stimulated renin secretion. However, significant suppression of renin secretion was still apparent compared with experiments where isoprenaline was infused alone. 4. These observations indicate that ADH inhibits renin secretion and that this is effected by a direct action on the kidney. Although this may be partly mediated by the rise in renal perfusion pressure, an additional direct effect of ADH on the renin-producing cell, which is dependent on the availability of calcium ions, is proposed.

scholarly journals Stimulation of renin release by hyperoncotic perfusion of the isolated rat kidney.

1982 ◽  
Vol 50 (3) ◽  
pp. 400-404 ◽  
Author(s):  
A J Cohen ◽  
K Spokes ◽  
R S Brown ◽  
J S Stoff ◽  
P Silva
Keyword(s):  
Rat Kidney ◽  
Renin Release ◽  
Isolated Rat Kidney ◽  
Isolated Rat ◽  
Stimulation Of
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