Chronic Sodium-Potassium-ATPase Inhibition with Ouabain Impairs Renal Haemodynamics and Pressure Natriuresis in the Rat

1996 ◽  
Vol 91 (4) ◽  
pp. 497-502 ◽  
Author(s):  
Toshiaki Kurashina ◽  
Kent A. Kirchner ◽  
Joey P. Granger ◽  
Ami R. Patel
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Perfusion Pressure ◽  
Urinary Sodium Excretion ◽  
Renal Perfusion ◽  
Control Group ◽  
Renal Perfusion Pressure

1. Chronic Na+,K+-ATPase inhibition with ouabain induces hypertension in the rat. To examine the role of the kidney in this process, the effect of changes in renal perfusion pressure on glomerular filtration rate, renal blood flow and urinary sodium excretion were determined in rats treated intraperitoneally with ouabain (27.8 μg day−1 kg−1 body weight) or vehicle for 6 weeks. 2. After ouabain administration, baseline mean arterial pressure was significantly higher (P < 0.05) in ouabain-treated rats (151 ± 2 mmHg; n = 9) than in control rats (116 ± 4 mmHg; n = 8). 3. At equivalent renal perfusion pressures, glomerular filtration rate was significantly lower (P < 0.05) in ouabain-treated rats compared with control rats. Glomerular filtration rate was 721 ± 73μl/min at 150 mmHg, and fell significantly to 322 ± 64 μl/min at 100 mmHg. In the control group, glomerular filtration rate was well autoregulated. The glomerular filtration rate autoregulatory index was calculated to determine the ability to maintain glomerular filtration rate during changes in renal perfusion pressure (0 reflects perfect autoregulation; >1 reflects the absence of autoregulation). This index was greater in the ouabain group than in the control group (1.54 ± 0.2 compared with 0.29 ± 0.2; P < 0.05). Renal blood flow showed a similar pattern. 4. Absolute urinary sodium excretion rate was less in ouabain-treated rats than in control rats at equivalent renal perfusion pressures. The slope of the relationship between absolute urinary sodium excretion rate and renal perfusion pressure was greater (P < 0.05) in the control group than in the ouabain group (309.1 ± 57.1 compared with 82.1 ± 14.8 μmol min−1 mmHg−1). 5. Thus, chronic inhibition of Na+,K+-ATPase induces less efficient autoregulation of glomerular filtration rate and renal blood flow as well as a rightward shift in the pressure natriuresis relationship, such that a 25–30 mmHg higher renal perfusion pressure is necessary to excrete any given sodium load. These abnormalities may contribute to the development and maintenance of hypertension in this model.

Atrial appendectomy reduces ANF but not sodium excretion in acute vasopressin hypertension

1990 ◽  
Vol 258 (1) ◽  
pp. R77-R81
Author(s):  
R. S. Zimmerman ◽  
R. W. Barbee ◽  
A. Martinez ◽  
A. A. MacPhee ◽  
N. C. Trippodo
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Sprague Dawley ◽  
Renal Perfusion Pressure ◽  
Sprague Dawley Rats ◽  
Circulating Levels

The present study was designed to determine whether atrial appendectomy would decrease the sodium excretion associated with pressor doses of arginine vasopressin (AVP) infusion in rats by decreasing circulating levels of atrial natriuretic factor (ANF). Ten to 21 days after either sham (n = 9) or bilateral atrial appendectomy (n = 13) AVP (19 ng.kg-1.min-1) was infused for 90 min in anesthetized Sprague-Dawley rats. Atrial appendectomy decreased circulating ANF levels from 469 +/- 70 pg/ml in sham-operated animals to 259 +/- 50 pg/ml (P less than 0.05) in atrial-appendectomized animals after 90 min of AVP infusion. Despite a reduction in circulating levels of ANF, sodium excretion, potassium excretion, and urine flow increased and were not affected by bilateral atrial appendectomy. Glomerular filtration rate and mean arterial pressure significantly increased in both groups of rats. The present study supports non-ANF factors such as increases in renal perfusion pressure and/or glomerular filtration rate as potential mechanisms in AVP-induced natriuresis.

Renal autoregulation of blood flow and filtration rate in the rabbit

1979 ◽  
Vol 237 (6) ◽  
pp. F479-F482 ◽  
Author(s):  
C. E. Ott ◽  
R. C. Vari
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Filtration Rate ◽  
Pressure Range ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Rabbit Kidney ◽  
Renal Perfusion Pressure

Electromagnetic flow techniques and inulin clearance were used to determine the autoregulatory capabilities of the rabbit kidney in vivo. Renal blood flow was measured in 13 animals over a renal perfusion pressure range of 40–110 mmHg. Normal renal blood flow averaged 3.2 +/- 0.3 ml.min-1.g kidney-1 and was efficiently autoregulated above a renal artery pressure of 75 mmHg. For every 10 mmHg renal pressure change above 75 mmHg renal blood flow changed only 0.96%. Renal perfusion pressure was reduced from 102 +/- 3 to 74 +/- 2 mmHg in six animals. Over this pressure range glomerular filtration rate was not significantly decreased and averaged 4.2 +/- 0.5 ml/min at high pressure compared to 4.0 +/- 0.5 ml/min at low perfusion pressure. Results show that the rabbit kidney autoregulates renal blood flow and glomerular filtration rate efficiently above 75 mmHg. This range of autoregulation compares well with the autoregulatory range of the dog. The results also show that in the autoregulatory range the rabbit and the rat appear to autoregulate with equal efficiency but that the rabbit kidney begins to autoregulate at a low perfusion pressure than the average of approximately 100 mmHg usually found in the rat.

Autoregulation of renal blood flow and glomerular filtration rate in the pregnant rabbit

1987 ◽  
Vol 252 (1) ◽  
pp. R69-R72 ◽  
Author(s):  
L. L. Woods ◽  
H. L. Mizelle ◽  
J. E. Hall
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Filtration Rate ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Renal Perfusion Pressure ◽  
Pregnant Rabbit ◽  
In Pregnancy

Our purpose was to determine whether renal autoregulatory capability is retained in pregnancy despite the marked renal vasodilation that occurs at this time. Renal blood flow and glomerular filtration rate (GFR) were measured in anesthetized pregnant (22–27 days gestation) and nonpregnant rabbits during step reductions in renal perfusion pressure from control (100 +/- 3 mmHg) to 50 mmHg. Control renal blood flow and GFR were significantly higher in pregnant animals, averaging 65 +/- 5 and 13.1 +/- 1.1 ml/min, respectively, compared with 50 +/- 5 and 9.4 +/- 1.2 ml/min in nonpregnant rabbits. Filtration fraction was also significantly elevated in pregnant animals (0.33 +/- 0.02 vs. 0.27 +/- 0.01 in nonpregnant rabbits). During step reductions in renal perfusion pressure, renal blood flow was well autoregulated down to approximately 70 mmHg in both nonpregnant and pregnant animals, falling by only 9 +/- 4 and 12 +/- 5%, respectively. Likewise, GFR was also well autoregulated, falling by 10 +/- 2 and 8 +/- 3% in nonpregnant and pregnant animals, respectively, when perfusion pressure was reduced from 90 to 70 mmHg. These results suggest that renal autoregulation is preserved in pregnancy despite the fact that the renal circulation is already markedly vasodilated.

Effect of Hypoxia and Hypercapnic Acidosis on Renal Autoregulation in the Dog: Role of Renal Nerves

1983 ◽  
Vol 65 (5) ◽  
pp. 533-538 ◽  
Author(s):  
Robert J. Anderson ◽  
Richard G. Pluss ◽  
William T. Pluss ◽  
Jon Bell ◽  
Gary G. Zerbe
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Filtration Rate ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Renal Nerves ◽  
Hypercapnic Acidosis ◽  
Renal Perfusion Pressure

1. Previous studies suggest that hypoxia and hypercapnic acidosis exert a renal nerve mediated adverse effect on renal haemodynamic function. We therefore examined the effect of hypoxia and hypercapnic acidosis on renal blood flow and glomerular filtration rate responses to lowering renal perfusion pressure from 125 to 75 mmHg in the anaesthetized dog. To study the role of renal nerves in these responses, paired innervated and denervated kidneys were studied in each animal. 2. Hypoxia (Po2 43 ± 3 mmHg) affected neither renal blood flow nor glomerular filtration rate responses to decreasing renal perfusion pressure. 3. Hypercapnic acidosis (Pco2 71 ±2 mmHg; pH 7.03 ± 0.01) significantly decreased both renal blood flow and glomerular filtration rate as renal perfusion pressure was lowered. This effect of hypercapnic acidosis could be abolished by renal denervation. 4. These findings suggest that hypercapnic acidosis results in renal nerve stimulation, which prevents the usual decrease in renal afferent arteriolar tone that occurs in response to lowering of renal perfusion pressure.

Action of Angiotensin I Converting Enzyme Inhibitor on the Control of Renal Function in the Cat

1979 ◽  
Vol 56 (4) ◽  
pp. 365-371 ◽  
Author(s):  
E. J. Johns
Keyword(s):  
Blood Flow ◽  
Enzyme Activity ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Nerve Stimulation ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Perfusion Pressure ◽  
Converting Enzyme ◽  
Sodium Clearance

1. The renal responses to low level renal nerve stimulation and reduction in renal perfusion pressure within the autoregulatory range were measured before and after blockade of converting enzyme activity. Experiments were carried out using the unilaterally nephrectomized cat with the nerves of the remaining kidney acutely sectioned. 2. Renal nerves were stimulated to cause a 14% fall in blood flow for 15 min. Glomerular filtration rate was unchanged but sodium excretion and the ratio of sodium clearance to glomerular filtration rate fell significantly. 3. Renal nerve stimulation after blockade of converting enzyme activity was associated with a significant fall in glomerular filtration rate. The reductions in sodium excretion and in the ratio of sodium clearance to glomerular filtration rate were as large as in the absence of the blocking drug. 4. Reduction in renal perfusion pressure was associated with autoregulation of both renal blood flow and glomerular filtration rate but with large falls in sodium excretion and the ratio of sodium clearance to glomerular filtration rate. 5. After blockade of converting enzyme activity blood flow was still autoregulated in response to similar perfusion pressure reduction and glomerular filtration rate fell significantly. The ratio of sodium clearance to glomerular filtration rate, and sodium excretion, were reduced to the same extent as in the absence of the drug. 6. This information suggests that regulation of glomerular filtration rate associated with nerve stimulation or pressure reduction may be mediated by the intrarenal formation of angiotensin II, possibly acting at the efferent arteriole. They also indicate that angiotensin II is probably not involved in causing the increased sodium reabsorption.

Effect of a kinin antagonist on renal function and haemodynamics during alterations in sodium balance in conscious normotensive rats

1990 ◽  
Vol 78 (2) ◽  
pp. 165-168 ◽  
Author(s):  
Paolo Madeddu ◽  
Nicola Glorioso ◽  
Aldo Soro ◽  
Paolo Manunta ◽  
Chiara Troffa ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Renal Function ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Sodium Intake ◽  
Urinary Sodium Excretion

1. To evaluate whether sodium intake can modulate the action of endogenous kinins on renal function and haemodynamics, a receptor antagonist of bradykinin was infused in conscious normotensive rats maintained on either a normal or a low sodium diet. 2. The antagonist inhibited the hypotensive effect of exogenously administered bradykinin. It did not change the vasodepressor effect of acetylcholine, dopamine or prostaglandin E2. 3. The antagonist did not affect mean blood pressure, glomerular filtration rate, renal blood flow or urinary sodium excretion, in rats on sodium restriction. It did not change mean blood pressure, glomerular filtration rate or urinary sodium excretion, but decreased renal blood flow, in rats on a normal sodium intake. 4. The kallikrein–kinin system has a role in the regulation of renal blood flow in rats on a normal sodium diet.

Glomerular filtration dynamics during renal vasodilation with acetylcholine in the dog

1983 ◽  
Vol 244 (6) ◽  
pp. F606-F611 ◽  
Author(s):  
C. E. Thomas ◽  
C. E. Ott ◽  
P. D. Bell ◽  
F. G. Knox ◽  
L. G. Navar
Keyword(s):  
Glomerular Filtration Rate ◽  
Proximal Tubule ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Renal Perfusion Pressure ◽  
Effective Filtration Pressure ◽  
Single Nephron ◽  
Flow Dependency

The reason for the failure of glomerular filtration rate (GFR) to exhibit plasma flow dependency during pharmacologic vasodilation remains unclear although it has been suggested on the basis of experiments in rats that vasodilators may lead to a reduction in the glomerular filtration coefficient (Kf). To evaluate the applicability of this hypothesis to the dog, the effects of vasodilation with acetylcholine on glomerular dynamics and Kf were evaluated in two groups of dogs. One group (n = 19) was studied at spontaneous arterial pressures to allow maximum vasodilation to occur. In the other group (n = 5), renal arterial pressure was reduced and maintained at approximately 89 mmHg. Glomerular filtration rate and single nephron glomerular filtration rate were not altered significantly during acetylcholine infusion in either of the two groups. Both whole kidney and superficial filtration fractions decreased significantly. At spontaneous arterial pressures, transglomerular hydrostatic pressure was not altered significantly because of equivalent increases in proximal tubule pressure and in glomerular pressure. In the dogs studied at reduced renal perfusion pressure, glomerular capillary pressure did not change, but proximal tubule pressure increased slightly. Average effective filtration pressures and Kf were not significantly altered during the infusion of acetylcholine either at spontaneous or reduced renal perfusion pressures. These observations indicate that Kf in the dog is not significantly decreased by acetylcholine and that GFR is not affected during infusion of this agent because the effective filtration pressure is not significantly altered.

Role of the Renal Nerves in Modulating Renin Release During Pressure Reduction at the Feline Kidney

1985 ◽  
Vol 69 (2) ◽  
pp. 185-195 ◽  
Author(s):  
Edward J. Johns
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Renin Secretion ◽  
Renal Nerves ◽  
Pressure Reduction ◽  
Renal Perfusion Pressure

1. Experiments were undertaken in pentobarbitone-anaesthetized cats to determine how reflex activation of the renal nerves altered the responsiveness of the kidney to release renin during reductions in renal perfusion pressure. Reflex activation of the renal nerves was achieved by reducing carotid sinus perfusion pressure by 30 mmHg, which increased systemic blood pressure. During this period renal perfusion pressure was regulated at control levels and neither renal blood flow nor glomerular filtration rate changed, but there was a significant decrease in sodium excretion and increase in renin secretion. Renal denervation abolished both these latter responses. 2. Renal perfusion pressure reduction, by 25-30 mmHg, had no effect on renal blood flow or glomerular filtration rate but significantly decreased sodium excretion and increased renin secretion. Simultaneous reduction of carotid sinus and renal perfusion pressures had no effect on renal blood flow or glomerular filtration rate, decreased sodium excretion, and the magnitude of the increase in renin secretion was significantly greater than that obtained with reduction in renal perfusion pressure alone. Renal denervation abolished the increase in renin secretion during these manoeuvres. 3. During atenolol administration, renal haemodynamics and sodium excretion responses to renal pressure reduction were similar to those obtained in the absence of the drug. Renin secretion was increased, but significantly less than in the absence of atenolol. Simultaneous carotid sinus and renal pressure reductions during atenolol administration had no effect on renal haemodynamics, reduced sodium excretion and increased renin secretion, the magnitude of which was significantly greater than that recorded with only renal pressure reduction in the presence of atenolol. 4. Direct electrical stimulation of the renal nerves, at frequencies which caused a 5-10% reduction in renal blood flow, did not change glomerular filtration rate, decreased sodium excretion by 30% and increased the rate of renin secretion twofold. In the presence of atenolol, such renal nerve stimulation reduced renal blood flow to the same degree, did not change filtration rate, decreased sodium excretion by 37% but did not change renin secretion. 5. These results show that the magnitude of the release of renin in response to renal pressure reduction is dependent on activity within the renal nerves, being blunted after denervation, and enhanced during reflex activation of the renal nerves.

Pressure-Diuresis-Natriuresis Response in Hyperthyroid and Hypothyroid Rats

1994 ◽  
Vol 87 (3) ◽  
pp. 323-328 ◽  
Author(s):  
Félix Vargas ◽  
Noemí M. Atucha ◽  
J. Mario Sabio ◽  
Tomás Quesada ◽  
Joaquín García-Estañ
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Perfusion Pressure ◽  
Normal Pressure ◽  
Renal Perfusion ◽  
Renal Perfusion Pressure ◽  
Pressure Natriuresis ◽  
Renal Responses ◽  
Water And Sodium Excretion

1. Renal responses to changes in renal perfusion pressure were studied in anaesthetized hyperthyroid (thyroxine, 300 μg day−1 kg−1) and hypothyroid (methimazole, 0.03% via drinking water) rats to determine whether an abnormality in the pressure-diuresis-natriuresis phenomenon is involved in the resetting of kidney function in these disorders. 2. There were no significant differences between control and hypothyroid rats with respect to the relationships between renal perfusion pressure and absolute or fractional water and sodium excretion. However, in hyperthyroid rats the pressure-diuresis-natriuresis mechanism was impaired. 3. Renal blood flow and glomerular filtration rate were well autoregulated and there were no differences between control and hypothyroid rats at every level of renal perfusion pressure. A significantly lower glomerular filtration rate was observed in hyperthyroid rats when data were expressed per gram kidney weight, but glomerular filtration rate was similar to that of control rats when normalized by body weight. 4. The shift in the pressure-diuresis-natriuresis response of hyperthyroid rats is mainly due to an increase in tubular reabsorption. Blunting of the renal pressure-diuresis-natriuresis mechanism in hyperthyroid rats may represent the functional resetting of the kidney necessary for sustained hypertension. However, a normal pressure-natriuresis response was observed in hypothyroid rats, in which blood pressure was markedly reduced.

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