Effect of aortic clamping on proximal reabsorption and sodium excretion in the rat

1977 ◽  
Vol 232 (2) ◽  
pp. F92-F96 ◽  
Author(s):  
R. W. Osgood ◽  
N. H. Lameire ◽  
M. I. Sorkin ◽  
J. H. Stein
Keyword(s):  
Sodium Excretion ◽  
Perfusion Pressure ◽  
Left Kidney ◽  
Extracellular Volume ◽  
Extracellular Fluid ◽  
Renal Perfusion ◽  
Ringer Solution ◽  
Aortic Clamping ◽  
Group I ◽  
Before And After

It has been suggested that aortic clamping prior to expansion of the extracellular fluid volume prevents the natriuretic response normally seen in this setting. To further evaluate this finding, two groups of re-collection micropuncture studies were performed before and after 7.5% body wt expansion with Ringer solution. Group I, immediate-clamp studies, n, 11. After control collections, perfusion pressure to the left kidney was decreased to 75 mmHg followed by Ringer loading. Group II, delayed-clamp studies, n, 8. After control collections, Ringer solution was given for 40 min. Then the left renal perfusion pressure was reduced to 75 mmHg and the Ringer infusion was continued at the same rate. In the immediate-clamp group, there was no change in total kidney glomerular filtration rate (GFR) (1.16 vs. 1.11 ml/min), nephron GFR (40 vs. 39 nl/min), tubular fluid-to-plasma inulin ratio (2.40 vs. 2.28), or filtrate delivery out of the proximal tubule (18 vs. 18 ndium excretion were not significantly altered. In the delayed-clamp studies, there was also no change in total or nephron GFR, but the tubular fluid-to-plasma inulin ratio fell from 2.52 to 1.65 (P less than .001) and distal delivery rose 9 nl/min after expansion (P less than .001). Sodium excretion increased 3.83 mueq/min and fractional sodium excretion rose 2.28%, both values being markedly greater than in the immediate-clamp studies (P less than .005 for both). These results demonstrate that immediate clamping obviates the fall in proximal reabsorption and the natriuretic response to Ringer loading and suggests that intrarenal adjustments are a major determinant of the magnitude of the natriuretic response to expansion of the extracellular volume

Effect of Renal Perfusion Pressure on Renal Interstitial Hydrostatic Pressure and Sodium Excretion

Hypertension ◽  
1995 ◽  
Vol 25 (4) ◽  
pp. 866-871 ◽  
Author(s):  
Tetsuya Nakamura ◽  
Tetsuo Sakamaki ◽  
Toshiaki Kurashina ◽  
Kunio Sato ◽  
Zenpei Ono ◽  
...  
Keyword(s):  
Hydrostatic Pressure ◽  
Sodium Excretion ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Renal Perfusion Pressure

Functional adaptation to reduced renal mass in early development

1982 ◽  
Vol 242 (2) ◽  
pp. F190-F196 ◽  
Author(s):  
R. L. Chevalier
Keyword(s):  
Renal Mass ◽  
Left Kidney ◽  
Extracellular Fluid ◽  
Functional Adaptation ◽  
Fluid Loss ◽  
Group Iii ◽  
Arterial Blood ◽  
India Ink ◽  
Group I ◽  
Group Ii

To determine whether reduced renal mass in the newborn results in acceleration of normal renal development, the response to unilateral nephrectomy (N) before 36 h of age was compared with sham-operated (S) guinea pigs during the period of most rapid nephron maturation. Studies were performed at 7-13 days (group I) and 19-25 days (group II). Mean arterial blood pressure (AP), left kidney glomerular filtration rate (LKGFR), and urine sodium excretion (UNaV) were measured. Superficial single nephron GFR (sSNGFR) and proximal fractional water reabsorption (FRH2O) were measured by micropuncture, and the number of glomeruli (NG) was determined by India ink perfusion. In view of the susceptibility of the neonate to extracellular fluid loss, groups I and II were plasma infused to maintain euvolemia and group II was compared with 19- to 25-day-old hydropenic animals (group III). Increase in body weight with age was unaffected by neonatal N. In group IN, the compensatory increase in sSNGFR was greater than SNGFR for deeper nephrons, which normally contribute most to GFR at this age. In group IIN there was an 80% adaptive increase in LKGFR that could not be entirely explained by the rise in SNGFR. Since NG in group IIN was greater than in group IIS and similar to that in adulthood, the enhanced adaptation in LKGFR in group IIN may be due in part to earlier recruitment of a population of underperfused glomeruli. FRH2O did not change significantly with age and did not differ in N and S groups. Animals in group III developed a rise in hematocrit during the experiment, and AP, LKGFR, and UNaV were lower in group IIIN than in group IIN. It is concluded that following N at birth, the sequence of renal functional maturation is accelerated while glomerulotubular balance is preserved. As a result of these adaptative changes, homeostasis is maintained and body growth proceeds without impairment.

scholarly journals Transcriptomic analysis reveals inflammatory and metabolic pathways that are regulated by renal perfusion pressure in the outer medulla of Dahl-S rats

2018 ◽  
Vol 50 (6) ◽  
pp. 440-447 ◽  
Author(s):  
Louise C. Evans ◽  
Alex Dayton ◽  
Chun Yang ◽  
Pengyuan Liu ◽  
Theresa Kurth ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Perfusion Pressure ◽  
Left Kidney ◽  
Respiratory Control ◽  
Renal Perfusion ◽  
Renal Physiology ◽  
Sequencing Analysis ◽  
Functional Changes ◽  
Renal Perfusion Pressure ◽  
Novel Approach

Studies exploring the development of hypertension have traditionally been unable to distinguish which of the observed changes are underlying causes from those that are a consequence of elevated blood pressure. In this study, a custom-designed servo-control system was utilized to precisely control renal perfusion pressure to the left kidney continuously during the development of hypertension in Dahl salt-sensitive rats. In this way, we maintained the left kidney at control blood pressure while the right kidney was exposed to hypertensive pressures. As each kidney was exposed to the same circulating factors, differences between them represent changes induced by pressure alone. RNA sequencing analysis identified 1,613 differently expressed genes affected by renal perfusion pressure. Three pathway analysis methods were applied, one a novel approach incorporating arterial pressure as an input variable allowing a more direct connection between the expression of genes and pressure. The statistical analysis proposed several novel pathways by which pressure affects renal physiology. We confirmed the effects of pressure on p-Jnk regulation, in which the hypertensive medullas show increased p-Jnk/Jnk ratios relative to the left (0.79 ± 0.11 vs. 0.53 ± 0.10, P < 0.01, n = 8). We also confirmed pathway predictions of mitochondrial function, in which the respiratory control ratio of hypertensive vs. control mitochondria are significantly reduced (7.9 ± 1.2 vs. 10.4 ± 1.8, P < 0.01, n = 6) and metabolomic profile, in which 14 metabolites differed significantly between hypertensive and control medullas ( P < 0.05, n = 5). These findings demonstrate that subtle differences in the transcriptome can be used to predict functional changes of the kidney as a consequence of pressure elevation.

Interstitial dynamics in rats with early stage experimental cirrhosis of the liver

1989 ◽  
Vol 256 (3) ◽  
pp. F497-F503
Author(s):  
E. Sanz ◽  
C. Caramelo ◽  
J. M. Lopez-Novoa
Keyword(s):  
Sodium Excretion ◽  
Interstitial Fluid ◽  
Early Stage ◽  
Fluid Pressure ◽  
Extracellular Fluid ◽  
Ringer Solution ◽  
Urine Flow ◽  
Cirrhosis Of The Liver ◽  
Experimental Cirrhosis ◽  
Albumin Infusion

Pathogenesis of edema in cirrhosis of the liver is still incompletely understood. The present study was designed to examine interstitial fluid dynamics in cirrhotic, non-ascitic rats, measuring interstitial fluid pressure by means of a subcutaneous plastic capsule in basal conditions during extracellular fluid volume expansion with Ringer solution and during albumin infusion. Urine flow and sodium excretion and plasma and interstitial fluid volumes were simultaneously measured. Cirrhotic rats exhibited reduced urine flow and sodium excretion, both in basal conditions and in response to expansion maneuvers. Plasma and interstitial fluid volumes were higher in cirrhotic than in control animals. Remarkable alterations were present in capsular pressures in cirrhotic rats. In the control rats, basal capsular pressure values were negative, and they increased after Ringer infusion and markedly decreased with albumin infusion. In contrast, in cirrhotic rats, basal capsular pressures were in the positive range and they remained nearly constant during ringer infusion and albumin administration. These results suggest that in cirrhotic rats there are significant alterations in systemic interstitial dynamics, even before ascites formation. Altered systemic capillary dynamics may therefore be important early changes that precede and thus contribute to the formation of edema in cirrhosis.

Modulation of natriuresis by sympathetic nerves and angiotensin II in conscious dogs

1989 ◽  
Vol 256 (3) ◽  
pp. F485-F489
Author(s):  
P. B. Persson ◽  
H. Ehmke ◽  
U. Kogler ◽  
H. Kirchheim
Keyword(s):  
Angiotensin Ii ◽  
Sodium Excretion ◽  
Perfusion Pressure ◽  
Recovery Period ◽  
Sympathetic Nerves ◽  
Renal Perfusion ◽  
Ang Ii ◽  
Sympathetic Nerve Stimulation ◽  
Converting Enzyme Inhibition ◽  
Pressure Independent

The effects of renal perfusion pressure and reflex sympathetic nerve stimulation on sodium excretion were studied in six conscious foxhounds on a normal sodium diet. This was done before, during common carotid occlusion (CCO), and during a recovery period following CCO. Three protocols were used 1) control (n = 6), 2) converting-enzyme inhibition (CEI, n = 6), and 3) CEI combined with a constant renal artery pressure (RAP, n = 5). In protocol 1, CCO increased RAP markedly (140.5 +/- 5.1 vs. 103.0 +/- 4.4 mmHg; P less than 0.001) along with a considerable natriuresis (128.4 +/- 20.1 vs. 86.3 +/- 15.1 mumol Na+/min; P less than 0.05). In protocol 2, CEI increased control sodium excretion but did not impair the natriuresis by CCO. Maintaining RAP at control levels in protocol 3 lead to an antinatriuresis (53.1 +/- 16.8 vs. 128.3 +/- 32.2 mumol Na+/min; P less than 0.05). Creatinine clearance was unaffected by all procedures. In conclusion, a change in ANG II formation shifts but does not impair the natriuretic response to CCO. A moderate sympathetic activation has a pronounced pressure-independent antinatriuretic effect, which is not mediated by angiotensin II.

scholarly journals Endothelin mediates renal vascular memory of a transient rise in perfusion pressure due to NOS inhibition

1999 ◽  
Vol 276 (4) ◽  
pp. F629-F634 ◽  
Author(s):  
Xin-Zhou Zhang ◽  
Chris Baylis
Keyword(s):  
Perfusion Pressure ◽  
Left Kidney ◽  
Renal Perfusion ◽  
Transient Increase ◽  
Transient Rise ◽  
Group 3 ◽  
Group 2 ◽  
The Right ◽  
Renal Vascular ◽  
Renal Responses

We investigated the renal responses to NO synthase (NOS) inhibition with N-monomethyl-l-arginine (l-NMA; 30 mg/kg) in anesthetized rats in which renal perfusion pressure (RPP) to the left kidney was mechanically adjusted. Acutel-NMA increased blood pressure (BP, ∼20%) and renal vascular resistance (RVR) rose (∼50%) in the right kidneys that were always exposed to high RPP. In group 1, the left kidney was exposed to a transient increase (5 min) in RPP which was then normalized, and the rise in RVR was similar to the right kidney. In group 2 the left kidney was never exposed to high RPP, and the rise in RVR was attenuated relative to the right kidney. In group 3, rats were pretreated with the endothelin (ET) receptor antagonist Bosentan, immediately before exposure of the left kidney to a transient increase in RPP, and the rise in RVR was also attenuated relative to the right kidney. NOS inhibition resulted in a natriuresis and diuresis in the right kidneys, and ∼50% of the natriuresis persisted in the left kidney of group 2, in the absence of any rise in RPP. ET antagonism completely prevented the natriuresis and diuresis in response to acutel-NMA in both left and right kidneys. These data suggest that transient exposure to high RPP by NOS inhibition prevents an appropriate vasodilatory response when RPP is lowered, due to the intrarenal action of ET.

Effect of furosemide on renal handling of glucose in the rat

1977 ◽  
Vol 232 (5) ◽  
pp. F438-F442
Author(s):  
S. Boonjarern ◽  
P. K. Mehta ◽  
M. E. Laski ◽  
W. R. Earnest ◽  
N. A. Kurtzman
Keyword(s):  
Control Period ◽  
Extracellular Volume ◽  
Urinary Flow ◽  
Renal Handling ◽  
Group Iii ◽  
Group I ◽  
Before And After ◽  
Glucose Recovery ◽  
Extracellular Volume Expansion ◽  
Renal Tubular

Clearance and intratubular microinjection studies were performed in rats during extracellular volume expansion before and after furosemide administration to evaluate renal tubular transport of glucose. Three groups of animals were studied: group I, intact rats; group II, acutely thyroparathyroidectomized rats; and group III, thyroparathyroidectomized rats receiving parathyroid extract after a control period. In all groups furosemide caused a significant increase in the urinary flow rate and sodium excretion. There was no significant change in filtered glucose and glucose excretion. After early distal tubular injections of [14C]glucose, recovery was complete both before and after furosemide infusion. Furosemide had no effect on [14C]glucose recovery after the late proximal injection. These results indicate that furosemide has no effect on the renal handling of glucose in normoglycemic rats. There is no evidence for glucose reabsorption in the nephronal segments distal to the early distal tubular segment in this experimental state. Our data suggest, but do not prove, that no glucose is transported by the rat nephron beyond the pars recta during normoglycemia.

Interaction of renal beta 1-adrenoceptors and prostaglandins in reflex renin release

1983 ◽  
Vol 244 (4) ◽  
pp. F418-F424 ◽  
Author(s):  
U. Kopp ◽  
G. F. DiBona
Keyword(s):  
Sodium Excretion ◽  
Perfusion Pressure ◽  
Carotid Sinus ◽  
Urinary Sodium Excretion ◽  
Renal Perfusion ◽  
Prostaglandin Synthesis ◽  
Urinary Sodium ◽  
Secretion Rate ◽  
Renin Secretion ◽  
Renal Perfusion Pressure

Anesthetized dogs with isolated carotid sinus preparation were used to examine the mechanisms involved in the increase in renin secretion rate produced by carotid baroreceptor reflex renal nerve stimulation (RNS) at constant renal perfusion pressure. Lowering carotid sinus pressure by 41 +/- 5 mmHg for 10 min increased mean arterial pressure and heart rate, caused no or minimal renal hemodynamic changes, decreased urinary sodium excretion, and increased renin secretion rate. Metoprolol, a beta 1-adrenoceptor antagonist, given in the renal artery, did not affect the decrease in urinary sodium excretion but attenuated the increase in renin secretion rate, from 1,764 +/- 525 to 412 +/- 126 ng/min (70 +/- 8%). Indomethacin or meclofenamate, prostaglandin synthesis inhibitors, did not affect the decrease in urinary sodium excretion but attenuated the increase in renin secretion rate, from 1,523 +/- 416 to 866 +/- 413 ng/min (51 +/- 18%). Addition of metoprolol to indomethacin-pretreated dogs attenuated the increase in renin secretion rate from 833 +/- 327 to 94 +/- 60 ng/min (86 +/- 10%). These results indicate that reflex RNS at constant renal perfusion pressure results in an increase in renin secretion rate that is largely mediated by renal beta 1-adrenoceptors and is partly dependent on intact renal prostaglandin synthesis. The beta 1-adrenoceptor-mediated increase in renin secretion rate is independent of and not in series with renal prostaglandins.

Role of renal interstitial hydrostatic pressure in the pressure diuresis response

1989 ◽  
Vol 256 (1) ◽  
pp. F63-F70 ◽  
Author(s):  
J. Garcia-Estan ◽  
R. J. Roman
Keyword(s):  
Hydrostatic Pressure ◽  
Sodium Excretion ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Renal Capsule ◽  
Interstitial Pressure ◽  
Renal Perfusion Pressure ◽  
Residual Response

The present study examines the role of renal interstitial hydrostatic pressure (RIHP) in the pressure-diuretic and -natriuretic response. The relationships between RIHP, sodium excretion, and renal perfusion pressure (RPP) were determined in antidiuretic and volume-expanded (VE) rats with an intact or decapsulated kidney. RIHP was measured by use of the implanted capsule technique. RIHP increased significantly from 7.5 +/- 0.8 to 12.0 +/- 1.4 mmHg in VE animals and from 3.3 +/- 0.4 to 5.2 +/- 0.7 mmHg in antidiuretic rats after RPP was varied from 100 to 150 mmHg. The pressure-natriuretic response of the antidiuretic rats was blunted compared with that observed in the VE rats. Decapsulation of the kidney in VE rats lowered RIHP and reduced, but did not eliminate, the pressure-natriuretic response. To determine whether this residual response was related to changes in interstitial pressure in the medulla, cortical (CIHP) and medullary interstitial hydrostatic pressures (MIHP) were simultaneously measured in VE rats with an intact or decapsulated kidney. In control rats CIHP and MIHP were similar at all levels of RPP studied. In rats with the renal capsule removed MIHP was higher than CIHP and rose significantly from 6.7 +/- 0.8 to 9.2 +/- 0.8 mmHg when RPP was varied from 100 to 150 mmHg. These results indicate that pressure diuresis and natriuresis is accompanied by changes in RIHP and the response is modulated by the basal level of RIHP. These findings suggest that changes in MIHP may serve as an intrarenal signal for this response.

Urinary sodium, phosphate, and hydrogen excretion following unilateral kidney clamping

1978 ◽  
Vol 56 (3) ◽  
pp. 428-434 ◽  
Author(s):  
Gérard E. Plante ◽  
Hubert Hermkens
Keyword(s):  
Sodium Phosphate ◽  
Renal Plasma Flow ◽  
Left Kidney ◽  
Critical Role ◽  
Extracellular Volume ◽  
Urinary Sodium ◽  
Ammonium Excretion ◽  
Titratable Acid ◽  
Group I ◽  
Group Ii

The influence of extracellular volume on compensatory adaptation of sodium, phosphate, and hydrogen excretion after unilateral kidney exclusion was examined in the dog. Ammonium chloride was administered to all animals to raise urinary hydrogen excretion. Eleven dogs (group I) were studied under relative hydropenia and 11 (group II) were volume expanded with isotonic NaCl. Six animals (group III) prepared as group II were sham operated.In groups I and II, plasma bicarbonate decreased by 1.1 and 1.2 mM/ℓ after unilateral kidney clamping, while serum phosphate rose from 5.3 to 6.1 and from 3.6 to 3.9 mg%, respectively. The following parameters are those obtained from the left kidney before and after contralateral clamping. Urinary sodium remained unchanged after clamping in group I but rose from 422 to 681 μequiv./min in group II. In contrast, urinary phosphate increased from 83 to 233 and from 94 to 189 μg/min in groups I and II, respectively.Measured titratable acid and urinary ammonium excretion remained unchanged in group I. A small but significant decrement in ammonium was obtained with time in group II. Glomerular filtration and renal plasma flow were not influenced by contralateral clamping, but filtration fraction was lower in group II than in group I. No change occurred in group III.Extracellular volume appears to play a critical role in the physiological expression of contralateral natriuresis after unilateral clamping whereas compensatory phosphaturia is obtained in both hydropenic and volume-expanded animals.

Sign in / Sign up

Export Citation Format

Share Document