Do vasopressin and oxytocin have synergistic renal effects in the conscious rat?

1995 ◽  
Vol 144 (3) ◽  
pp. 441-448 ◽  
Author(s):  
R J Windle ◽  
J M Judah ◽  
M L Forsling
Keyword(s):  
Filtration Rate ◽  
Fractional Excretion ◽  
Potassium Excretion ◽  
Conscious Rat ◽  
Renal Effects ◽  
Fractional Excretion Of Sodium ◽  
Dose Dependent ◽  
Higher Doses ◽  
Sodium And Potassium ◽  
Tubular Component

Abstract The renal effects of arginine vasopressin and oxytocin were studied in the conscious unrestrained rat infused with 0·077 m NaCl. Peptides were infused at rates of 24 and 160 pmol/min (vasopressin) or 30 and 200 pmol/min (oxytocin) either alone or as a combination of the two lower or two higher doses. The rates of infusion were selected to give ratios of oxytocin:vasopressin similar to those seen in the plasma of euhydrated and dehydrated rats. Vasopressin produced dose-dependent antidiuretic and natriuretic responses, the natriuresis commencing after 15–30 min infusion. Oxytocin produced dose-dependent diuretic and natriuretic responses, the natriuresis commencing within the first 15 min of infusion. Combined infusion of vasopressin and oxytocin produced dose-dependent antidiuretic responses which were comparable to those seen with vasopressin alone. The natriuretic response from combined infusion at the higher rate appeared to have the greater magnitude for individual 15-min periods of the vasopressin response combined with the longer duration of the oxytocin response. Although the total natriuretic response was therefore greater, this difference failed to reach significance. Only the higher rates of infusion of vasopressin and oxytocin significantly increased the clearance of sodium, by 53 ± 23 and 62 ± 18% and glomerular filtration rate (GFR) by 23 ± 4 and 23 ± 4% respectively. The clearance of sodium during the combined hormone infusion was significantly greater (109 ± 21%), while the rise in GFR at 23 ± 5% was comparable to that seen when each hormone was given separately. Both fractional excretion of sodium and potassium excretion were also significantly elevated by this combined infusion, suggesting an additional tubular component to the response. Although no synergistic effect of neurohypophysial hormones on the antidiuresis was found in the conscious rat, they may act together to promote sodium excretion Journal of Endocrinology (1995) 144, 441–448

The effect of vasopressin and oxytocin on glomerular filtration rate in the conscious rat: contribution to the natriuretic response

1994 ◽  
Vol 141 (1) ◽  
pp. 59-67 ◽  
Author(s):  
M L Forsling ◽  
J M Judah ◽  
R J Windle
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Plasma Concentrations ◽  
Fractional Excretion ◽  
Conscious Rat ◽  
Arterial Blood ◽  
Fractional Excretion Of Sodium ◽  
Dose Dependent ◽  
Higher Doses

Abstract Urine flow, sodium excretion, mean arterial blood pressure and glomerular filtration rate (GFR) were detennined in the conscious unrestrained rat infused with hypotonic saline. The effects of vasopressin infused at 24 and 160 pmol/min and oxytocin infused at 30 and 200 pmol/min were determined. The lower doses of each hormone gave plasma concentrations within the physiological range whereas the higher doses produced plasma concentrations equivalent to those seen following dehydration. Vasopressin produced dose-dependent antidiuretic and natriuretic responses. Hormone infused at both rates increased the clearance of sodium, but only the higher dose caused a significant increase in GFR. Fractional excretion of sodium was significantly elevated by both doses. Oxytocin produced dose-dependent diuretic and natriuretic responses. Again both rates of infusion increased the clearance of sodium, but only the higher dose caused a significant increase in GFR. The lower dose caused a significant increase in the fractional excretion of sodium. It appears, therefore, that increases in GFR may have a role in the natriuretic response to both hormones. However, this response can also be seen when GFR remains unchanged. This fact, together with the observed increases in the fractional excretion of sodium, indicates that these hormones have additional tubular actions. Journal of Endocrinology (1994) 141, 59–67

Three peptides from the ANF prohormone NH(2)-terminus are natriuretic and/or kaliuretic

1990 ◽  
Vol 258 (5) ◽  
pp. F1401-F1408 ◽  
Author(s):  
D. R. Martin ◽  
J. B. Pevahouse ◽  
D. J. Trigg ◽  
D. L. Vesely ◽  
J. E. Buerkert
Keyword(s):  
Atrial Natriuretic Factor ◽  
Wistar Rats ◽  
Urine Volume ◽  
Fractional Excretion ◽  
Potassium Excretion ◽  
Terminal Portion ◽  
Urine Sodium ◽  
Fractional Excretion Of Sodium ◽  
Urinary Potassium ◽  
Sodium And Potassium

The present investigation was designed to determine whether peptides derived from the NH(2)-terminal portion of the 126-amino acid prohormone (pro) of atrial natriuretic factor (ANF) have natriuretic and diuretic properties similar to ANF. Three peptides consisting of amino acids 1-30 [(proANF-(1-30)], 31-67 [proANF-(31-67)], and 79-98 (proANF-(79-98)] of the ANF prohormone were tested and compared with the COOH-terminus peptide (ANF) with respect to their ability to increase urine volume, urine sodium and potassium excretion, and glomerular filtration rate (GFR) in anesthetized Munich-Wistar rats. Each of these peptides except proANF-(79-98) caused a significant diuresis (P less than 0.05) when infused at their respective 100 ng.kg body wt-1.min-1 concentrations for 120 min. ProANFs-(1-30), (31-67), (79-98), and (99-126) (ANF) increased sodium excretion by 231, 973, 167, and 1,405%, respectively. The fractional excretion of sodium compared with control was significant at P less than 0.05, P less than 0.01, and P less than 0.05 for proANFs (1-30), (31-67), and (99-126), respectively. ProANF-(79-98) did not significantly increase the fractional excretion of sodium, but it was the only peptide from the NH(2)-terminus of the prohormone that significantly increased the fractional excretion of potassium's ProANF-(31-67) did not increase urinary potassium excretion. ProANF-(1-30), (79-98), and ANF significantly (P less than 0.05) increased urinary potassium excretion. None of these peptides significantly enhanced GFR. In conclusion, three peptides from the NH(2)-terminus of the ANF prohormone as well as ANF (the COOH-terminus) have either natriuretic, kaliuretic, and/or diuretic properties, but the respective ability of each of these peptides to produce these effects varies considerably.

Hemodynamic mechanisms in CNS-induced natriuresis in the conscious rat

1983 ◽  
Vol 244 (4) ◽  
pp. F376-F382 ◽  
Author(s):  
S. L. Bealer
Keyword(s):  
Blood Pressure ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Urine Volume ◽  
Sodium Concentration ◽  
Potassium Excretion ◽  
Conscious Rat ◽  
Electrolytic Lesions ◽  
Sodium And Potassium

These experiments were designed to determine 1) the effects of increased CSF sodium concentration on renal hemodynamics in the conscious rat, and 2) the role of the periventricular tissue surrounding the anteroventral third ventricle (AV3V) in the natriuretic and hemodynamic responses during this treatment. After electrolytic lesions of AV3V periventricular tissue or control surgery, blood pressure, glomerular filtration rate, effective renal blood flow, urine volume, and sodium and potassium excretion were measured before and during intraventricular (IVT) infusion of either isotonic or hypertonic saline solutions in conscious hydrated rats. Blood pressure, glomerular filtration rate, and sodium and potassium excretion increased during IVT infusion of concentrated sodium solutions in control rats but not in animals with lesions in the AV3V region. These data support the hypothesis that the natriuretic response to increased CSF sodium concentration in the rat is due to a pressor response and/or increased glomerular filtration rate and demonstrate that ablation of AV3V periventricular tissue blunts the natriuretic response, possibly through diminished central pressor mechanisms and/or decreased central control of glomerular filtration rate.

Renal and pressor action of angiotensin in the normal dog

1965 ◽  
Vol 208 (6) ◽  
pp. 1093-1099 ◽  
Author(s):  
John K. Healy ◽  
Carlos Barcena ◽  
J. M. Brian O'Connell ◽  
George E. Schreiner
Keyword(s):  
Filtration Rate ◽  
Pressor Response ◽  
Urine Flow ◽  
Sodium Reabsorption ◽  
Potassium Excretion ◽  
Control Blood Pressure ◽  
Electrolyte Excretion ◽  
Initial Depression ◽  
High Doses ◽  
Higher Doses

The renal and pressor actions of angiotensin in relation to dose were studied in unanesthetized dogs. Low doses caused depression of urine flow, electrolyte excretion, glomerular filtration rate (GFR), and Cpah. With higher doses, the initial depression of urine flow, GFR, and Cpah was greater, but subsequently these functions rose toward control values. In fact, diuresis occurred, accompanied by natriuresis, chloruresis, and kaliuresis. The natriuresis occurred at a time when GFR was significantly depressed. In longer experiments at high doses it was found that the natriuresis declined after 50 min despite continued angiotensin infusion; however, potassium excretion gradually increased throughout. These results help clarify the confusing literature regarding the effects of angiotensin on renal function in dogs and also support the hypothesis that angiotensin can block tubular sodium reabsorption. The pressor response was found to be proportional to the logarithm of the dose of angiotensin. It was also inversely related to the control blood pressure of the dog.

Low concentrations of ANP cause pressure-dependent natriuresis in the isolated kidney

1988 ◽  
Vol 255 (3) ◽  
pp. F391-F396 ◽  
Author(s):  
J. D. Firth ◽  
A. E. Raine ◽  
J. G. Ledingham
Keyword(s):  
Filtration Rate ◽  
Perfusion Pressure ◽  
Rat Kidney ◽  
Fractional Excretion ◽  
Renal Perfusion ◽  
Isolated Kidney ◽  
Renal Perfusion Pressure ◽  
Low Concentrations ◽  
Fractional Excretion Of Sodium ◽  
Perfused Rat Kidney

The effect of alteration in renal perfusion pressure on the response of the isolated perfused rat kidney to concentrations of alpha-human atrial natriuretic peptide (ANP) within the pathophysiological range has been examined. At a perfusion pressure of 90 mmHg ANP concentrations of 50, 200, and 1,000 pmol/l were without effect on any parameter tested. At a perfusion pressure of 130 mmHg 50 pmol/l ANP produced an increase of 3.13 +/- 0.68 mumol/min in sodium excretion (UNa V), compared with a fall of 0.33 +/- 1.04 mumol/min in controls (P less than 0.02); fractional excretion of sodium (FENa) rose by 1.45 +/- 0.36% vs. -0.12 +/- 0.47% (P less than 0.05); glomerular filtration rate (GFR) was unchanged. At 200 and 1,000 pmol/l larger changes in UNa V and FENa were seen; only at 1,000 pmol/l was a significant effect on GFR observed. In contrast, frusemide (furosemide) at concentrations of 10 and 100 mumol/l was natriuretic at both 90 and 130 mmHg, with lesser absolute but greater proportional changes being seen at the lower pressure. It was concluded 1) the response of the isolated kidney to ANP is critically dependent on perfusion pressure, 2) at elevated levels of perfusion pressure the isolated kidney can respond to levels of ANP within the upper physiological and pathophysiological range.

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.

Role of prostaglandins in the renal response to calcium infusion

1990 ◽  
Vol 258 (4) ◽  
pp. F1096-F1099
Author(s):  
V. Lahera ◽  
M. J. Fiksen-Olsen ◽  
J. C. Romero
Keyword(s):  
Filtration Rate ◽  
Bolus Injection ◽  
Excretion Rate ◽  
Fractional Excretion ◽  
Concurrent Administration ◽  
Excretory Function ◽  
Fractional Excretion Of Sodium ◽  
Calcium Infusion ◽  
Renal Excretory Function

The effects of intrarenal infusions of calcium gluconate (10 and 100 micrograms Ca.kg-1.min-1) on renal hemodynamics and on renal excretory function were studied in anesthetized mongrel dogs. In one group, the two doses of calcium were infused for 30 min each (1 ml/min). In a second group, the same doses were administered 30 min after the start of an infusion of prostaglandin (PG) inhibitors (intrarenal indomethacin, 10 micrograms.kg-1.min-1, or intravenous bolus injection of meclofenamate, 5 mg/kg). No change with physiological significance was observed during the infusion of 10 micrograms Ca.kg-1.min-1. However, the infusion of 100 micrograms Ca.kg-1.min-1 induced increases (P less than 0.05) in glomerular filtration rate (50%), sodium excretion rate (180%), and fractional excretion of sodium (160%), with respect to control precalcium values. All these changes were prevented by the concurrent administration of PG synthesis inhibitors. Urinary PGE2 and 6-keto-PGF1 alpha increased 220 and 85%, respectively, during the infusion of 100 micrograms Ca.kg-1.min-1, but both decreased (P less than 0.05) below basal levels during the concurrent administration of PG synthesis inhibitors. The infusion of 100 micrograms Ca.kg-1.min-1 decreased (P less than 0.05) renal blood flow by 16% during the administration of PG synthesis inhibitors. These results suggest that PGs are mediating the increase in hemodynamic and excretory factors induced by the intrarenal infusion of 100 micrograms Ca.kg-1.min-1.

Unimpaired excretion of an acute salt load in conscious hypoproteinaemic dogs

1988 ◽  
Vol 75 (3) ◽  
pp. 271-276 ◽  
Author(s):  
J. A. Joles ◽  
H. A. Koomans ◽  
P. Boer ◽  
E. J. Dorhout Mees
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Plasma Protein ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Isotonic Saline ◽  
Fractional Excretion ◽  
Sodium Reabsorption ◽  
Filtration Fraction ◽  
Fractional Excretion Of Sodium

1. The role of hypoproteinaemia in the sodium retention seen in conditions such as the nephrotic syndrome is incompletely known. 2. To define the influence of severe hypoproteinaemia on kidney function, we studied the effect of an intravenous infusion of an isotonic saline load (133 mmol of sodium), as 1 litre of Ringer lactate solution, on sodium excretion and renal haemodynamics in conscious dogs before and after reduction of plasma protein from 68 ± 3 to 36 ±2 g/l by repeated plasmapheresis and a low protein diet. 3. During hypoproteinaemia, 2 days after a period of plasmapheresis, glomerular filtration rate and effective renal plasma flow were lower than in the control study. After the sodium load, both rose to values nearly identical with the pre-infusion levels found in normoproteinaemia, the filtration fraction remaining unchanged. This contrasted with the rise in filtration fraction after expansion in normoproteinaemia, where filtration fraction increased from 32 to 39% due to a rise in glomerular filtration rate. 4. After expansion, natriuresis rose to similar levels in normoproteinaemia (0.18 ±0.06 mmol/min) and hypoproteinaemia (0.20 ± 0.06 mmol/min), and increments in fractional excretion of sodium, potassium and chloride were also similar. However, baseline excretion was higher in the hypoproteinaemic dogs due to their overhydrated condition in this period immediately after plasmapheresis. 5. The fractional excretion of lithium, an alleged marker of proximal tubular sodium reabsorption, rose to comparable levels. 6. Hence, both the increase in filtration and decrease in reabsorption of sodium after an isotonic saline load are not affected by severe reduction in plasma protein concentration. Apparently, the pathways to augment natriuresis after acute expansion function normally in hypoproteinaemia.

Effect of inhibition of MAO and COMT on intrarenal dopamine and serotonin and on renal function

2001 ◽  
Vol 280 (1) ◽  
pp. R248-R254 ◽  
Author(s):  
Yongqing Wang ◽  
Theresa J. Berndt ◽  
Jennifer M. Gross ◽  
Michael A. Peterson ◽  
Mathew J. So ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Glomerular Filtration Rate ◽  
Monoamine Oxidase ◽  
Filtration Rate ◽  
Interstitial Fluid ◽  
Fractional Excretion ◽  
Urine Flow ◽  
Arterial Blood ◽  
Fractional Excretion Of Sodium

The purpose of the present investigation was to study the effects of inhibition of monoamine oxidase (MAO) and/or catechol- O-methyltransferase (COMT), enzymes involved in the degradation of dopamine (DA) and serotonin (5-HT), on intrarenal DA and 5-HT, as reflected in the renal interstitial fluid (RIF) microdialysate and urine, and on renal function. Inhibition of MAO selectively increased RIF 5-HT from 3.16 ± 0.38 to 8.03 ± 1.83 pg/min ( n = 7, P < 0.05), concomitant with decreases in mean arterial blood pressure and glomerular filtration rate (2.09 ± 0.18 to 1.57 ± 0.22 ml/min, n = 7, P < 0.05). Inhibition of COMT significantly increased RIF DA (3.47 ± 0.70 to 8.68 ± 1.96 pg/min, n = 9, P < 0.05), urinary DA (2.00 ± 0.16 to 2.76 ± 0.26 ng/min, n = 9, P < 0.05), and absolute excretion of sodium (6.42 ± 2.00 to 9.82 ± 1.62 μmol/min, n = 10, P < 0.05). Combined inhibition of MAO and COMT significantly increased RIF DA, urinary DA, and urinary 5-HT, which was accompanied with increases in urine flow rate, and absolute (3.03 ± 0.59 to 8.40 ± 1.61 μmol/min, n = 9, P < 0.01) and fractional excretion of sodium. We conclude that inhibition of MAO selectively increases RIF 5-HT. COMT appears to be more important than MAO in the metabolism of intrarenal DA. Physiological increases in intrarenal DA/5-HT induced by inhibition of their degrading enzymes are accompanied with significant alterations of renal function.

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