Stretch receptor model for renin release with evidence from perfused rat kidney

1976 ◽  
Vol 231 (3) ◽  
pp. 936-944 ◽  
Author(s):  
JC Fray
Keyword(s):  
High Pressure ◽  
Perfusion Pressure ◽  
Rat Kidney ◽  
Granular Cell ◽  
Sodium Concentration ◽  
Stretch Receptor ◽  
Renin Activity ◽  
Renin Release ◽  
Perfusion Medium ◽  
Renal Vasoconstriction

Control of renin release was studied in isolated rat kidneys perfused with Krebs-Henseleit solution containing albumin. Cumulative perfusate renin activity (PRA) as measured by radioimmunoassay was increased by low perfusion pressure and suppressed by high pressure. Renal vasoconstriction induced by infusion of phenylephrine or methoxamine increased PRA, whereas vasodilatation by papaverine suppressed renin activity. The increased renin activity induced by phenylephrine was blocked by high pressure or papaverine. Changing sodium concentration in the perfusion medium had no effect on basal renin release. A mathematical analysis for an intrarenal stretch receptor indicates that renin release is related to the elastic modulus, the internal and external hydrostatic pressures, and the internal and external radii. Calculations based on this model also indicate that renin release is most sensitive to changes in the ratio of the radii. It is proposed that basodilatation or high perfusion pressure may increase the stretch of the afferent arteriole and depolarize the granular cell membrane, whereas vasoconstriction or low pressure may decrease stretch and thus hyperpolarize the cell.

Stimulation of renin release in perfused kidney by low calcium and high magnesium

1977 ◽  
Vol 232 (4) ◽  
pp. F377-F382 ◽  
Author(s):  
J. S. Fray
Keyword(s):  
Sodium Excretion ◽  
Calcium Concentration ◽  
Perfusion Pressure ◽  
Rat Kidney ◽  
Sodium Concentration ◽  
Renin Release ◽  
Isolated Perfused Rat Kidney ◽  
Low Calcium ◽  
Perfused Rat Kidney ◽  
Stimulation Of

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.

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.

The effects of ionophores (A23187 and RO2-2985) on renin secretion and renal vasoconstriction

1977 ◽  
Vol 199 (1135) ◽  
pp. 199-212 ◽  
Keyword(s):  
Rat Kidney ◽  
Ionic Composition ◽  
Calcium Flux ◽  
Renin Release ◽  
Perfusion Medium ◽  
Ionic Flux ◽  
Renal Vasoconstriction ◽  
Calcium Dependent ◽  
Clear Cut ◽  
Calcium And Magnesium

The hypothesis that renin release and renal vasoconstriction are both controlled by changes in net ionic flux of calcium has been supported by previous work from this laboratory, and in order to test the concept further the effects of ionophores have been studied. These substances, which are peptides derived from bacterial culture, act by chelating ions and transporting them across cell membranes. Two ionophores, A23187 and RO2-2985, were chosen for their known ability to transport calcium and magnesium. As in the previous experiments, the isolated perfused rat kidney was used and the effects of the ionophores in different concentrations and with different ionic composition of the perfusate were investigated. The results were most clear-cut with A23187 which seems to be more specific in transport of calcium and magnesium. This ionophore in higher concentrations (2 x 10 –6 mol l –1 ) caused marked vasoconstriction and inhibition of renin release, whereas at lower concentrations (2 x 10 –7 mol l –1 ) there was no vasoconstriction but very marked inhibi­tion of renin release. Both the renal vasoconstriction and the inhibition of renin release were calcium dependent since the effects were abolished by calcium-free perfusate in the presence of the ionophore. In the case of RO2-2985 the results were not so clear-cut but in higher concentrations (2 x 10 –5 mol l –1 ) vasoconstriction occurred together with inhibition of renin release. However, unlike A23187, the vasoconstrictor effect was biphasic with an immediate rise, followed by decline, and then a second­ary rise. The first component was shown to be dependent on calcium in the perfusion medium, and the second upon magnesium. Inhibition of renin release was most closely related to the presence of calcium in the perfusate but this was not as clear-cut a demonstration as with A23187. As a whole, therefore, the evidence supports the link between renin release, renal vasoconstriction and calcium flux.

Changes in plasma renin activity and aldosterone concentration in response to endothelin injection in dogs

1989 ◽  
Vol 121 (3) ◽  
pp. 361-364 ◽  
Author(s):  
Atsuhiro Otsuka ◽  
Hiroshi Mikami ◽  
Katsutoshi Katahira ◽  
Takeshi Tsunetoshi ◽  
Kaori Minamitani ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Total Peripheral Resistance ◽  
Inhibitory Action ◽  
Peripheral Resistance ◽  
Plasma Renin ◽  
Renin Activity ◽  
Renin Release ◽  
Renal Vasoconstriction

Abstract. The effects of endothelin on the renin-aldosterone system were examined by injecting it intravenously at low (40 pmol/kg) and high (400 pmol/kg) doses into pentobarbital-anesthetized dogs. Plasma renin activity and aldosterone concentration together with hemodynamic parameters were measured before and 60 min after endothelin injection. The lower dose of endothelin induced no significant increase in mean blood pressure or total peripheral resistance. It caused a slight decrease of plasma renin activity from 10.3 ± 1.6 to 5.9 ± 1.3 μg · l−1 · h−1 (p <0.1) and a decrease of aldosterone concentration from 364 ± 68 to 231 ± 58 ng/l (p <0.05) with an increase in total peripheral resistance (p <0.05), but it did not cause any clear change in the plasma renin activity or aldosterone concentration. Thus, endothelin increases the blood pressure mainly by vasoconstriction. The finding of a slight decrease in the plasma renin activity after the lower dose of endothelin, together with our previous finding that endothelin inhibits renin release from isolated rat glomeruli, suggests that endothelin inhibits renin release in vivo. With the higher dose of endothelin, stimulation of renin release secondary to renal vasoconstriction might have counteracted the direct inhibitory action of endothelin. The decrease in aldosterone concentration may have been due to the direct inhibitory action of endothelin on aldosterone release or it may be a secondary effect induced by suppression of plasma renin activity.

Renin Release from Isolated Rat Glomeruli

1976 ◽  
Vol 51 (s3) ◽  
pp. 97s-99s ◽  
Author(s):  
S. Holdsworth ◽  
A. McLean ◽  
B. J. Morris ◽  
E. Dax ◽  
C. I. Johnston
Keyword(s):  
Rat Kidney ◽  
Pressure Change ◽  
Sodium Concentration ◽  
Renin Release ◽  
High Yield ◽  
Juxtaglomerular Cells ◽  
Direct Proportion ◽  
Isolated Glomeruli ◽  
Sympathetic Nervous

1. By the use of a mechanical graded sieving technique a high yield of isolated glomeruli has been obtained from rat kidney. 2. Microscopy and renin assay have shown the presence of renin-containing juxtaglomerular cells attached to these glomeruli. 3. The viability of isolated glomeruli has been confirmed by the ability of the cells to survive and divide in tissue culture and by their exclusion of vital dyes. 4. In superfusion after washout of extracellular renin, the glomeruli actively release constant amounts of renin over 3 h in direct proportion to the number superfused. 5. Decreasing sodium concentration from 140 to 110 mol/l with constant osmolarity of 305 mosmol/l stimulated renin release by a direct effect on juxtaglomerular cells. 6. Catecholamines stimulated renin release in vitro in proportion to the potency of their action on β-adrenoreceptors. 7. The system of superfusion of isolated glomeruli provides a technique for studying the influence of mediators leading to renin release acting directly on juxtaglomerular cells, independent of pressure change, tubular sodium, the sympathetic nervous system and circulating hormones.

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.

Renal Vasoconstriction in Glycerol-Induced Acute Renal Failure. Studies in the Isolated Perfused Rat Kidney

1978 ◽  
Vol 55 (3) ◽  
pp. 249-252
Author(s):  
K. G. Hofbauer ◽  
K. Bauereiss ◽  
A. Konrads ◽  
F. Gross
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Vascular Resistance ◽  
Rat Kidney ◽  
Renal Vascular Resistance ◽  
Renin Release ◽  
Pass System ◽  
Renal Vasoconstriction ◽  
Renal Vascular

1. Acute renal failure was produced in rats by the intramuscular injection of glycerol (6.1 mol/l, 10 ml/kg). Either 2 or 4–6 h later the right kidney was isolated and perfused for 1 h with an electrolyte solution containing a gelatin preparation (Haemaccel, 35 g/l) at pressures between 90 and 100 mmHg in a single-pass system. 2. In kidneys taken from rats with acute renal failure renal vascular resistance was markedly increased immediately after the start of the perfusion as compared with control kidneys taken from untreated rats. During the following 30 min of perfusion the resistance progressively decreased and, at 1 h of perfusion, was similar to that in control kidneys or only moderately elevated. 3. Despite the reduction of renal vascular resistance glomerular filtration rate was still markedly impaired after 1 h of perfusion and fractional reabsorption of sodium and water as well as the secretion of p-aminohippurate were diminished. Renal venous renin concentration and renin release were lower in kidneys taken from rats with acute renal failure than in the control experiments. 4. These results suggest that the increase in renal vascular resistance and the stimulation of renin release after injection of glycerol in vivo are the consequence of extra-rather than intra-renal mechanisms.

Renal perfusion pressure and renin secretion in the rainbow trout, Salmo gairdneri

1981 ◽  
Vol 59 (7) ◽  
pp. 1220-1226 ◽  
Author(s):  
J. R. Bailey ◽  
D. J. Randall
Keyword(s):  
Plasma Renin Activity ◽  
Perfusion Pressure ◽  
Plasma Renin ◽  
Renal Perfusion ◽  
Renin Secretion ◽  
Renin Activity ◽  
Renin Release ◽  
Salmo Gairdneri ◽  
Renal Perfusion Pressure

In the trout, Salmo gairdneri, a significant correlation between the amount of blood loss and plasma renin activity was established. This increase in plasma renin activity could be due to stimulation of an intrarenal receptor, thus an isolated nonfiltering perfused kidney preparation was developed to test this hypothesis. It was found that a decrease in renal perfusion pressure resulted in an increase in renin release (as measured by perfusate renin activity) but an increase in renal perfusion pressure had no effect on renin release. The increase in renin secretion in response to a decreased renal perfusion pressure was not affected by sympathetic nervous system blocking agents, whereas angiotensin II will apparently inhibit renin secretion in vitro. It was concluded that a baroreceptor response, similar to that found in mammals, is found in fishes and a model mechanism for renin secretion in fishes is proposed.

Decreased Plasma Renin Activity and Renin Release in Rats with Phaeochromocytoma

1977 ◽  
Vol 53 (5) ◽  
pp. 447-452
Author(s):  
J. C. S. Fray ◽  
P. V. H. Mayer
Keyword(s):  
Sodium Chloride ◽  
Plasma Renin Activity ◽  
Perfusion Pressure ◽  
Plasma Renin ◽  
Renin Activity ◽  
Renin Release ◽  
High Sodium ◽  
Sodium Chloride Loading ◽  
And Control ◽  
Renin Content

1. We have examined the response of renin to chronic low and high sodium chloride intake in rats with transplanted phaeochromocytoma. 2. Phaeochromocytoma suppressed the usual elevated plasma renin activity observed during sodium deprivation. 3. Studies in isolated perfused kidneys indicated that sodium-deprived phaeochromocytoma rats released substantially less renin than sodium-deprived control rats despite an almost identical renal renin content in both sets of animals. In addition, low perfusion pressure (50 mmHg) failed to stimulate renin release in kidneys from these phaeochromocytoma rats. 4. Additional experiments demonstrated that chronic sodium chloride loading suppressed plasma renin activity, renin content and renin release in both phaeochromocytoma and control rats. Both sodium-loaded phaeochromocytoma and sodium-loaded control rats were unresponsive to low perfusion pressure. 5. We conclude that noradrenaline-secreting phaeochromocytoma impairs the response of plasma renin activity in the rat by inhibiting renin release. We also conclude that chronic sodium chloride loading has a similar effect, but the mechanisms remain to be determined.

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