The role of calcium in the control of renin release from the isolated rat kidney

1980 ◽  
Vol 58 (1) ◽  
pp. 60-66 ◽  
Author(s):  
Alexander G. Logan ◽  
Alice Chatzilias
Keyword(s):  
Rat Kidney ◽  
Experimental Period ◽  
Renin Secretion ◽  
Renin Release ◽  
Base Line ◽  
Isolated Perfused Kidney ◽  
Renal Vasoconstriction ◽  
Perfusate Flow ◽  
Perfused Kidney

The effect of verapamil and manganese on isoproterenol- and glucagon-evoked renin secretion and on norepinephrine-induced renal vasoconstriction was studied in the isolated perfused kidney. Results for renin secretion and perfusate flow rates were expressed as the ratio of the average of the two values which deviated furthest from base line during the experimental period to the average of two control values determined at the beginning of each experiment. Norepinephrine significantly reduced (p < 0.001) the perfusate flow ratio to 0.35 ± 0.06 (mean ± SEM) without having any effect on renin secretion. During Ca2+-free perfusion, norepinephrine-induced renal vasoconstriction was completely abolished and concomitantly the renin secretion ratio increased significantly (p < 0.001) to 6.28 ± 1.24. Verapamil attenuated and manganese chloride abolished norepinephrine-induced renal vasoconstriction. Renin secretion increased significantly (p < 0.001) to 9.26 ± 1.79 and 9.92 ± 1.93 in the verapamil and manganese experiments, respectively. Verapamil and manganese themselves did not significantly alter renin secretion or perfusate flow and neither inhibited renin secretion induced by isoproterenol and glucagon. In conclusion, extracellular Ca2+ and net Ca2+ influx are prerequisites for norepinephrine to produce renal vasoconstriction and to inhibit renin release in the isolated perfused kidney. On the other hand, renin secretion evoked by isoproterenol and glucagon does not seem to require the movement of extracellular calcium into juxtaglomerular cells and it is speculated that the level of adenylate cyclase activity may be an important determinant of the rate of renin release.

Influence of sodium diet on L-NAME effects on renin release and renal vasoconstriction

1994 ◽  
Vol 267 (5) ◽  
pp. F798-F804 ◽  
Author(s):  
J. Gardes ◽  
M. F. Gonzalez ◽  
F. Alhenc-Gelas ◽  
J. Menard
Keyword(s):  
Salt Intake ◽  
Rat Kidney ◽  
Renin Secretion ◽  
Renin Release ◽  
Renal Vasoconstriction ◽  
Perfusate Flow ◽  
Dose Dependent Decrease ◽  
Renal Vascular ◽  
Dose Dependent Increase ◽  
Dose Dependent

The intervention of the L-arginine-NO pathway in renal vasodilation and renin secretion was studied in an isolated perfused rat kidney model. NG-nitro-L-arginine methyl ester (L-NAME, 1-25 microM), an inhibitor of nitric oxide (NO) synthesis, caused a dose-dependent increase in perfusion pressure (PP) and a dose-dependent decrease in renal perfusate flow. Renin was inhibited independently of the rise in PP, since the effect of L-NAME on renin release was the same when PP was maintained constant. Exposure of rats to low [salt depleted (SD)] or high [salt repleted (SR)] salt intake for 1 mo influenced the renal vascular response to L-NAME (3 microM). Isolated SR rat kidney vasculature vasoconstricted to a greater extent after inhibition of NO synthase than did that of SD kidneys. A similar fall in renin release was observed after L-NAME in both groups, despite a higher renin secretion rate in SD than in SR rats. These results suggest that NO-dependent vasodilation counteracts the renal vasoconstrictor effect of sodium loading.

α-Adrenergic Suppression of Renin Secretion in the Rat Independent of Renal Vasoconstriction

1979 ◽  
Vol 57 (s5) ◽  
pp. 161s-163s
Author(s):  
R. Vandongen ◽  
K. D. Strang ◽  
Marianne H. Poesse ◽  
W. H. Birkenhager
Keyword(s):  
Perfusion Pressure ◽  
Rat Kidney ◽  
Renal Perfusion ◽  
Inhibitory Effect ◽  
Renin Secretion ◽  
Renin Release ◽  
Adrenergic Stimulation ◽  
Renal Vasoconstriction ◽  
Adrenergic Mechanism ◽  
Perfused Rat Kidney

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.

Inhibitory Role of Ca2+ in the Control of Renin Secretion: A Study Using Supervised Dispersed Rat Renal Cortical Cells

1989 ◽  
Vol 77 (3) ◽  
pp. 273-279 ◽  
Author(s):  
Karen Pardy ◽  
B. C. Williams ◽  
A. R. Noble
Keyword(s):  
Rat Kidney ◽  
Renin Secretion ◽  
Renin Release ◽  
Kidney Cortex ◽  
Cortical Cells ◽  
Rat Kidney Cortex ◽  
Cyclic Monophosphate ◽  
Cortex Cell ◽  
The Mean

1. The role of Ca2+ in the control of renin release was investigated using a collagenase-dispersed rat kidney cortex cell preparation. 2. Superfusion with a series of low [Ca2+] buffers in either ascending or descending order of concentration increased renin release. Exposure to 0.06 mmol/l Ca2+ increased release by 120% (P < 0.001) when presented as the first buffer in ascending order of concentration and by 79% (P < 0.001) when presented as the fourth and last in a series of descending order. 3. The Ca2+ entry blocking drug diltiazem in a range of concentrations increased renin release and at 10−5 mol/l diltiazem the mean stimulation was 35% (P < 0.01). 4. 8-(N,N-Diethylamino)octyl-3,4,5-trimethoxybenzoate (TMB-8) reduces the release of Ca2+ from intracellular stores and, studied over a range of concentrations, this compound increased renin release. At 10−5 mol/l TMB-8 the mean increase was 44% (P < 0.001). 5. None of these experimental manipulations, low [Ca2+], diltiazem or TMB-8, had any effect on the release of adenosine 3′:5′-cyclic monophosphate into the cell superfusate, indicating that a decrease in intracellular [Ca2+] increases renin release by a mechanism which is independent of changes in adenosine 3′:5′-cyclic monophosphate production. 6. Effects of low [Ca2+], diltiazem and TMB-8 on renin secretion were all shown to be reversible when superfusion with control buffer was resumed.

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 ◽  
...  
Keyword(s):  
Rat Kidney ◽  
Renin Secretion ◽  
Renin Release ◽  
Isolated Perfused Rat Kidney ◽  
Renal Vasoconstriction ◽  
Perfused Rat Kidney ◽  
Stimulation Of

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.

Evidence for the existence of endothelin-B receptor subtypes and their physiological roles in the rat

1996 ◽  
Vol 271 (1) ◽  
pp. R254-R261 ◽  
Author(s):  
M. Gellai ◽  
T. Fletcher ◽  
M. Pullen ◽  
P. Nambi
Keyword(s):  
Radioligand Binding ◽  
Rat Kidney ◽  
Receptor Subtypes ◽  
Sprague Dawley ◽  
Vascular Effects ◽  
Renal Vasoconstriction ◽  
Eta Receptor ◽  
Etb Receptor ◽  
Endothelin B

The physiological roles of endothelin-B (ETB) receptor subtypes in systemic and renal hemodynamics were assessed in conscious Sprague-Dawley rats. Mean arterial pressure, hindlimb flow, and renal blood flow were measured via an implanted catheter and pulsed Doppler flow probes. Bolus intravenous injections of sarafotoxin 6c (S6c), a selective ETB agonist, elicited transient dose-dependent vasodilation, followed by sustained vasoconstriction in the systemic bed, but only vasoconstriction in the renal bed. RES-701-1, a selective ETB antagonist, blocked the dilator and potentiated the constrictor effect; SB-209670, a mixed ET receptor antagonist, attenuated both responses to S6c. In follow-up studies, the role of endogenous ET was assessed by administration of the antagonists alone: RES-701-1, SB-209670, and the ETA-selective antagonist BQ-123. RES-701-1 unmasked a significant systemic and renal vasoconstriction, which was attenuated by SB-209670 but not by BQ-123. SB-209670 and BQ-123 had no effect on basal hemodynamic parameters. Data from radioligand binding experiments showed that RES-701-1 binds with high affinity to the cloned human ETB receptor but poorly to the ETB receptor predominant in the rat kidney. Collectively, the results indicate that 1) the vascular effects of ET in the rat are mediated by two ETB receptor subtypes: an RES-701-1-sensitive subtype, mediating vasodilation, and an RES-701-1-insensitive subtype, mediating vasoconstriction; 2) the predominant role of endogenous ET is vasodilation; and 3) the ETA receptor plays a negligible role in the control of vascular tone in the rat.

Effect of 6-aminonicotinamide on renin release in isolated rat kidney: possible role for the pentose pathway

1985 ◽  
Vol 249 (2) ◽  
pp. F213-F219
Author(s):  
S. G. Rostand ◽  
J. Work
Keyword(s):  
Rat Kidney ◽  
Renin Secretion ◽  
Renin Release ◽  
Sprague Dawley ◽  
Bicarbonate Buffer ◽  
Rate Limiting Step ◽  
Sprague Dawley Rats ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
Renin Content ◽  
Pentose Pathway

To study the association between renal renin release and the pentose pathway, we perfused nonfiltering kidneys from Sprague-Dawley rats with Krebs-Ringer bicarbonate buffer containing 5 mM glucose and 14 g/100 ml bovine serum albumin in the presence or in the absence of 0.25 mM 6-aminonicotinamide (6AN), an inhibitor of glucose-6-phosphate dehydrogenase, the rate-limiting step of the pentose pathway. Eleven kidneys perfused in the absence of 6AN had a renin secretion rate of 7.4 +/- 2.2 ng ANG I X min-1 X ml-1. In six kidneys perfused in the presence of 6AN, renin release was depressed to 0.56 +/- 0.24 ng ANG I X min-1 X ml-1. The renal renin content for four control kidneys was 56 +/- 3.3 ng ANG I X mg-1 X h-1 while in four kidneys perfused with 6AN renal renin content was lower, 35 +/- 2.9 ng ANG I X mg-1 X h-1. In the presence of 5 mM lactate, the renin release of eight nonfiltering kidneys was 0.31 +/- 0.06 ng ANG I X min-1 X ml-1. The addition of 6AN did not further depress renin secretion in the presence of lactate. 6-Aminonicotinamide also completely blocked furosemide-stimulated renin release without having any effect on glomerular filtration rate or furosemide-induced natriuresis. However, 6AN did not inhibit stimulation of renin secretion by isoproterenol. We conclude that 6-aminonicotinamide interferes with renin release by nonfiltering kidneys and also inhibits furosemide-stimulated renin release but does not affect beta-adrenergic-stimulated renin secretion. Glucose but not lactate is important for maintaining augmented rates of renin secretion in nonfiltering kidneys. 6-Aminonicotinamide significantly reduced renal renin content in the presence of glucose.(ABSTRACT TRUNCATED AT 250 WORDS)

The Effects of Calcium and Calcium-Ionophores (X 537 a and a 23187) on Renin Release in the Isolated Perfused Rat Kidney

1978 ◽  
Vol 55 (s4) ◽  
pp. 163s-166s ◽  
Author(s):  
U. Schwertschlag ◽  
E. Hackenthal ◽  
R. Hackenthal ◽  
G. H. Rohs
Keyword(s):  
Indirect Effect ◽  
Indirect Effects ◽  
Vascular Tone ◽  
Rat Kidney ◽  
Renin Release ◽  
Direct And Indirect Effects ◽  
Calcium Depletion ◽  
A 23187 ◽  
Perfusate Flow ◽  
Perfused Rat Kidney

1. Calcium depletion from the medium of the isolated perfused kidney reduced renin release and renal perfusate flow. 2. Reintroduction of calcium increased renin release and perfusate flow. 3. The ionophore X 537 A (0·1–4 μmol/l) increased renin release both in the presence and absence of calcium in the medium. 4. The ionophore A 23187 (1–10 nmol/l) increased as well as decreased renin release. There was a positive correlation between direction of this effect and renal perfusate flow. 5. The results are compatible with the view that the effects of calcium and ionophores on renin release are the sum of direct and indirect effects of these agents, the predominant indirect effect being the modification of vascular tone.

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.

Effect of bradykinin and kininogens in isolated rat kidney vasoconstricted by angiotensin II

1990 ◽  
Vol 258 (5) ◽  
pp. F1273-F1281 ◽  
Author(s):  
J. Gardes ◽  
T. Baussant ◽  
P. Corvol ◽  
J. Menard ◽  
F. Alhenc-Gelas
Keyword(s):  
Molecular Weight ◽  
Angiotensin Ii ◽  
High Molecular Weight ◽  
Rat Kidney ◽  
Renin Secretion ◽  
Ang Ii ◽  
Urinary Kallikrein ◽  
High Molecular Weight Kininogen ◽  
Perfusate Flow ◽  
Isolated Rat

The hemodynamic and endocrine effects of bradykinin and kininogens were investigated using a closed-circuit isolated rat kidney perfused with angiotensin II (ANG II). ANG II induced vasoconstriction, stimulation of urinary kallikrein release, and inhibition of renin secretion. Bradykinin markedly increased renal perfusate flow (RPF) and produced a slight but significant diuresis and natriuresis. The inhibitory effect of ANG II on renin secretion was delayed. Urinary kallikrein secretion was unchanged. The effect of bradykinin was suppressed by the competitive kinin antagonist [DArg,Hyp3,Thi5,8,DPhe7]bradykinin. Kallikrein-sensitive rat high-molecular-weight kininogen produced a progressive rise in renal perfusate flow. Exocrine function and renin and kallikrein secretions were unchanged. Immunoreactive kinins, identified as bradykinin by high-pressure liquid chromatography, were liberated into the perfusate. Perfusate immunoreactive high-molecular-weight kininogen decreased in parallel as a result of consumption. The kalikrein-resistant T-kininogen was not hydrolyzed to release a kinin, had no effect on renal function, and its concentration in the perfusate remained constant. These results suggest that kinin can be produced in the renal circulation from kallikrein-sensitive circulating kininogens and can antagonize the vasoconstrictor effect of ANG II and alter renal hemodynamics. They provide evidence that the kallikrein-kinin system can participate with the renin-angiotensin system in the control of renal blood flow.

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