The natriuretic actions of vasopressin in the female rat: variations during the 4 days of the oestrous cycle

1996 ◽  
Vol 148 (3) ◽  
pp. 457-464 ◽  
Author(s):  
M L Forsling ◽  
Y Zhou ◽  
R J Windle
Keyword(s):  
Sodium Excretion ◽  
Filtration Rate ◽  
Significant Rise ◽  
Urine Flow ◽  
Oestrous Cycle ◽  
Female Rat ◽  
Plasma Vasopressin ◽  
Reproductive Cycles ◽  
Dose Dependent Increase ◽  
Dose Dependent

Abstract The renal actions of vasopressin were studied in the conscious female rat. Vasopressin caused a dose-dependent increase in sodium excretion when administered at 40–160 pmol/min. The highest dose, which increased sodium excretion from 10·4 ± 0·3 μmol/min (n=32) to 18·3 ± 0·8 μmol/min (n=8, P<0·001), also caused a significant rise in glomerular filtration rate (GFR). The antidiuretic and natriuretic responses to vasopressin varied significantly over the 4 days of the oestrous cycle. Both responses were greatest on pro-oestrus, being −57 ± 3 and 52 ± 3% above the control values with 80 pmol vasopressin/min. Responses of similar magnitude were also seen on dioestrus day 1. On these two cycle days the effects on urine flow and sodium excretion were accompanied by a significant increase in GFR. Smaller antidiuretic and natriuretic responses were seen on oestrus and dioestrus day 2, without concomitant changes in GFR. As the plasma vasopressin concentrations produced by hormone infusion were similar on each day of the cycle, the renal responsiveness to vasopressin appears to vary over the 4 days of the oestrous cycle. This may be important in terms of alteration and possible disturbances of fluid balance which may occur during reproductive cycles and pregnancy. Journal of Endocrinology (1996) 148, 457–464

Renal responses to oxytocin during the 4 days of the oestrous cycle in the rat

1997 ◽  
Vol 154 (2) ◽  
pp. 347-353 ◽  
Author(s):  
R J Windle ◽  
M L Forsling
Keyword(s):  
Sodium Excretion ◽  
Dose Range ◽  
Virgin Female ◽  
Urine Flow ◽  
Oestrous Cycle ◽  
Female Rats ◽  
Female Rat ◽  
Oxytocin Infusion ◽  
Renal Responses ◽  
Dose Dependent

Abstract Oxytocin was administered to virgin female rats at doses of 25–200 pmol/min during 0·077 mol NaCl/l infusion at 150 μl/min on each day of the oestrous cycle. The resultant rates of urine flow, glomerular filtration (GFR) and electrolyte excretion were determined. Oxytocin caused significant increases in urine flow (P<0·001) and sodium excretion (P<0·001); both responses being dose-dependent (P<0·02 and P<0·01 respectively). Significant variations in the renal responsiveness to the hormone occurred over the 4 days of the oestrous cycle. On oestrus the lowest dose of 25 pmol oxytocin/min produced a significant increase in urine flow (from 139·5 ± 4·3 to 165·6 ± 7·1 μl/min, P<0·005) and a dose of 50 pmol/min produced a significant increase in sodium excretion (from 10·6 ± 0·1 to 14·5 ± 0·7 μmol/min, P<0·005). Significant increases in urine flow and sodium excretion were seen on pro-oestrus with hormone administration rates of 50 and 100 pmol/min respectively and on dioestrus day 2 with a rate of 100 pmol/min. On dioestrus day 1 no increase in urine flow or sodium excretion was seen over the dose range of oxytocin administration. A dose of 100 pmol oxytocin/min significantly increased GFR on pro-oestrus and dioestrus day 2, but not on the other 2 days of the cycle. The circulating hormone concentrations produced by oxytocin infusion were similar on each day of the cycle and so could not account for the differences seen. Therefore, these results suggest varying renal responsiveness to oxytocin during the reproductive cycle of the female rat. Journal of Endocrinology (1997) 154, 347–353

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.

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.

Effects of intrarenal adenosine on renal function and medullary blood flow in the rat

1988 ◽  
Vol 255 (6) ◽  
pp. F1230-F1234 ◽  
Author(s):  
M. Miyamoto ◽  
Y. Yagil ◽  
T. Larson ◽  
C. Robertson ◽  
R. L. Jamison
Keyword(s):  
Blood Flow ◽  
Sodium Excretion ◽  
Systemic Circulation ◽  
Urinary Flow ◽  
Medullary Blood Flow ◽  
Vasa Recta ◽  
Potent Vasodilator ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Higher Doses

Adenosine is a potent vasodilator of the systemic circulation. Infusion of adenosine into the aorta causes water and sodium retention and a fall in glomerular filtration rate and renal blood flow. The effect of adenosine on medullary blood flow is unknown. Because systemic vasodilatory effects may confound its renal actions, adenosine was infused into the renal artery of anesthetized Munich-Wistar rats at doses of 2, 6, and 15 micrograms/min. A marked dose-dependent increase in urinary flow and sodium excretion was observed. Inulin and p-aminohippuric acid clearance did not change significantly. Blood flow in vasa recta in the exposed renal papilla, as determined by fluorescence videomicroscopy, increased significantly only with the highest dose of adenosine. In control animals infused with the vehicle only, there was no change in any of the above variables. These results indicate that direct intrarenal infusion of adenosine in the rat increases urinary flow and sodium excretion and at higher doses also increases vasa recta blood flow. The effects on urinary flow and sodium excretion were therefore mediated by a mechanism other than an increase in vasa recta blood flow.

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.

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.

Induction of Lysinuria in the Rat by Two Para-Substituted Guanidinophenylalanines

1978 ◽  
Vol 54 (6) ◽  
pp. 673-677
Author(s):  
C. W. I. Owens
Keyword(s):  
Intravenous Infusion ◽  
Sodium Excretion ◽  
Renal Excretion ◽  
Urine Flow ◽  
Methyl Derivative ◽  
Dose Dependent

1. p-Guanidino- and p-guanidinomethyl-phenylalanine increase the renal excretion of lysine especially and, to some extent, cystine in the phenylalanine-loaded rat. The methyl derivative is the more effective. 2. The lysinuria is dose-dependent, reversible, pronounced when the intravenous infusion of analogue exceeds 10 μmol min−1 kg−1 and does not appear to be secondary to changes in urine flow or sodium excretion. 3. A mechanism for induced basic aminoaciduria conditions is suggested.

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.

Atrial peptide potentiates renal responses to volume expansion in conscious dogs

1989 ◽  
Vol 256 (1) ◽  
pp. R284-R289
Author(s):  
C. H. Metzler ◽  
D. J. Ramsay
Keyword(s):  
Sodium Excretion ◽  
Urine Volume ◽  
Extracellular Fluid ◽  
Urinary Sodium Excretion ◽  
Urine Flow ◽  
Conscious Dogs ◽  
Physiological Dose ◽  
Peptide Secretion ◽  
Renal Responses ◽  
Dose Dependent

Experiments were performed to compare the renal responses to atrial peptide infusion in conscious dogs with normal and expanded extracellular fluid volumes to test the hypothesis that the renal responses to atrial peptide infusions are dependent on the prevailing fluid and electrolyte status in the animal. Atrial peptide-(99-126) was infused intravenously in doses of either 0, 5, 25, or 100 ng.kg-1.min-1 in conscious dogs prepared with chronic catheters in the femoral artery and vein and the urinary bladder. In dogs with normal extracellular fluid volume, atrial peptide caused small increases in urinary sodium excretion with the high physiological (25 ng.kg-1.min-1) and pharmacological (100 ng.kg-1.min-1) doses. Urine volume and potassium excretion were increased only at the highest pharmacological dose. In contrast, atrial peptide infusion in dogs that were volume expanded by infusion of hypertonic saline showed dramatic, dose-dependent increases in sodium excretion and urine flow with all doses tested. The low, physiological dose of atrial peptide (5 ng.kg-1.min-1) increased sodium excretion and urine flow rate in volume-expanded dogs more than the pharmacological dose in normal dogs (n = 4). These results demonstrate that the renal responses to atrial peptide infusion are potentiated in dogs that are volume expanded and suggest that under conditions where atrial peptide secretion would be enhanced, small changes in plasma atrial peptide concentration can have significant effects on renal function.

Arginine vasopressin potentiates natriuretic effect of atrial peptide

1989 ◽  
Vol 256 (3) ◽  
pp. H925-H927
Author(s):  
L. M. Graczak ◽  
L. K. Nicolodi ◽  
D. A. Hartupee ◽  
E. H. Blaine
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Glomerular Filtration ◽  
Arginine Vasopressin ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Dependent Manner ◽  
Functional Interaction ◽  
Natriuretic Effect ◽  
Dose Dependent

We investigated potentiation of atrial peptide (AP)-induced natriuresis by vasopressin in anesthetized rats. Increasing doses of vasopressin potentiated AP-induced natriuresis in a dose-dependent manner, e.g., sodium excretion during AP administration (290 ng/min) was 0.66 +/- 0.16, 2.02 +/- 0.68, 5.21 +/- 1.38 and 7.08 +/- 1.96 mu eq/min during infusion of 0.00, 0.78, 1.56, and 3.12 ng.kg-1.min-1 of vasopressin, respectively. Vasopressin alone had no effect on sodium excretion. In a second experiment, vasopressin (1.56 ng.kg-1.min-1) potentiated AP (128 ng/min)-induced natriuresis similar to that seen in the first experiment. In this experiment, glomerular filtration rate (GFR) and mean arterial pressure were monitored. Mean arterial pressure was no different between the groups treated with AP plus vasopressin and AP alone. Glomerular filtration was actually reduced in the group treated with vasopressin plus AP, suggesting that neither changes in GFR nor blood pressure were responsible for potentiation of the natriuresis. A third experiment compared the ability of 1-desamino-8-D-arginine vasopressin (dDAVP), a nonpressor analogue of vasopressin, to vasopressin in enhancing AP (145 ng/min)-induced natriuresis. The nonpressor analogue did not potentiate AP-induced natriuresis, whereas vasopressin had the same effect as in the first two experiments. These are the first studies to report a functional interaction between AP and vasopressin. They show that vasopressin potentiates AP-induced natriuresis without altering mean arterial pressure or GFR.

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