Renal Na+-K+-ATPase in renin release

1982 ◽  
Vol 243 (6) ◽  
pp. F598-F603
Author(s):  
M. A. Cruz-Soto ◽  
J. E. Benabe ◽  
J. M. Lopez-Novoa ◽  
M. Martinez-Maldonado
Keyword(s):  
Sodium Excretion ◽  
Filtration Rate ◽  
Urine Flow ◽  
Renin Secretion ◽  
Juxtaglomerular Cells ◽  
Secretory Rate ◽  
Level Of Activity ◽  
Anesthetized Dogs ◽  
Natriuretic Effect

The effects of ouabain and furosemide on renin secretion, renal function, and renal Na+-K+-ATPase were investigated in anesthetized dogs. Furosemide (2 mg/kg) induced significant diuresis, natriuresis, an increase in renal blood flow (RBF), and a fivefold increase in renin secretory rate (RSR), but no changes in glomerular filtration rate (GFR). Infusion of ouabain (1 microgram . kg-1 . min-1) into one renal artery during furosemide diuresis increased fractional sodium excretion from 22 +/- 2 to 30 +/- 3% from the ipsilateral kidney but did not change urine flow, RBF, or GFR, whereas RSR fell to control values (698 +/- 203 to 137 +/- 43). When ouabain preceded furosemide, the rise in RBF and RSR induced by furosemide was abolished but sodium excretion increased. Ouabain infused in vivo inhibited Na+-K+-ATPase in microsomal fractions from cortex (34%) and medulla (27%) as compared with control. Neither saline nor furosemide exerted any effect on Na+-K+-ATPase. Moreover, the effect of ouabain alone on Na+-K+-ATPase was not different from that of ouabain plus furosemide. No changes in Mg2+-ATPase were detected in any of the experiments. These results indicate that inhibition of renal Na+-K+-ATPase abolishes furosemide-induced renin secretion despite potentiation of the natriuretic effect of the diuretic. It is apparent that the level of activity of Na+-K+-ATPase is of prime importance for renin secretion. In addition, ouabain may act directly on the juxtaglomerular cells to inhibit renin secretion.

Diuretic and natriuretic properties of prestegane B, a mammalian lignan

1987 ◽  
Vol 253 (2) ◽  
pp. R375-R378
Author(s):  
G. E. Plante ◽  
C. Prevost ◽  
A. Chainey ◽  
P. Braquet ◽  
P. Sirois
Keyword(s):  
Glomerular Filtration Rate ◽  
Filtration Rate ◽  
Urine Flow ◽  
In Vivo Model ◽  
Similar Magnitude ◽  
Site Of Action ◽  
Normal Rat ◽  
Natriuretic Effect

The effect of increasing doses of prestegane B, a synthetic lignan, was examined in the anesthetized normal rat, using clearance methodology. Increasing doses of prestegane B 0.5, 1.0, 2.0, and 5.0 mg) were administered intravenously in our separate groups of hydropenic rats. Urine flow increased by 2.8 +/- 0.3, 4.5 +/- 0.5, 7.7 +/- 0.5, and 18.2 +/- 0.8 microliters/min, respectively, above control values. The rise of urinary sodium secretion was of similar magnitude and averaged 0.4 +/- 0.1, 0.8 +/- 0.2, 1.1 +/- 0.3, and 2.4 +/- 0.3 mu eq/min, respectively. No significant change in urinary phosphate excretion was obtained in all groups of rats, and glomerular filtration rate remained constant from control to experimental clearance periods. The natriuretic effect of prestegane B observed in this in vivo model could be related to the inhibition of the Na+-K+-adenosine triphosphate activity demonstrated in vitro in previous studies from our laboratory. The action of this substance is likely to be situated beyond the proximal tubule, since urinary phosphate was not altered. Prestegane B mimics the effects of other endogenous diuretic and natriuretic hormones, but its site of action and its effect on renal hemodynamics are obviously different.

Effect of vasopressin on sodium excretion and plasma antinatriferic activity in the dog

1976 ◽  
Vol 231 (1) ◽  
pp. 28-33 ◽  
Author(s):  
VM Buckalew ◽  
KA Dimond
Keyword(s):  
Glomerular Filtration Rate ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Urine Flow ◽  
Potassium Excretion ◽  
State Control ◽  
Sham Control ◽  
Anesthetized Dogs ◽  
Renal Tubular ◽  
Steady State Control

Vasopressin (VP) was administered for 1 h intravenously to hydropenic, anesthetized dogs in doses of 1.0-1.25 mU/kg per min. In 14 experiments, sodium excretion (UNA V) increased from a mean of 13 +/- 5 to a peak of 96 +/- 21 mueq/min 40 min after beginning infusion (P less than .001). Urine flow and potassium excretion increased from 0.18 +/-.04 ml/min and 20 +/- 2 meuq/min to peak values of 0.6 +/- .08 ml/min and 61 +/- 9 mueq/min, respectively (P less than .001), with no significant increase in glomerular filtration rate. No significant changes in UNA V occurred in eight sham control experiments of in six experiments in which VP was given at 75 muU/kf per min. To test the hypothesis that VP might be natriuretic indirectly by releasing a natriuretic substance, plasms ultrafiltrates were tested for toad bladder antinatriferic activity(AA). During steady-state control, AA was -10 +/- 3%. Thirty and sixty minutes after beginning VP, AA increased to -24 +/- 3% (P less than .05) and -26 +/- 2% (P less than .001), respectiviely. No significant change in plasma AA occurred in either sham controls or in animals given the subnatriuretic VP dose. Incubation of plasma with 1,000 muU/ml VP caused no increase in AA. The data show that VP natriuresis is accompanied by an increase in plasms AA. The results suggest that vasopressin natriuresis in hydropenic dogs at least in part to the release of a humoral inhibitor of renal tubular sodium transport.

Atrial extracts increase glomerular filtration rate in vivo

1985 ◽  
Vol 248 (1) ◽  
pp. F24-F30 ◽  
Author(s):  
D. Beasley ◽  
R. L. Malvin
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Recovery Period ◽  
Plasma Renin ◽  
Urine Flow ◽  
Constant Infusion ◽  
Natriuretic Effect

We measured the effect of a constant infusion of rat atrial extract on the glomerular filtration rate (GFR), renal plasma flow (RPF), and plasma renin concentration (PRC) of bioassay rats. The infusion rate of the atrial extract was 0.038 ml/min, which represented 1.25 mg of homogenized atrial tissue/min. To ensure that dead space was cleared, clearance measurements during the atrial extract infusion were not begun until urine flow had increased and 300 microliter of urine had been excreted. In the first series of rats, control GFR was 0.69 +/- 0.05, increased to 1.04 +/- 0.06 during infusion of atrial extract, and then decreased to 0.72 +/- 0.08 ml X min-1 X 100 g-1 during the recovery period. In a second series, RPF was also measured. GFR increased from 0.92 +/- 0.02 to 1.15 +/- 0.05 ml X min-1 X 100 g-1, while RPF was unchanged. In both series, the increase in GFR was statistically significant. Constant infusion of atrial extracts had no significant effect on PRC. These studies provide evidence that an atrial factor can cause a large increase in GFR, which may contribute to the natriuretic effect of atrial extracts.

scholarly journals Endothelin induces diuresis and natriuresis in the rat by acting on proximal tubular cells through a mechanism mediated by lipoxygenase products.

1991 ◽  
Vol 2 (1) ◽  
pp. 57-69
Author(s):  
N Perico ◽  
R P Cornejo ◽  
A Benigni ◽  
B Malanchini ◽  
J R Ladny ◽  
...  
Keyword(s):  
Glomerular Filtration Rate ◽  
Atrial Natriuretic Peptide ◽  
Glomerular Filtration ◽  
Plasma Flow ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Lipoxygenase Products ◽  
Natriuretic Effect

Besides being a potent renal vasoconstrictor, endothelin causes diuresis and natriuresis. At which site along the nephron and how endothelin alters water and sodium handling in the tubule remain to be clarified. It was found that endothelin (75 pmol) given as an i.v. infusion in vivo to rats caused diuresis and urinary sodium excretion to double but did not affect glomerular filtration rate and renal plasma flow. On raising the dose of endothelin to 150 pmol, a further increase in diuresis and natriuresis was found, whereas glomerular filtration rate fell 33% and renal plasma flow fell 36%; 300 pmol of endothelin reduced glomerular filtration rate by 73% and renal plasma flow by 77% but did not significantly affect diuresis and absolute sodium excretion. It did, however, increase fractional sodium excretion eightfold. Lithium clearance studies of changes in tubular handling of water and sodium indicated that infusion of 150 pmol of endothelin to rats caused a reduction in absolute (pre, 84.7 +/- 5.9; post, 47.9 +/- 6.1 microEq/min/100 g) and fractional (pre, 85.7 +/- 3.0; post, 64.7 +/- 6.4%) proximal reabsorption of sodium. Endothelin infusion (150 pmol) was not associated with any significant change in plasma atrial natriuretic peptide levels, which on average remained comparable to those in rats given the vehicle alone (49.7 +/- 8.4 versus 46.3 +/- 5.6 pg/mL). In the isolated perfused rat kidney preparation, exposure to 150 pmol of endothelin significantly increased fractional sodium excretion over preinjection values (pre, 2.2 +/- 0.2; post, 7.3 +/- 1.0%) despite a marked decrease in glomerular filtration rate and renal perfusate flow. Additional in vivo experiments showed that oral administration of the specific 5-lipoxygenase inhibitor L-651,392 to rats prevented the increase in urine flow rate (pre, 5.7 +/- 0.1; post, 6.6 +/- 0.8 microL/min), and in absolute (pre, 0.33 +/- 0.04; post, 0.37 +/- 0.05 microEq/min) and fractional (pre, 0.10 +/- 0.02; post, 0.11 +/- 0.03%) sodium excretion caused by bolus i.v. infusion of endothelin (150 pmol). Similarly, a specific leukotriene C4/D4 receptor antagonist, L-649,923, also prevented the diuretic and natriuretic effect of 150 pmol of endothelin i.v. infusion. These findings show that (1) endothelin has a diuretic and natriuretic effect that is independent of its action on renal hemodynamics; (2) this effect depends on a direct action on the proximal tubules; (3) atrial natriuretic peptide does not appear to be involved in this effect; and (4) the diuretic and natriuretic responses to endothelin are mediated by 5-lipoxygenase products.

Inhibition of nitric oxide synthesis attenuates pressure-induced natriuretic responses in anesthetized dogs

1993 ◽  
Vol 264 (1) ◽  
pp. F79-F87 ◽  
Author(s):  
D. S. Majid ◽  
A. Williams ◽  
L. G. Navar
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Sodium Excretion ◽  
Renin Angiotensin System ◽  
Fractional Excretion ◽  
Urine Flow ◽  
Synthesis Inhibition ◽  
Fractional Excretion Of Sodium ◽  
Anesthetized Dogs ◽  
Pressure Natriuresis

Inhibition of nitric oxide (NO) synthesis by intrarenal administration of nitro-L-arginine (NLA) leads to decreases in urinary sodium excretion (UNaV) in association with the increases in renal vascular resistance (RVR). In the present study, we examined the ability of the kidney to alter its sodium excretion in response to acute changes in renal arterial pressure (RAP) in anesthetized dogs before and during intrarenal infusion of NLA (50 micrograms.kg-1.min-1). NO synthesis inhibition in 11 dogs increased RVR by 32 +/- 4% and decreased renal blood flow (RBF) by 25 +/- 3%, outer cortical blood flow by 25 +/- 6%, urine flow by 37 +/- 14%, UNaV by 71 +/- 5%, and fractional excretion of sodium (FENa) by 71 +/- 4%. Glomerular filtration rate was not significantly changed during NLA infusion. As previously reported, there was suppression of the RBF autoregulation plateau during NO synthesis inhibition. In addition, there was a marked attenuation of urine flow and UNaV responses to reductions in RAP (150 to 75 mmHg), with significant reductions in the slopes of the relationships between RAP vs. UNaV and RAP vs. FENa during NLA infusion. Similar responses were observed in nine other dogs treated with the angiotensin receptor antagonist losartan, indicating that an augmented activity of the renin-angiotensin system is not responsible for attenuation of the slope of the pressure-natriuresis relationship during NLA infusion. These data suggest that NO may participate in the mediation of the pressure-natriuresis response.

scholarly journals Effects of costimulation of dopamine D1- and D2-like receptors on renal function

1998 ◽  
Vol 275 (4) ◽  
pp. R986-R994 ◽  
Author(s):  
Pedro A. Jose ◽  
Laureano D. Asico ◽  
Gilbert M. Eisner ◽  
Felice Pocchiari ◽  
Claudio Semeraro ◽  
...  
Keyword(s):  
Dopamine Receptor ◽  
Sodium Transport ◽  
Sodium Excretion ◽  
Rank Order ◽  
Sch 23390 ◽  
Urine Flow ◽  
Dopamine Receptor Agonist ◽  
Vasodilatory Effect

In vitro studies have suggested that dopamine D1- and D2-like receptors interact to inhibit renal sodium transport. We used Z-1046, a dopamine receptor agonist with the rank-order potency D3 ≥ D4 > D2 > D5 > D1, to test the hypothesis that D1- and D2-like receptors interact to inhibit renal sodium transport in vivo in anesthetized rats. Increasing doses of Z-1046, administered via the right renal artery, increased renal blood flow (RBF), urine flow, and absolute and fractional sodium excretion without affecting glomerular filtration rate. For determination of the dopamine receptor involved in the renal functional effects of Z-1046, another group of rats received Z-1046 at 2 μg ⋅ kg−1 ⋅ min−1( n = 10) in the presence or absence of the D2-like receptor antagonist domperidone and/or the D1-like antagonist SCH-23390. Domperidone alone had no effect but blocked the Z-1046-mediated increase in urine flow and sodium excretion; it enhanced the increase in RBF after Z-1046. SCH-23390 by itself decreased urine flow and sodium excretion without affecting RBF and blocked the diuretic, natriuretic, and renal vasodilatory effect of Z-1046. We conclude that the renal vasodilatory effect of Z-1046 is D1-like receptor dependent, whereas the diuretic and natriuretic effects are both D1- and D2-like receptor dependent.

On the interaction of calcium, sodium, and water transport in the diuresing kidney

1968 ◽  
Vol 46 (2) ◽  
pp. 275-280 ◽  
Author(s):  
O. Schück ◽  
J. H. Cort
Keyword(s):  
Renal Function ◽  
Linear Relation ◽  
Filtration Rate ◽  
Urine Flow ◽  
Water Reabsorption ◽  
Osmotic Diuresis ◽  
Anesthetized Dogs ◽  
Permeability For Water ◽  
Solute Excretion ◽  
Tubular Permeability

Diuresis was induced in cats by infusion of 3% glucose in 10% ethanol. When urine flow had stabilized at high levels a solution of the Ca salt of ethylenediaminetetraacetate (Na2CaEDTA) was infused as a control for the effect of the EDTA molecule on renal function. The infusion was then changed over to the same molar rate of Na2EDTA, which resulted in a 30% decrease in serum Ca levels. Ca was then repleted rapidly as CaCl2 given intravenously, and the infusion was shifted back to Na2CaEDTA. The decrease in extracellular Ca concentration was associated with a significant antidiuresis. In further experiments on anesthetized dogs, osmotic diuresis was induced either by (a) infusion of hyperosmotic mannitol solutions, which were then shifted over to hypertonic NaCl, or (b) the same solutions in reverse order. Ca excretion correlated in linear fashion with Na excretion, but not with total solute excretion or with filtration rate. When Ca was added to the mannitol infusion, Na excretion increased in linear relation to Ca. It is suggested that Ca (a) decreases tubular permeability for water reabsorption and (b) decreases Na reabsorption, while Na (c) decreases Ca reabsorption. Mechanisms a and b would appear to involve membrane transport directly in the proximal tubule.

Renal actions of endothelin: interaction with prostacyclin

1990 ◽  
Vol 259 (4) ◽  
pp. F645-F652 ◽  
Author(s):  
S. Y. Chou ◽  
A. Dahhan ◽  
J. G. Porush
Keyword(s):  
Blood Pressure ◽  
Filtration Rate ◽  
Prostaglandin Synthesis ◽  
Urine Flow ◽  
Renin Release ◽  
Arterial Blood ◽  
Anesthetized Dogs ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Arterial Plasma ◽  
Prostacyclin Synthesis

The renal actions of endothelin were examined by infusing it intrarenally in anesthetized dogs at 4 ng.min-1.kg-1 without affecting arterial blood pressure or cardiac output. Endothelin infusion caused a transient and significant increase in renal blood flow (RBF) by 13 +/- 2%, followed by large decreases in RBF and glomerular filtration rate (GFR; by 26 +/- 2 and 23 +/- 7%, respectively) but did not alter urine flow rate or absolute sodium excretion. After endothelin infusion, renal venous and arterial plasma 6-ketoprostaglandin F1 alpha increased from 250 +/- 58 and 117 +/- 31 to 1,044 +/- 249 and 617 +/- 211 pg/ml, respectively, and its renal output increased from 339 +/- 99 to 963 +/- 202 pg.min-1.g-1 (P less than 0.01 for all). The renal prostacyclin synthesis was augmented by endothelin without stimulating the renal renin release or norepinephrine output. Inhibition of prostaglandin synthesis with indomethacin partially prevented the early renal vasodilation induced by endothelin, which then caused a more pronounced decline in RBF and GFR (by 65 +/- 7 and 54 +/- 8%, respectively). With suppression of prostacyclin synthesis, inhibition of renin release by endothelin was observed. Thus the vasoconstrictive effects of endothelin on renal hemodynamics are significantly modified by its ability to enhance production of vasodilators, including prostacyclin.

Activation of histamine H3 receptors inhibits renal noradrenergic neurotransmission in anesthetized dogs

2001 ◽  
Vol 280 (5) ◽  
pp. R1450-R1456 ◽  
Author(s):  
Tomoyuki Yamasaki ◽  
Isao Tamai ◽  
Yasuo Matsumura
Keyword(s):  
Receptor Antagonist ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urine Flow ◽  
Urinary Sodium ◽  
Renal Nerve ◽  
Anesthetized Dogs ◽  
Induced Changes ◽  
Antidiuretic Action

To investigate the possible involvement of histamine H3 receptors in renal noradrenergic neurotransmission, effects of (R)alpha-methylhistamine (R-HA), a selective H3-receptor agonist, and thioperamide (Thiop), a selective H3-receptor antagonist, on renal nerve stimulation (RNS)-induced changes in renal function and norepinephrine (NE) overflow in anesthetized dogs were examined. RNS (0.5–2.0 Hz) produced significant decreases in urine flow and urinary sodium excretion and increases in NE overflow rate (NEOR), without affecting renal hemodynamics. When R-HA (1 μg · kg−1 · min−1) was infused intravenously, mean arterial pressure and heart rate were significantly decreased, and there was a tendency to reduce basal values of urine flow and urinary sodium excretion. During R-HA infusion, RNS-induced antidiuretic action and increases in NEOR were markedly attenuated. Thiop infusion (5 μg · kg−1 · min−1) did not affect basal hemodynamic and excretory parameters. Thiop infusion caused RNS-induced antidiuretic action and increases in NEOR similar to the basal condition. When R-HA was administered concomitantly with Thiop infusion, R-HA failed to attenuate the RNS-induced antidiuretic action and increases in NEOR. However, in the presence of pyrilamine (a selective H1-receptor antagonist) or cimetidine (a selective H2-receptor antagonist) infusion, R-HA attenuated the RNS-induced actions, similarly to the case without these antagonists. Thus functional histamine H3 receptors, possibly located on renal noradrenergic nerve endings, may play the role of inhibitory modulators of renal noradrenergic neurotransmission.

Natriuretic effect of atriopeptin III in rats with papillary necrosis

1989 ◽  
Vol 257 (5) ◽  
pp. F859-F865 ◽  
Author(s):  
J. Garcia-Estan ◽  
K. Takezawa ◽  
R. J. Roman
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Hydrostatic Pressure ◽  
Glomerular Filtration ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Renal Papilla ◽  
Papillary Necrosis ◽  
Juxtamedullary Nephron ◽  
Natriuretic Effect

This study compared the effects of atriopeptin III (AP III) on sodium excretion and renal interstitial hydrostatic pressure (RIHP) in control rats and in rats pretreated with 2-bromoethylamine (BEA) to produce papillary necrosis. In control rats, infusion of AP III (100 ng.kg-1.min-1) increased sodium excretion from 2.2 +/- 0.7 to 6.4 +/- 0.9 microeq.min-1.g kidney wt-1 and RIHP from 6.8 +/- 0.7 to 8.7 +/- 0.9 mmHg, whereas glomerular filtration rate and renal blood flow were unaltered. Similar results were obtained in rats pretreated with BEA 48 h before the experiment. In rats studied 6 wk after BEA treatment, the papilla was absent and there was atrophy of juxtamedullary nephrons. AP III did not alter sodium excretion or RIHP in this group of rats. These results indicate that 1) an intact renal papilla and/or juxtamedullary nephron population may be required for the natriuretic effect of AP III; 2) the papillary injury 48 h after BEA is not sufficient to abolish the natriuretic response to AP III; and 3) elevations in RIHP may play a role in the natriuretic response to AP III.

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