Renal autoregulation and pressure natriuresis during ANF-induced diuresis

1987 ◽  
Vol 253 (3) ◽  
pp. F424-F431 ◽  
Author(s):  
R. V. Paul ◽  
K. A. Kirk ◽  
L. G. Navar
Keyword(s):  
Arterial Pressure ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Sodium Reabsorption ◽  
Similar Response ◽  
Water Excretion ◽  
Renal Perfusion Pressure ◽  
Arterial Blood ◽  
Pressure Natriuresis ◽  
Atrial Natriuretic

We examined the autoregulation of renal blood flow (RBF) and glomerular filtration rate (GFR) in the anesthetized dog during selective renal arterial infusion of two different synthetic atrial natriuretic factor (ANF) analogues. Rat atriopeptin II (5 X 10(-8) M in renal arterial blood) caused increases in sodium and water excretion but left RBF and GFR unchanged. A similar response was seen with rat 8-33 atrial natriuretic peptide (ANP) (10(-9) M), but a twofold higher dose of this peptide produced a transient increase in RBF and a sustained 16% increase in GFR. The normal pattern of RBF autoregulation in response to decreases in renal perfusion pressure was not altered by either peptide. GFR was also efficiently autoregulated during ANF infusion; however, there was a threefold increase in the slope of the relationship between sodium excretion and arterial pressure (pressure natriuresis) during 8-33 ANP infusion (control 1.11 +/- 0.39, 8-33 ANP 4.00 +/- 0.86 mu eq/mmHg, P less than 0.01). We conclude that ANF-induced diuresis can be sustained without detectable changes in either the autoregulation-responsive or autoregulation-independent components of renal vascular resistance. Factors other than GFR, which are highly responsive to renal perfusion pressure, are important in modulating the natriuresis caused by ANF. The augmentation of pressure natriuresis within the GFR autoregulatory range suggests an influence of ANF on the magnitude of arterial pressure-induced changes in tubular sodium reabsorption.

Pressure natriuresis during saline expansion in newborn and adult dogs

1984 ◽  
Vol 246 (6) ◽  
pp. F828-F834 ◽  
Author(s):  
L. I. Kleinman ◽  
R. O. Banks
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Sodium Reabsorption ◽  
Renal Perfusion Pressure ◽  
Arterial Blood ◽  
Bilateral Carotid ◽  
Glomerular Filtrate ◽  
Pressure Natriuresis

Pressure natriuresis was studied in anesthetized saline-expanded adult (n = 10) and neonatal (n = 23) dogs. One group (protocol B) received ethacrynic acid and amiloride to block distal nephron function. Studies in the other group (protocol A) were done without diuretics. Renal arterial blood pressure was raised by bilateral carotid artery occlusion. Renal perfusion pressure was then lowered in steps by partially occluding the aorta proximal to the renal arteries. In protocol B carotid occlusion was associated with an increase in both absolute and fractional sodium excretion by adult and newborn dogs. Moreover, there was significant negative correlation (P less than 0.01) between absolute change in renal arterial pressure and change in tubular reabsorption of sodium per milliliter glomerular filtrate for both age groups. For each mmHg increase in blood pressure there was greater inhibition of sodium reabsorption in the puppy (0.55 mueq/ml glomerular filtrate) than in the adult (0.18 mueq/ml, P less than 0.05). In protocol A puppies, the inhibition of sodium reabsorption due to increases in renal perfusion pressure was less than that occurring in protocol B, indicating that some of the sodium escaping proximal nephron reabsorption was reabsorbed distally. Results of these studies indicate that during saline expansion pressure natriuresis is primarily a proximal tubular event, and the sensitivity of the proximal tubule to changes in renal arterial blood pressure is greater in the newborn than the adult kidney.

Urinary excretion of urodilatin is increased during pressure natriuresis in the isolated perfused rat kidney

1999 ◽  
Vol 277 (3) ◽  
pp. F347-F351
Author(s):  
Matthias Heringlake ◽  
Klaus Wagner ◽  
Jan Schumacher ◽  
Horst Pagel
Keyword(s):  
Perfusion Pressure ◽  
Rat Kidney ◽  
Renal Perfusion ◽  
Direct Relation ◽  
Renal Perfusion Pressure ◽  
Arterial Blood ◽  
Urinary Potassium ◽  
Perfused Rat Kidney ◽  
Pressure Natriuresis ◽  
Serial Measurements

The findings about mechanisms regulating production and excretion of urodilatin [ANP-(95–126)], a member of the atrial natriuretic peptide (ANP) family, are controversial. To elucidate a possible relationship between arterial blood pressure and renal urodilatin excretion, we studied the effects of different perfusion pressures on urine flow (UV), urinary sodium (UNaV), urinary potassium (UKV), and urodilatin excretion (UUROV), and the concentration of urodilatin in the perfusate (PURO) of isolated perfused rat kidneys. Kidneys were perfused for 180 min with constant perfusion pressures (80 and 120 mmHg, respectively; each, n = 4) in a closed circuit system. Samples of urine and perfusate were taken every 30 min. Mean UV, UNaV, UKV, and UUROV values were significantly higher with a perfusion pressure of 120 mmHg than with 80 mmHg, whereas PURO did not change significantly. Serial measurements revealed no direct relation of UUROV with either UNaV or UV. This suggests that renal perfusion pressure is a determinant of UUROV and that urinary and venous effluent concentrations of urodilatin (probably production) are not coupled directly and that UUROV and UNaV may dissociate during acute variations of sodium excretion and UV.

Abnormal renal hemodynamics and pressure-natriuresis relationship in Dahl salt-sensitive rats

1986 ◽  
Vol 251 (1) ◽  
pp. F57-F65 ◽  
Author(s):  
R. J. Roman
Keyword(s):  
Arterial Pressure ◽  
Plasma Levels ◽  
Sodium Excretion ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Urine Flow ◽  
Blood Flows ◽  
Renal Perfusion Pressure ◽  
Pressure Natriuresis ◽  
Renal Responses

The renal responses to changes in renal perfusion pressure (RPP) were compared in Dahl salt-resistant (R) rats and in prehypertensive and hypertensive Dahl salt-sensitive (S) rats to determine whether an abnormality in the pressure diuresis response is involved in the development of this form of hypertension. Possible differences in the neural and endocrine background to the kidney of S and R rats were eliminated by denervating the kidney and by holding plasma levels of vasopressin, aldosterone, corticosterone, and norepinephrine fixed by intravenous infusion. Arterial pressure averaged 124 +/- 1 mmHg in R rats, 133 +/- 1 mmHg in prehypertensive S rats, and 158 +/- 2 mmHg in hypertensive S rats. Control renal blood flows (RBF) and glomerular filtration rates (GFR) were not significantly different in the three groups. RBF was autoregulated over a range of pressures from 80 to 160 mmHg in normotensive S and R rats. GFR was autoregulated at pressures greater than 100 mmHg in R rats and greater than 120 mmHg in prehypertensive S rats. In contrast, RBF was only autoregulated at pressures greater than 110 mmHg in hypertensive Dahl S rats, and GFR was significantly reduced from control when RPP was lowered below 150 mmHg. In R rats, increasing RPP from 100 to 150 mmHg produced a fivefold increase in urine flow and sodium excretion. In prehypertensive or hypertensive Dahl S rats the slopes of the relationships between urine flow, sodium excretion, and RPP were less than half of those seen in R rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Plasma renin activity responses to graded decreases in renal perfusion pressure in fetal and newborn lambs

1992 ◽  
Vol 262 (3) ◽  
pp. R524-R529 ◽  
Author(s):  
N. D. Binder ◽  
D. F. Anderson
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Perfusion Pressure ◽  
Plasma Renin ◽  
Renal Perfusion ◽  
Renin Activity ◽  
Renal Perfusion Pressure ◽  
Arterial Blood ◽  
The Right ◽  
The Relationship

We examined the relationship between acute reductions in renal perfusion pressure, as approximated by femoral arterial blood pressure, and plasma renin activity in the uninephrectomized fetal lamb. Renal perfusion pressure was reduced and maintained at a constant value by controlled partial occlusion of the aorta above the renal artery. After 15 min of reduced blood pressure, blood samples were taken for determination of plasma renin activity. This protocol was performed 22 times in 11 fetal lambs. Additionally, three of the fetuses were delivered by cesarean section and studied as newborns for the first week of life. In the fetus, there was a linear relationship between log plasma renin activity and femoral arterial blood pressure (P less than 0.01). After birth, the relationship still existed, although it was shifted to the right (P less than 0.0001). We conclude that there is a significant relationship between plasma renin activity and renal perfusion pressure in the fetal lamb, and as early as 1 day after birth, this relationship shifts to the right in the newborn lamb.

ACE inhibition prevents Na and water retention and MABP increase during reduction of renal perfusion pressure

1995 ◽  
Vol 269 (3) ◽  
pp. R481-R489 ◽  
Author(s):  
W. Boemke ◽  
E. Seeliger ◽  
L. Rothermund ◽  
M. Corea ◽  
R. Pettker ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Angiotensin Converting Enzyme ◽  
Water Retention ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Plasma Aldosterone ◽  
Angiotensin Converting Enzyme Inhibition ◽  
Converting Enzyme ◽  
Renal Perfusion Pressure ◽  
Arterial Blood

Two groups of six dogs were studied during 4 control days and 4 days of reduced renal perfusion pressure (rRPP) servo controlled at 20% below the individual dog's 24-h mean arterial blood pressure (MABP) during control days, i.e., below the threshold for renin release. On rRPP days, endogenous activation of plasma aldosterone and angiotensin II was inhibited by the angiotensin-converting enzyme inhibitor captopril. The dogs were kept on a high-Na and high-water intake. Unlike studies during rRPP alone, there was no Na and water retention during rRPP+captopril. Glomerular filtration rate dropped by approximately 9%, and MABP remained in the range of control days. Plasma renin activity rose to values 14 times greater than control, whereas plasma aldosterone decreased by approximately 60%. Atrial natriuretic peptide remained in the range of controls. In conclusion, angiotensin-converting enzyme inhibition can prevent the otherwise obligatory Na and water retention and systemic MABP increase during a 20% reduction in renal perfusion pressure. This is achieved most likely via the captopril-induced fall in angiotensin II and plasma aldosterone levels.

Effect of renal perfusion pressure on sodium reabsorption from proximal tubules of superficial and deep nephrons

1986 ◽  
Vol 250 (3) ◽  
pp. F425-F429 ◽  
Author(s):  
J. A. Haas ◽  
J. P. Granger ◽  
F. G. Knox
Keyword(s):  
Proximal Tubule ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Proximal Tubules ◽  
Sodium Reabsorption ◽  
Renal Perfusion Pressure ◽  
Henle's Loop ◽  
Acute Change ◽  
Acute Changes ◽  
Superficial And Deep Nephrons

Previous studies in rats have demonstrated that superficial proximal tubule sodium reabsorption does not change in response to alterations in renal perfusion pressure (RPP). The first objective of the present study was to estimate sodium reabsorption in response to acute changes in RPP utilizing fractional lithium reabsorption (FRLi) as an index of fractional sodium reabsorption (FRNa) by the proximal tubule of the kidney as a whole. FRLi decreased in response to increases in RPP, suggesting that sodium reabsorption by the proximal tubule of some nephron population is decreased. Therefore, the second objective of the present study was to test the hypothesis that superficial and deep proximal tubules respond differently to changes in RPP by comparing proximal tubule sodium reabsorption from both nephron populations. In response to an acute change in RPP from 114 +/- 4 to 138 +/- 5 mmHg, FRNa by the proximal tubule and descending limb of Henle's loop in deep nephrons decreased from 71.3 +/- 2.3 to 55.8 +/- 5.6%, but FRNa by the superficial late proximal tubule was not changed: (44.3 +/- 4.8 to 45.1 +/- 3.9%). The urinary fractional reabsorption of sodium decreased from 96.7 +/- 0.6 to 94.5 +/- 0.5%. In summary, these studies demonstrate that increases in RPP have no effect on sodium reabsorption by the proximal tubule of superficial nephrons. In contrast, sodium delivery to the point of micropuncture in the descending limb of Henle's loop of deep nephrons was increased, suggesting inhibition of sodium reabsorption by proximal tubules of deep nephrons in response to increases in RPP.

Effects of renal perfusion pressure on the natriuresis induced by atrial natriuretic factor

1987 ◽  
Vol 253 (2) ◽  
pp. F234-F238
Author(s):  
A. A. Seymour ◽  
S. G. Smith ◽  
E. K. Mazack
Keyword(s):  
Vascular Resistance ◽  
Atrial Natriuretic Factor ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Renal Vascular Resistance ◽  
Base Line ◽  
Renal Perfusion Pressure ◽  
Natriuretic Factor ◽  
Renal Vascular ◽  
Atrial Natriuretic

Synthetic atrial natriuretic factor (ANF 101-126) was infused at 1, 5, 25, and 125 pmol X kg-1 X min-1 into the renal artery of anesthetized, one-kidney dogs. During administration of 25 and 125 pmol X kg-1 X min-1 of ANF 101-126, fractional sodium excretion (FENa) rose from 1.4 +/- 0.3 to 6.6 +/- 1.1 and 5.6 +/- 1.3% when renal perfusion pressure (RPP) was at its basal level (112 +/- 5 mmHg). When base-line RPP was lowered to 101 +/- 5 mmHg by tightening a suprarenal aortic constriction, the same doses raised FENa to only 5.6 +/- 1.6 and 5.1 +/- 1.6%. A larger reduction of beginning RPP to 82 +/- 4 mmHg suppressed the natriuretic responses to 25 and 125 pmol X kg-1 X min-1 of ANF 101-126 to only 1.4 +/- 0.8 and 0.8 +/- 0.3%, respectively.During the peak natriuretic dose of 25 pmol X kg-1 X min-1, renal vascular resistance (RVR) fell from 0.88 +/- 0.10 to 0.68 +/- 0.07, from 0.78 +/- 0.10 to 0.68 +/- 0.12, and from 0.60 +/- 0.06 to 0.61 +/- 0.06 mmHg X ml-1 X min-1 at RPP = RPP = 112, 101, and 82 mmHg, respectively. ANF 101-126 did not affect glomerular filtration rate (GFR) at any level of RPP tested. In conclusion, the natriuretic responses to ANF 101-126 occurred without changes in GFR and were modulated by the prevailing levels of renal perfusion pressure and renal vascular resistance.

Renal interstitial hydrostatic pressure and PGE2 in pressure natriuresis

1991 ◽  
Vol 260 (5) ◽  
pp. F643-F649 ◽  
Author(s):  
J. M. Gonzalez-Campoy ◽  
C. Long ◽  
D. Roberts ◽  
T. J. Berndt ◽  
J. C. Romero ◽  
...  
Keyword(s):  
Hydrostatic Pressure ◽  
Perfusion Pressure ◽  
Fractional Excretion ◽  
Renal Perfusion ◽  
Blood Flows ◽  
Renal Perfusion Pressure ◽  
Fractional Excretion Of Sodium ◽  
Anesthetized Dogs ◽  
Pressure Natriuresis ◽  
Indomethacin Treatment

The present study tested the hypothesis that the presence of renal prostaglandin E2 (PGE2) is necessary for full natriuretic response to increased renal interstitial hydrostatic pressure (RIHP) during increased renal perfusion pressure (RPP). In control untreated pentobarbital-anesthetized dogs (n = 7), fractional excretion of sodium (FENa) was 1.17 +/- 0.48, 1.07 +/- 0.24, and 2.69 +/- 0.57% at RPP of 90, 122, and 148 mmHg, respectively. These changes in FENa were associated with effective renal blood flows (ERBF) of 1.43 +/- 0.20, 1.49 +/- 0.23, and 1.99 +/- 0.40 ml.min-1.g kidney wt-1, respectively. Similarly, glomerular filtration rate (GFR) was 0.53 +/- 0.10, 0.71 +/- 0.10, and 0.72 +/- 0.14 ml.min-1.g kidney wt-1, respectively. Treatment with indomethacin, a cyclooxygenase inhibitor, significantly lowered FENa to 0.45 +/- 0.13, 0.77 +/- 0.21, and 1.19 +/- 0.59% at RPP of 91, 121, and 146 mmHg, respectively. Additionally, indomethacin treatment lowered ERBF (0.51 +/- 0.15, 0.52 +/- 0.10, and 0.85 +/- 0.21 ml.min-1.g kidney wt-1) and GFR (0.28 +/- 0.09, 0.34 +/- 0.09, and 0.47 +/- 0.09 ml.min-1.g kidney wt-1) at low, middle, and high RPP, respectively. PGE2 replacement (n = 6) into renal artery at 0.01 microgram.min-1.kg body wt-1 returned FENa, ERBF, and GFR to control levels over the same range of RPP, whereas prostacyclin (PGI2) infusion (n = 7) at the same dose did not. RIHP was 4.2 +/- 1.2, 4.2 + 0.5, and 7.5 +/- 1.7 mmHg with increasing RPP in control untreated group and increased to similar levels with indomethacin treatment and during PGE2 or PGI2 replacement.(ABSTRACT TRUNCATED AT 250 WORDS)

Abstract MP02: Acute Increases Of Renal Perfusion Pressure Activate Mechanistic Target Of Rapamycin Complex 1 And Increase Macrophage Infiltration In The Kidney Of Sprague Dawley Rats.

Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Satoshi Shimada ◽  
Chun Yang ◽  
Vikash Kumar ◽  
David L Mattson ◽  
Allen W Cowley
Keyword(s):  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Macrophage Infiltration ◽  
Target Of Rapamycin ◽  
Lipocalin 2 ◽  
Sprague Dawley ◽  
Ultrasonic Probe ◽  
Renal Perfusion Pressure ◽  
Mechanistic Target Of Rapamycin ◽  
Pressure Natriuresis

Studies were carried out to determine whether acute elevation of renal perfusion pressure (RPP) activates the mechanistic target of rapamycin complex 1 (mTORC1) and inflammation-related genes which may trigger a rapid infiltration of immune cells. RPP was elevated by 40 mmHg (HP group) for 30 minutes in male SD rats (n=5, 10-12 weeks of age) while measuring renal blood flow (RBF; Transonic ultrasonic probe) and urine flow rate. Sham rats (Sham group) were studied in the same way, but RPP was not changed. Since initial studies found that the acute increase of RPP resulted in activation of mTORC1 (pS6 S235/6 /S6; P<0.05) but not mTORC2 (pAKT T308 /AKT ), the effects of inhibition of mTORC1 with rapamycin (Rapa) pretreatment (1.5 mg/kg; n=10) were then determined (HP+Rapa group). RBF was well autoregulated in both HP and HP+Rapa treated rats averaging 6.9 ± 0.5 vs 7.0 ± 0.8 ml/min/gkw in HP (p=0.72) and 8.1 ± 0.8 vs 8.4 ± 0.5 in HP+Rapa group (p=0.34) with a 40 mmHg elevation of RPP. Pressure-natriuresis was unexpectedly blunted in HP+Rapa treated rats increasing from 0.40 ± 0.21 to 4.0 ± 1.1 in HP rats compared to 0.21 ± 0.07 to 2.3 ± 0.5 μmol/min/gkw; p<0.05) in the HP+Rapa treated rats. Urine volumes were similarly affected. Elevation of RPP increased the mTORC1 activity (pS6 S235/6 /S6) in renal cortex (2.8 ± 0.4 vs 4.8 ± 0.5 A.U.; p<0.05, n=5) and outer medulla (2.0 ± 0.3 vs 5.0 ± 0.6 A.U.; p<0.05, n=5) of HP rats compared to Sham. Rapa treatment suppressed this activation. rtPCR analysis found increased mRNA expression of lipocalin-2 (Lcn2; involved innate immune responses; p<0.05), heme oxygenase (Hmox1; p<0.05) and cyclooxygenase 2 (Cox2; p=0.08) in HP rats compared to Sham, responses which were generally blunted by Rapa. Importantly, as determined by immunohistochemistry, CD68 positive macrophage staining was significantly increased (p<0.001) with elevation of RPP in HP compared to sham rat kidneys. This was significantly reduced by Rapa treatment (p<0.001). We conclude that the mTORC1 pathway can be activated very quickly following elevations of RPP and appears to be responsible for rapid macrophage infiltration which is prevented by Rapa treatment. So too, inhibition of mTORC1 with Rapa reduced the pressure-diuresis response through yet unknown mechanisms.

Effect of interactions between nitric oxide and angiotensin II on pressure diuresis and natriuresis

1997 ◽  
Vol 273 (5) ◽  
pp. R1676-R1682 ◽  
Author(s):  
María Isabel Madrid ◽  
Miguel García-Salom ◽  
Jerónimo Tornel ◽  
Marc De Gasparo ◽  
Francisco J. Fenoy
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Renal Function ◽  
Angiotensin Ii ◽  
Methyl Ester ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Angiotensin Receptors ◽  
Water Excretion ◽  
Renal Perfusion Pressure

The present study examined the effect of an angiotensin II AT1 or AT2 receptor antagonist on the impairment of the pressure diuresis and natriuresis response produced by nitric oxide (NO) synthesis blockade. N ω-nitro-l-arginine methyl ester (l-NAME, 37 nmol ⋅ kg−1 ⋅ min−1) lowered renal blood flow and reduced the slopes of the pressure diuresis and natriuresis responses by 44 and 40%, respectively. Blockade of AT1 receptors with valsartan increased slightly sodium and water excretion at low renal perfusion pressure (RPP). Blockade of AT2 receptors with PD-123319 had no effect on renal function. The administration of valsartan or PD-123319 to rats given l-NAME had no effect on the renal vasocontriction induced by NO synthesis blockade. In addition, in rats givenl-NAME, valsartan elevated baseline excretory values at all RPP studied, but it had no effect on the sensitivity of the pressure diuresis and natriuresis response. However, the administration of PD-123319 tol-NAME-pretreated rats shifted the slopes of the pressure diuresis and natriuresis responses toward control values, indicating that the impairment produced by NO synthesis blockade on pressure diuresis is dependent on the activation of AT2 angiotensin receptors.

Sign in / Sign up

Export Citation Format

Share Document