In vivo diuretic actions of renal vasopressin V1 receptor stimulation in rats

1995 ◽  
Vol 268 (3) ◽  
pp. R796-R807 ◽  
Author(s):  
C. Ledderhos ◽  
D. L. Mattson ◽  
M. M. Skelton ◽  
A. W. Cowley
Keyword(s):  
Glomerular Filtration Rate ◽  
Receptor Agonist ◽  
Filtration Rate ◽  
Urine Flow ◽  
Vasopressin Receptor ◽  
Receptor Stimulation ◽  
Water Excretion ◽  
V2 Receptor ◽  
Volume Retention

The specific vasopressin V1 receptor agonist (V1AG; [Phe2,Ile3,Orn8]vasopressin) was infused (2.0 ng.kg-1.min-1) into the renal medullary interstitial space to determine the effects of selective medullary V1 receptor stimulation on sodium and water excretion in normal rats. Responses were compared with those of arginine vasopressin (AVP) and vasopressin V2 receptor stimulation resulting from infusion of a V1 receptor antagonist with AVP. Medullary infusion of V1AG or AVP in euvolemic rats produced no changes in hemodynamics or glomerular filtration rate. V1AG increased urine flow > 60% in euvolemic rats, whereas no change was observed with AVP. This response could not be explained by a rise of arterial pressure or by volume retention. With V2 stimulation in euvolemic rats, urine flow was decreased. In water diuretic rats, V1AG produced no change, whereas AVP infusion decreased urine flow. The results provide in vivo evidence that tubular V1 vasopressin receptor activity results in increased urine flow and thereby modulates the antidiuretic actions of vasopressin in the euvolemic state.

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.

V1- and V2-receptor contributions to ovine fetal renal and cardiovascular responses to vasopressin

1992 ◽  
Vol 262 (4) ◽  
pp. R636-R643
Author(s):  
M. G. Ervin ◽  
M. G. Ross ◽  
R. D. Leake ◽  
D. A. Fisher
Keyword(s):  
Receptor Agonist ◽  
Urine Osmolality ◽  
Cardiovascular Responses ◽  
Urine Flow ◽  
Receptor Blockade ◽  
Fetal Life ◽  
Receptor Stimulation ◽  
V2 Receptor ◽  
Ovine Fetal ◽  
Renal Responses

To assess the contributions of arginine vasopressin (AVP) V1- and V2-receptors to the ovine fetal responses to AVP, we studied V2-receptor stimulation in the presence of V1-receptor blockade, and selective V2-receptor stimulation in chronically catheterized fetal lambs. AVP administration (20 ng/kg) to the saline infused fetuses (n = 8; 132 +/- 2 days) significantly increased mean arterial pressure (MAP; 45 +/- 2 to 53 +/- 4 mmHg) and urine osmolality (Uosm; 134 +/- 13 to 379 +/- 42 mosmol/kgH2O) and decreased heart rate (HR; 168 +/- 3 to 147 +/- 5 beats/min) and urine flow (V; 0.48 +/- 0.10 to 0.19 +/- 0.03 ml/min). V1-receptor antagonist infusion, [d(CH2)5,Tyr(Me)]AVP (n = 7; 134 +/- 1 days) had no effect on fetal MAP, Uosm, HR, or V. V1-receptor blockade abolished the MAP response to AVP without affecting the HR and urinary responses. In a second series of animals (n = 6; 131 +/- 1 days), selective V2-receptor agonist infusion [desmopressin (DDAVP)] had no effect on fetal MAP or HR while initial changes in V and Uosm were identical to the effects of AVP alone. Our results demonstrate clear discrimination of V1- and V2-receptor-mediated events in the fetal MAP and renal responses to AVP. Moreover, the HR response to AVP is not mediated by the population of V1-receptors blocked by [d(CH2)5,Tyr(Me)]AVP or V2-receptors stimulated by DDAVP, suggesting the presence of additional AVP receptor subclass(es) during fetal life.

Effects of glucagon on glomerular filtration rate and urea and water excretion

1992 ◽  
Vol 263 (1) ◽  
pp. F24-F36 ◽  
Author(s):  
M. Ahloulay ◽  
N. Bouby ◽  
F. Machet ◽  
M. Kubrusly ◽  
C. Coutaud ◽  
...  
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Flow Rate ◽  
Filtration Rate ◽  
Urine Flow ◽  
Urine Flow Rate ◽  
Urea Synthesis ◽  
Physiological Level ◽  
Water Excretion ◽  
Urea Excretion

Clearance experiments were performed in anesthetized male Wistar rats to reevaluate the renal effects of glucagon (Gluc) on glomerular filtration rate (GFR) and solute and water excretion. After an 80-min control period, these effects were evaluated in the last 80 min of a 2-h intravenous Gluc infusion. Gluc induced significant increases in GFR (+20%), urine flow rate (+150%), free water reabsorption (+50%), urea synthesis and urea excretion (+66%), and nonurea solute excretion (+67%). In addition, fractional urea excretion (FEurea) increased by 43% (P less than 0.01). Additional experiments showed that increases in either urea excretion or urine flow rate (induced by appropriate infusion of urea or half-dilute saline), similar to those seen after Gluc, could not account for the increased FEurea. All significant effects of Gluc were also observed during infusion of antidiuretic hormone or during water diuresis. The tubular effects of Gluc could be explained by a reduction in proximal reabsorption. The dose of Gluc required to induce all the effects described above was 12 ng.min-1.100 g body wt-1, a dose producing an approximately 10-fold supraphysiological peripheral plasma concentration but a “physiological” level for the liver. Infusion of 1.2 ng induced almost no change in renal function, and infusion of 120 ng induced no greater effects than 12 ng. These results suggest 1) that Gluc, a hormone liberated after protein ingestion, exerts coordinated effects on liver and kidney to increase simultaneously urea synthesis and excretion and to promote water conservation and 2) that these effects could, at least in part, be indirect and depend on the Gluc-induced stimulation of hepatocyte metabolism.

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.

Sodium and Water Excretion in Nephrotic Patients: Effects of Changes in Renal Haemodynamics

1990 ◽  
Vol 79 (2) ◽  
pp. 123-129 ◽  
Author(s):  
Michael Allon ◽  
Charles B. Pasque ◽  
Mariano Rodriguez
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Plasma Flow ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Urine Volume ◽  
Sodium Reabsorption ◽  
Plasma Volume Expansion ◽  
Water Excretion ◽  
Significant Change

1. Eight nephrotic patients were studied in order to evaluate the effects of acute changes in renal plasma flow and glomerular filtration rate on renal solute and water handling, in the absence of plasma volume expansion. 2. The subjects were studied first after the administration of captopril, a manoeuvre that increased renal plasma flow without a significant change in glomerular filtration rate, and a second time after receiving combined therapy with captopril and ibuprofen, a manoeuvre that decreased glomerular filtration rate without a significant change in renal plasma flow. 3. After captopril therapy, despite the increase in renal plasma flow, there was no significant change in proximal sodium reabsorption (as estimated from fractional lithium reabsorption), urine volume or urine osmolality. 4. The decrease in glomerular filtration rate observed after the administration of captopril plus ibuprofen was associated with decreases in fractional excretion of sodium and urine volume, and an increase in urine osmolality. The changes in these parameters of tubular function were proportionate to the changes in glomerular filtration rate. Fractional proximal sodium reabsorption increased substantially. 5. These observations suggest that, in the absence of plasma volume expansion, an increase in renal plasma flow does not increase sodium or water excretion by the nephrotic kidney. Moreover, during acute decreases in glomerular filtration rate, glomerulotubular balance appears to be disrupted, resulting in disproportionately high rates of proximal tubule sodium reabsorption.

Renal responses to graded hemorrhage in conscious pig

1990 ◽  
Vol 259 (1) ◽  
pp. R119-R125 ◽  
Author(s):  
J. L. Sondeen ◽  
G. A. Gonzaludo ◽  
J. A. Loveday ◽  
G. E. Deshon ◽  
C. B. Clifford ◽  
...  
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Arterial Pressure ◽  
Filtration Rate ◽  
Urine Flow ◽  
Electrolyte Excretion ◽  
Flow Probe ◽  
Ureteral Catheter ◽  
Time Points ◽  
Renal Responses

We developed a conscious pig model with a chronically instrumented kidney to measure renal blood flow (RBF), glomerular filtration rate (GFR), and excretory functions during hemorrhage. Seven to 10 days before experimentation, pigs were splenectomized, arterial and venous catheters were implanted, an ultrasonic flow probe was placed on the renal artery, and a pyelostomy was performed for nonocclusively placing a ureteral catheter. Measurements were taken before hemorrhage, and at hemorrhage volumes of 7, 14, 21, and 28 ml/kg (equivalent to 10.5, 21, 31, and 42% of the estimated blood volume), or at corresponding time points for controls. RBF was decreased by 30% when 21% of the blood (14 mg/kg) was removed, before arterial pressure, GFR, or urine flow or excretion was changed. At volumes of hemorrhage greater than 14 ml/kg, there were progressive decreases in RBF, GFR, urine flow rate, osmotic and electrolyte excretion, and arterial pressure. Thus pigs, like humans, respond to hypovolemia with an early redistribution of blood flow away from the kidney.

DIAGNOSIS AND TREATMENT: ACUTE RENAL FAILURE

PEDIATRICS ◽  
1965 ◽  
Vol 35 (3) ◽  
pp. 478-481
Author(s):  
Malcolm A. Holliday
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Glomerular Filtration Rate ◽  
Renal Disease ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Obstructive Uropathy ◽  
Urine Flow ◽  
Water Restriction ◽  
Plasma Electrolyte

ACUTE RENAL FAILURE is an uncommon emergency which faces pediatricians. It is usually easy to recognize. The management in the early phase is critical to the survival potential of the patient. The purpose of this review is to cite the causes, characteristics, and principally the management of acute renal failure. Renal failure is defined as a state in which there is not sufficient kidney function to prevent the development of severe uremia or to maintain plasma electrolyte values in a range compatible with ordinary activities. Clinically the condition is associated with mental confusion, stupor, and frequently convulsions. Persistent hiccoughs, irregular respirations, and muscle cramps also may occur. Usually though not always, there is obvious oliguria. Since urine flow is ordinarily but 0.2-2,0% of glomerular filtration rate, and since glomerular filtration rate reduction to 5-10% may be associated with uremia, it is possible to have renal failure without oliguria. It is also possible to have physiological oliguria (< 300 ml per square meter) in response to rigid water restriction that is not related to renal failure. Hence, the term must be defined in terms of its effect on plasma composition rather than in terms of urine flow. The presence of certain clinical conditions known to result in acute renal failure should alert the physician. These include: nephrotoxie agents; hemoglobinuria or myoglobinuria; shock with anoxic damage; acute, diffuse renal disease; acute dehydration in patients with chronic advanced renal disease; and acute obstructive uropathy. Nephrotoxic agents, hemoglobinuria, and shock all result in acute tubular necrosis, and recovery depends upon the capacity of the nephron to regenerate on an intact basement membrane.

Meclofenamate and urine concentration with and without exposure of the renal papilla

1981 ◽  
Vol 240 (5) ◽  
pp. F423-F429 ◽  
Author(s):  
R. J. Roman ◽  
C. Lechene
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Urine Osmolality ◽  
Urine Concentration ◽  
Prostaglandin Synthesis ◽  
Urine Flow ◽  
Renal Papilla ◽  
Arterial Blood ◽  
Pelvic Urine

The recent finding that inhibitors of prostaglandin synthesis prevent the fall in urine concentration produced by papillary exposure challenges the hypothesis that contact between the pelvic urine and papilla is essential to the renal concentrating process. The present study examines the change in urine osmolality produced by exposure of the renal papilla in rats given meclofenamate. In control animals urine osmolality(Uosmol) decreased 57% after 2 h of exposure of the renal papilla. In rats given meclofenamate 4 mg/kg urine osmolality increased 16%, urine flow decreased 30%, and glomerular filtration rate was unchanged in the nonexposed kidney. Meclofenamate, however, did not alter the decrease in Uosmol seen in the kidney with the exposed papilla. Meclofenamate 10 mg/kg was also ineffective in preventing the fall in urine osmolality produced by papillary exposure, although this higher dose decreased glomerular filtration rate and arterial blood pressure. These results are consistent with the finding that pelvic urine urea is important to the urinary concentrating process and with the hypothesis that urine osmolality falls after papillary exposure because contact between pelvic urine and papilla is interrupted.

scholarly journals The intrinsic circadian clock in podocytes controls glomerular filtration rate

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Camille Ansermet ◽  
Gabriel Centeno ◽  
Svetlana Nikolaeva ◽  
Marc P. Maillard ◽  
Sylvain Pradervand ◽  
...  
Keyword(s):  
Glomerular Filtration Rate ◽  
Circadian Clock ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Transcriptome Profiling ◽  
Circadian Rhythmicity ◽  
Water Excretion ◽  
Key Indicator ◽  
Genes Encoding ◽  
Urine Formation

Abstract Glomerular filtration rate (GFR), or the rate of primary urine formation, is the key indicator of renal function. Studies have demonstrated that GFR exhibits significant circadian rhythmicity and, that these rhythms are disrupted in a number of pathologies. Here, we tested a hypothesis that the circadian rhythm of GFR is driven by intrinsic glomerular circadian clocks. We used mice lacking the circadian clock protein BMAL1 specifically in podocytes, highly specialized glomerular cells critically involved in the process of glomerular filtration (Bmal1lox/lox/Nphs2-rtTA/LC1 or, cKO mice). Circadian transcriptome profiling performed on isolated glomeruli from control and cKO mice revealed that the circadian clock controls expression of multiple genes encoding proteins essential for normal podocyte function. Direct assessment of glomerular filtration by inulin clearance demonstrated that circadian rhythmicity in GFR was lost in cKO mice that displayed an ultradian rhythm of GFR with 12-h periodicity. The disruption of circadian rhythmicity in GFR was paralleled by significant changes in circadian patterns of urinary creatinine, sodium, potassium and water excretion and by alteration in the diurnal pattern of plasma aldosterone levels. Collectively, these results indicate that the intrinsic circadian clock in podocytes participate in circadian rhythmicity of GFR.

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