Effects of atriopeptin and chicken heart extract in Gallus domesticus

1986 ◽  
Vol 251 (3) ◽  
pp. R543-R551 ◽  
Author(s):  
C. M. Gregg ◽  
R. F. Wideman
Keyword(s):  
Sodium Excretion ◽  
Filtration Rate ◽  
Urine Flow ◽  
Limited Capacity ◽  
Chicken Heart ◽  
Fractional Sodium Excretion ◽  
The Difference ◽  
Renal Vascular ◽  
Single Comb ◽  
Portal Infusion

Effects of Ser-Leu-Arg-Arg-atriopeptin III (ANP) and chicken heart extract (CHE) were compared during unilateral renal portal infusion in anesthetized Single Comb White Leghorn chickens. The purpose was to determine whether renal effects were glomerular and/or tubular. Both CHE and ANP caused substantial decreases in mean arterial pressure but had different renal actions. ANP caused small but significant increases in both absolute and fractional sodium excretion, but these effects were modest compared with those reported in mammals. Although there was a tendency for higher fractional sodium excretion in the portal infused kidney, the difference was not significant (0.1 less than P greater than 0.05). ANP also increased glomerular filtration rate (GFR), urine flow rate (UFR), and osmolal clearance and decreased estimated renal vascular resistance. In contrast, CHE decreased GFR and increased resistance. In contrast, CHE decreased GFR and increased fractional potassium excretion in the infused kidney. After CHE infusion was stopped, GFR and UFR increased, and there was a further transient kaliuresis. No natriuretic effects were ever seen with CHE. Chickens apparently lack potent mammalian-type cardiac natriuretic factor(s) and/or have a limited capacity for natriuresis in response to mammalian ANP. Because hypotension was the most prominent avian response to both CHE and ANP, endogenous vasoactive factor(s) in chicken hearts may function to regulate blood pressure rather than blood volume.

scholarly journals THE STUDY OF RENOPROTECTIVE PROPERTIES OF ERYTROPOETIN DERIVATIVES ON THE KIDNEY ISCHEMIA-REPERFUSION MODEL

2018 ◽  
Vol 25 (6) ◽  
pp. 73-77 ◽  
Author(s):  
V. V. Elagin ◽  
D. A. Kostina ◽  
O. I. Bratchikov ◽  
M. V. Pokrovsky ◽  
T. G. Pokrovskaya
Keyword(s):  
Acute Kidney Injury ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Fractional Sodium Excretion ◽  
Male Wistar Rats ◽  
Microcirculatory Disorders

Aim.The research was designed to study the renoprotective properties of erythropoietin derivatives on the kidney ischemiareperfusion experimental model.Materials and methods.The renoprotective properties of asialo erythropoietin (0.4 μg/kg and 2.4 μg/kg 30 minutes before the induction of ischemia) and carbamylated darbepoetin (50 μg/kg 24 hours before the ischemic stimulus) were studied in comparison with erythropoietin and darbepoetin in a series of experiments on male Wistar rats on a 40-minute bilateral model of renal ischemia-reperfusion. The renoprotective properties were evaluated by the results of biochemical markers of acute kidney injury, the dynamics of glomerular filtration rate and fractional sodium excretion, as well as the severity of microcirculatory disorders.Results.It was found that the prophylactic use of asialo erythropoietin (dose-dependent) and carbamylated darbepoetin leads to a decrease in the serum concentration of markers of acute renal damage, an increase in the glomerular filtration rate, a decrease in fractional sodium excretion, and a decrease in microcirculatory disorders.Conclusion.Asialo erythropoietin and carbamylated darbepoetin have the pronounced renoprotective properties and are the promising agents for the prevention and treatment of acute kidney injury.

Chronic atrial appendectomy alters sodium excretion in conscious monkeys

1988 ◽  
Vol 254 (4) ◽  
pp. R699-R705
Author(s):  
B. A. Benjamin ◽  
C. H. Metzler ◽  
T. V. Peterson
Keyword(s):  
Sodium Excretion ◽  
Volume Expansion ◽  
Sham Group ◽  
Venous Pressure ◽  
Urine Flow ◽  
Central Venous ◽  
Renal Response ◽  
Fractional Sodium Excretion ◽  
Blood Volume Expansion ◽  
Atrial Natriuretic

The purpose of this study is to determine whether chronic removal of atrial appendages alters renal response to volume expansion in the conscious monkey. Chronic bilateral atrial appendectomy (ATX) was performed in six animals. Six additional animals served as sham-operated controls. Monkeys were studied 1-2 wk after chronic surgery. The protocol consisted of three consecutive 10-min urine collections followed by 20% ischemic blood volume expansion (VE) and 120 min of post-VE measurements. In sham animals, VE caused an increase in plasma atrial natriuretic peptide (ANP) levels (48 +/- 7 pg/ml to a peak of 108 +/- 34 pg/ml). Urine flow increased from 0.43 +/- 0.07 to 1.07 +/- 0.24 ml/min, sodium excretion increased from 17.9 +/- 2.6 to 74.9 +/- 12.0 mu eq/min, and fractional sodium excretion increased from 0.67 +/- 0.10 to 2.43 +/- 0.28%. ATX attenuated the increase in ANP (34 +/- 8 pg/ml to a peak of 38 +/- 9 pg/ml) in four of six animals. In these animals, renal response to VE was significantly attenuated. Urine flow increased from 0.21 +/- 0.05 to 0.30 +/- 0.01 ml/min, sodium excretion increased from 19.3 +/- 6.02 to 37.8 +/- 5.05 mu eq/min, and fractional sodium excretion increased from 0.79 +/- 0.08 to 1.43 +/- 0.17%. Renal response of two ATX animals with normal increases in atrial natriuretic factor was similar to the sham group. Effect of volume expansion on mean arterial pressure, central venous pressure, and renal hemodynamics was not altered by ATX. These findings demonstrate that bilateral atrial appendectomy in the monkey attenuates the increase in ANP and reduces renal response to VE.

Supersensitivity to norepinephrine in chronically denervated kidneys: evidence for a postsynaptic effect

1987 ◽  
Vol 65 (11) ◽  
pp. 2219-2224 ◽  
Author(s):  
J. Krayacich ◽  
R. L. Kline ◽  
P. F. Mercer
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Fractional Excretion ◽  
Urine Flow ◽  
Fractional Excretion Of Sodium ◽  
Infusion Of Norepinephrine

Denervation supersensitivity in chronically denervated kidneys increases renal responsiveness to increased plasma levels of norepinephrine. To determine whether this effect is caused by presynaptic (i.e., loss of uptake) or postsynaptic changes, we studied the effect of continuous infusion of norepinephrine (330 ng/min, i.v.) and methoxamine (4 μg/min, i.v.), an α1 adrenergic agonist that is not taken up by nerve terminals, on renal function of innervated and denervated kidneys. Ganglionic blockade was used to eliminate reflex adjustments in the innervated kidney and mean arterial pressure was maintained at preganglionic blockade levels by an infusion of arginine vasopressin. With renal perfusion pressure controlled there was a significantly greater decrease in renal blood flow (−67 ± 9 vs. −33 ± 8%), glomerular filtration rate (−60 ± 9 vs. −7 ± 20%), urine flow (−61 ± 7 vs. −24 ± 11%), sodium excretion (−51 ± 15 vs. −32 ± 21%), and fractional excretion of sodium (−50 ± 9 vs. −25 ± 15%) from the denervated kidneys compared with the innervated kidneys during the infusion of norepinephrine. During the infusion of methoxamine there was a significantly greater decrease from the denervated compared with the innervated kidneys in renal blood flow (−54 ± 10 vs. −30 ± 14%), glomerular filtration rate (−51 ± 11 vs. −19 ± 17%), urine flow (−55 ± 10 vs. −39 ± 10%), sodium excretion (−70 ± 9 vs. −59 ± 11%), and fractional excretion of sodium (−53 ± 10 vs. −41 ± 10%). These results suggest that vascular and tubular supersensitivity to norepinephrine in chronically denervated kidneys is due to postsynaptic changes involving α1-adrenergic receptors.

Neural not tubular dopamine increases glomerular filtration rate in perfused rat kidneys

1986 ◽  
Vol 250 (4) ◽  
pp. F674-F679 ◽  
Author(s):  
A. D. Baines ◽  
R. Drangova
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Sch 23390 ◽  
Inulin Clearance ◽  
Fractional Sodium Excretion ◽  
Adrenergic Antagonists ◽  
Chronic Denervation ◽  
Endogenous Substrates

We examined the effect of endogenous neural and tubular dopamine production on renal function in isolated perfused kidneys. Nerves and proximal tubules in perfused kidneys produce dopamine from endogenous substrates. Surgical denervation 5-14 days before perfusion removed neural dopamine production and decreased dopamine excretion 32% (P less than 0.05), inulin clearance 7% (P less than 0.05), and sodium excretion 57% (P less than 0.01). Carbidopa, which abolished neural and tubular dopamine production, produced similar functional effects. Haloperidol, Sch 23390, and (+)butaclamol, but not (-)butaclamol, added during perfusion increased renovascular resistance 4-5% (P less than 0.001) and decreased inulin clearance 20% (P less than 0.001). Sch 23390 reduced fractional sodium excretion (P less than 0.01), but haloperidol and butaclamol did not. Chronic denervation or carbidopa blocked the reduction of inulin clearance by haloperidol, but alpha- and beta-adrenergic antagonists did not. Fractional sodium excretion increased after adding haloperidol to denervated or adrenergic blocked kidneys. Denervation blocked the effect of Sch 23390 on inulin clearance but not on sodium excretion. Haloperidol inhibited dopamine excretion. Thus dopamine released from acutely severed nerves in perfused kidneys increases glomerular filtration rate (GFR). Dopamine produced by tubules of chronically denervated kidneys did not influence GFR but stimulated sodium excretion by an Sch 23390-sensitive mechanism.

Role of kinin and renal ANG II blockade in acute effects of ACE inhibitors in low-renin hypertension

1997 ◽  
Vol 272 (2) ◽  
pp. H679-H687
Author(s):  
M. Naitoh ◽  
H. Suzuki ◽  
K. Arakawa ◽  
A. Matsumoto ◽  
A. Ichihara ◽  
...  
Keyword(s):  
Glomerular Filtration Rate ◽  
Receptor Antagonist ◽  
Flow Rate ◽  
Ace Inhibitors ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Urinary Sodium Excretion ◽  
Urine Flow ◽  
Ang Ii ◽  
Low Renin Hypertension

In conscious deoxycorticosterone acetate (DOCA) salt-hypertensive dogs, the angiotensin-converting enzyme (ACE) inhibitors captopril and imidaprilat significantly decreased mean arterial pressure (MAP) and significantly increased urine flow rate, effective renal plasma flow (ERPF), glomerular filtration rate, and urinary sodium excretion. However, the angiotensin type 1 (AT1) receptor antagonist losartan caused a significant increase only in urinary sodium excretion without significant changes in MAP, urine flow rate, ERPF, and glomerular filtration rate. Simultaneous infusion of a bradykinin receptor antagonist inhibited the ACE inhibitor-induced reduction in MAP and increase in ERPF. DOCA salt treatment markedly suppressed plasma angiotensin II (ANG II) concentration (P < 0.001), although it decreased renal ANG II content only slightly (P < 0.05). Comparison of the expression of renal AT1 receptor mRNA in control kidneys with that in DOCA salt-hypertensive kidneys revealed no significant change. These results suggest that, in low-renin hypertension, inhibition of the relatively maintained ANG II production in the kidney participates in the natriuretic action of ACE inhibitors. However, hypotensive and other renal effects are mainly due to the action of bradykinin.

Renal Function Correlates of Postnatal Diuresis in Preterm Infants

PEDIATRICS ◽  
1988 ◽  
Vol 82 (1) ◽  
pp. 50-58 ◽  
Author(s):  
Khurshid S. Bidiwala ◽  
John M. Lorenz ◽  
Leonard I. Kleinman
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Preterm Infants ◽  
Sodium Excretion ◽  
Urine Output ◽  
Filtration Rate ◽  
Fluid Intake ◽  
Intake Rate ◽  
Fractional Sodium Excretion ◽  
The Face

A characteristic pattern of fluid homeostasis occurs in the first week of life in many preterm infants. Initially, urine output is low independent of fluid intake, subsequently a diuresis occurs, and finally urine output begins to vary with intake. Renal clearance measurements were made during each of these three phases to elucidate the renal mechanisms involved. Periods during which the ratio of urine output to fluid intake was ≥1 and urine output was ≥3 mL/kg/h were defined as diuretic. Of 22 preterm infants studied from 12 to 120 hours of age, 17 had at least one period of diuresis. In these infants, urine output, fluid intake rate, output to intake ratio, glomerular filtration rate, and fractional sodium excretion were lowest at 12 to 24 hours of age. During diuresis, urine output tripled without a significant change in fluid intake so that output to intake increased to levels exceeding unity. Diuresis was associated with significant increases in glomerular filtration rate and fractional sodium excretion. By 108 to 120 hours of age, urine output decreased despite an increase in fluid intake. This was accompanied by a decrease in glomerular filtration rate. These results suggest that the initial antidiuretic phase is the result of a low fractional sodium excretion in the face of a low glomerular filtration rate. Subsequently, diuresis and natriuresis occur as a result of abrupt, nonmaturational increases in glomerular filtration rate and fractional sodium excretion. With cessation of diuresis, glomerular filtration rate and fractional sodium excretion decrease and water and electrolyte output begin to vary appropriately with intake.

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.

scholarly journals Bosentan Normalizes the GFR Response to Renal Nerve Stimulation Following Reversible Unilateral Ureteric Obstruction in the Rat

2014 ◽  
pp. 713-722
Author(s):  
F. T. HAMMAD ◽  
A. M. WHEATLEY ◽  
G. DAVIS
Keyword(s):  
Glomerular Filtration Rate ◽  
Flow Rate ◽  
Nerve Stimulation ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Urine Flow ◽  
Ureteric Obstruction ◽  
Renal Nerve ◽  
Renal Nerve Stimulation ◽  
Unilateral Ureteric Obstruction

We investigated the renal response to direct renal nerve stimulation, 2 weeks following reversal of 24-h unilateral (left) ureteric obstruction. Renal nerve stimulation caused a 13-15 % fall in renal blood flow, in 4 groups of anesthetized rats following ureteric obstruction (n=9) or a sham operation (n=7) both with (n=9) and without (n=7) treatment with the mixed ETA/B receptor antagonist, bosentan. In the sham-operated rats, renal nerve stimulation did not change glomerular filtration rate but reduced urine flow rate (37±3 %, P<0.001), and absolute (38±4 %, P<0.001) and fractional (35±5 %, P<0.01) sodium excretion. Following unilateral ureteric obstruction, renal nerve stimulation increased glomerular filtration rate by 22±3 % (P<0.01), but reduced urine flow rate (14±2 %, P<0.001) and fractional sodium excretion (23±5 %, P<0.01). Bosentan treatment had no effect on baseline or renal responses to renal nerve stimulation in the sham group but normalized the renal response to renal nerve stimulation in the unilateral ureteric obstruction group. We conclude that 14 days after a 24-h period of unilateral ureteric obstruction there is an increase in GFR in response to direct renal nerve stimulation, which is due, in part, to the actions of endothelin at the time of obstruction.

Renal nerves and renal responses to head-up tilt in dogs

1987 ◽  
Vol 252 (5) ◽  
pp. R979-R986
Author(s):  
T. V. Peterson ◽  
N. L. Hurst ◽  
J. A. Richardson
Keyword(s):  
Arterial Pressure ◽  
Sodium Excretion ◽  
Renal Denervation ◽  
Urine Flow ◽  
Renal Nerves ◽  
Fluid Reabsorption ◽  
Fractional Sodium Excretion ◽  
Head Up Tilt ◽  
Anesthetized Dogs ◽  
Renal Responses

Experiments were performed in anesthetized dogs to compare the effects of acute and chronic unilateral renal denervation on the renal responses to head-up tilt and to assess denervation hypersensitivity to infused norepinephrine (NE). Responses of the denervated kidney were compared with those of the contralateral innervated kidney in each animal. With acute denervation, 40 min of 45 degrees head-up tilt decreased urine flow (V) 37%, absolute sodium excretion (UNaV) 53%, and fractional sodium excretion (FENa+) 44% in the innervated kidneys, but no decreases occurred in the denervated kidneys. NE infusion (125 ng X kg-1 X min-1) increased arterial pressure by 11 mmHg and increased V, UNaV, and FENa+ in both kidneys. In the chronically denervated animals (2-4 wk prior to experiment) tilt decreased V by 32%, UNaV by 44%, and FENa+ by 21% in the innervated kidneys, but again no changes occurred in the denervated kidneys. NE infusion in this group also increased arterial pressure approximately 11 mmHg and caused V, UNaV, and FENa+ to increase in the innervated kidneys but decrease in the denervated kidneys. These results demonstrate that the renal responses to tilt are abolished by both acute and chronic renal denervation even though the chronically denervated kidney is hypersensitive to NE-stimulated fluid reabsorption. Therefore endogenous plasma NE levels must not increase enough during tilt such that this hypersensitivity phenomenon can compensate for chronic ablation of the renal nerves.

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.

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