Blockade of Renin Release by Lanthanum

1974 ◽  
Vol 48 (s2) ◽  
pp. 31s-32s
Author(s):  
A. G. Logan ◽  
I. Tenyi ◽  
T. Quesada ◽  
W. S. Peart ◽  
A. S. Breathnach ◽  
...  

1. The effects of lanthanum on renin release and renal vasoconstriction were studied in the isolated perfused rat kidney. 2. Lanthanum reduced noradrenaline-induced renal vasoconstriction. 3. Lanthanum prevented isoprenaline-induced and glucagon-induced stimulation of renin secretion.

1977 ◽  
Vol 232 (4) ◽  
pp. F377-F382 ◽  
Author(s):  
J. S. Fray

These experiments were designed to test whether changing perfusate calcium or magnesium concentrations affected renin release in the isolated perfused rat kidney, and whether kidneys removed from sodium-loaded or sodium-deprived rats released the same amount of renin in response to identical stimuli. Kidneys were perfused with Kreb-Henseleit solution containing albumin. Renin release was inversely related to perfusate calcium concentration, whereas renin release was directly related to perfusate magnesium. Although a low calcium medium or low perfusion pressure (50 mmHg) stimulated renin release, the release was substantially greater in the sodium-deprived rats. Increasing the perfusate sodium concentration from 85 to 206 mM increased excretion, but did not alter renin release. It is concluded that a) low perfusate calcium and high magnesium concentrations stimulate renin release, b) kidneys removed from sodium-deprived rats released substantially more renin thatn those from sodium-loaded rats, and c) changing perfusate sodium concentration alters sodium excretion, but does not affect renin release.


1979 ◽  
Vol 57 (s5) ◽  
pp. 161s-163s
Author(s):  
R. Vandongen ◽  
K. D. Strang ◽  
Marianne H. Poesse ◽  
W. H. Birkenhager

1. The effect of α-adrenergic stimulation, with phenylephrine, on isoprenaline-provoked renin secretion was studied in the isolated perfused rat kidney. 2. Infusion of phenylephrine increased renal perfusion pressure and prevented renin secretion in response to isoprenaline. 3. Renal vasoconstriction was abolished and the response in renin secretion to isoprenaline was restored by α-adrenoreceptor blockade with phenoxybenzamine. 4. In contrast, when renal vasoconstriction was prevented by dihydrallazine, suppression of renin release by phenylephrine still occurred. 5. These observations support an inhibitory effect of a non-vascular α-adrenergic mechanism on renin release. It is suggested that the α-receptor mediating this effect is directly related to the renin-producing juxtaglomerular cell.


1985 ◽  
Vol 180 (1) ◽  
pp. 133-136 ◽  
Author(s):  
R. Loutzenhiser ◽  
M. Epstein ◽  
C. Horton ◽  
R. Hamburger

1973 ◽  
Vol 32 (2) ◽  
pp. 290-296 ◽  
Author(s):  
ROBERT VANDONGEN ◽  
W. STANLEY PEART ◽  
GRAHAME W. BOYD

1975 ◽  
Vol 49 (6) ◽  
pp. 609-612
Author(s):  
R. Vandongen ◽  
Dianne M. Greenwood

1. The effect of adrenaline and noradrenaline on renin secretion in the isolated perfused rat kidney was examined. The doses of catecholamines used were such that renal vasoconstriction and therefore increases in renal perfusion pressure were avoided. Under these conditions adrenaline and noradrenaline significantly increased renin secretion rates, compared with control experiments in which no catecholamine was infused. 2. Mean renal perfusion pressure during both adrenaline and noradrenaline infusion paralleled the control study by showing a progressive fall. 3. Administration of phenoxybenzamine did not impair the stimulation of renin secretion by adrenaline whereas this was prevented by racemic propranolol. 4. These observations suggest that catecholamines stimulate renin secretion by an intrarenal effect which is largely independent of changes in renal perfusion pressure. It is postulated that the beta-adrenoceptors mediating renin secretion are an integral component of the renin-producing cell.


1990 ◽  
Vol 415 (6) ◽  
pp. 713-717 ◽  
Author(s):  
Rainer Nobiling ◽  
Klaus Münter ◽  
Christian P. Bührle ◽  
Eberhard Hackenthal

1987 ◽  
Vol 28 (2) ◽  
pp. 221-227 ◽  
Author(s):  
Shosaku NARUMI ◽  
Toshiyuki YASUI ◽  
Mamoru YOSHIZAWA ◽  
Minako KAWAMURA ◽  
Hiromichi SUZUKI ◽  
...  

1976 ◽  
Vol 51 (s3) ◽  
pp. 101s-104s
Author(s):  
R. Vandongen ◽  
Dianne M. Greenwood

1. The effect of diazoxide (17·3 μmol min—1 g—1) and frusemide (0·12 μmol min—1 g—1) on renin secretion was examined in the isolated perfused rat kidney. These substances are potential renal vasodilators with opposite effects on urine sodium excretion. 2. Both agents significantly increased renin secretion rate above control values. In the case of frusemide this was not altered by ureteric occlusion and presumed absence of urine flow. 3. Mean renal perfusion pressure decreased to the same extent with diazoxide and frusemide infusion as in the control experiments and no additional vasodilatory effect was observed on the basis of changes in flow rate of perfusate. 4. These observations identify an intrarenal site of action for diazoxide and frusemide on renin secretion. The apparent independence of this stimulatory action on renal vasodilatation and urine flow suggests a direct effect on the renin-producing cell.


1983 ◽  
Vol 24 (1) ◽  
pp. 58-65 ◽  
Author(s):  
Jiro Misumi ◽  
François Alhenc-Gelas ◽  
Michel Marre ◽  
Jeanine Marchetti ◽  
Pierre Corvol ◽  
...  

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