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.

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.

Role of connexin40 in the autoregulatory response of the afferent arteriole

2012 ◽  
Vol 303 (6) ◽  
pp. F855-F863 ◽  
Author(s):  
Charlotte Mehlin Sorensen ◽  
Isaiah Giese ◽  
Thomas Hartig Braunstein ◽  
Jens Christian Brasen ◽  
Max Salomonsson ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Significant Role ◽  
Knockout Mice ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Tubuloglomerular Feedback ◽  
Wild Type ◽  
Renal Perfusion Pressure ◽  
Acute Changes ◽  
Arteriolar Diameter

Connexins in renal arterioles affect autoregulation of arteriolar tonus and renal blood flow and are believed to be involved in the transmission of the tubuloglomerular feedback (TGF) response across the cells of the juxtaglomerular apparatus. Connexin40 (Cx40) also plays a significant role in the regulation of renin secretion. We investigated the effect of deleting the Cx40 gene on autoregulation of afferent arteriolar diameter in response to acute changes in renal perfusion pressure. The experiments were performed using the isolated blood perfused juxtamedullary nephron preparation in kidneys obtained from wild-type or Cx40 knockout mice. Renal perfusion pressure was increased in steps from 75 to 155 mmHg, and the response in afferent arteriolar diameter was measured. Hereafter, a papillectomy was performed to inhibit TGF, and the pressure steps were repeated. Conduction of intercellular Ca2+changes in response to local electrical stimulation was examined in isolated interlobular arteries and afferent arterioles from wild-type or Cx40 knockout mice. Cx40 knockout mice had an impaired autoregulatory response to acute changes in renal perfusion pressure compared with wild-type mice. Inhibition of TGF by papillectomy significantly reduced autoregulation of afferent arteriolar diameter in wild-type mice. In Cx40 knockout mice, papillectomy did not affect the autoregulatory response, indicating that these mice have no functional TGF. Also, Cx40 knockout mice showed no conduction of intercellular Ca2+changes in response to local electrical stimulation of interlobular arteries, whereas the Ca2+response to norepinephrine was unaffected. These results suggest that Cx40 plays a significant role in the renal autoregulatory response of preglomerular resistance vessels.

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.

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.

Renal Vascular Resistance and Aortic Pressure as Determinants of Sodium Reabsorption

1973 ◽  
Vol 51 (9) ◽  
pp. 654-664 ◽  
Author(s):  
S. M. Zweig ◽  
T. M. Daugharty ◽  
L. E. Earley
Keyword(s):  
Vascular Resistance ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Aortic Pressure ◽  
Renal Vascular Resistance ◽  
Sodium Reabsorption ◽  
Renal Perfusion Pressure ◽  
Bilateral Carotid ◽  
Infusion Of Norepinephrine ◽  
Renal Vascular

During induced renal vasodilatation, angiotensin and norepinephrine result in an increased excretion of sodium (UNaV), which has been attributed to transmission of elevated aortic pressure (PA) to peritubular capillaries and not to direct effects of the drugs on sodium reabsorption. The importance of PA, intrarenal hemodynamics, and other possible effects of angiotensin and norepinephrine was examined in anesthetized dogs in which one kidney was vasodilated by denervation or acetylcholine, and the opposite kidney served as control. During elevation of aortic pressure, following bilateral carotid occlusion and vagotomy (B.C.O. and V), infusion of angiotensin and norepinephrine, increased UNaV occurred on only the vasodilated side. Changes in UNaV on both sides are related inversely to renal vascular resistance (R.V.R.) before elevation PA, but not to changes in R.V.R., glomerular filtration rate (G.F.R.), or filtration fraction following elevation of PA. When renal perfusion pressure was controlled during aortic constriction, persistent increases in UNaV and urine flow rate were abolished during infusion of norepinephrine and after B.C.O. and V, and markedly reduced during infusion of angiotensin. These effects could not be attributed to changes in intrarenal hemodynamics. Thus increased sodium and water excretion following infusion of norepinephrine and angiotensin, and B.C.O. and V, can be largely attributed to an interplay of increased renal perfusion pressure and reduced preset renal vascular resistance.

Effect of intrarenal volume expansion on proximal sodium reabsorption

1988 ◽  
Vol 255 (6) ◽  
pp. F1178-F1182 ◽  
Author(s):  
J. A. Haas ◽  
J. P. Granger ◽  
F. G. Knox
Keyword(s):  
Hydrostatic Pressure ◽  
Proximal Tubule ◽  
Volume Expansion ◽  
Rat Kidney ◽  
Extracellular Volume ◽  
Proximal Tubules ◽  
Sodium Reabsorption ◽  
Polyethylene Matrix ◽  
Interstitial Volume ◽  
Superficial And Deep Nephrons

The objective of the present study was to examine the effect of direct expansion of the renal interstitial volume on sodium reabsorption by proximal tubules of superficial and deep nephrons in the absence of systemic extracellular volume expansion. Renal interstitial volume expansion was achieved by injection of 50 microliter of 2.5% albumin in 0.9% saline into the renal interstitium via a polyethylene matrix that was chronically implanted in the interstitium of the rat kidney. Renal interstitial volume expansion increased renal interstitial hydrostatic pressure from 3.8 +/- 0.5 to 6.8 +/- 1.1 mmHg, P less than 0.05 (n = 5 rats). Fractional reabsorption of sodium by the superficial late proximal tubule decreased from 45.7 +/- 5.6 to 34.2 +/- 5.4%, P less than 0.05, and by the proximal tubule and descending limb of Henle's loop of deep nephrons it decreased from 73.9 +/- 2.9 to 57.2 +/- 6.3%, P less than 0.05 (n = 8 rats). Thus expansion of the renal interstitial volume increased renal interstitial hydrostatic pressure and decreased sodium reabsorption by the proximal tubules of superficial and deep nephrons.

L-arginine improves transmission of perfusion pressure to the renal interstitium in Dahl salt-sensitive rats

1994 ◽  
Vol 266 (6) ◽  
pp. R1730-R1735 ◽  
Author(s):  
A. R. Patel ◽  
J. P. Granger ◽  
K. A. Kirchner
Keyword(s):  
Hydrostatic Pressure ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Renal Capsule ◽  
Renal Perfusion Pressure ◽  
Renal Interstitium ◽  
Pressure Natriuresis ◽  
Acute Changes ◽  
The Relationship

L-Arginine normalizes pressure natriuresis in Dahl salt-sensitive (DS) rats. To determine the role of renal interstitial hydrostatic pressure (RIHP) in this phenomenon, we measured RIHP determined by servo-null during acute changes in renal perfusion pressure in anesthetized DS rats receiving L-arginine (300 mg.kg-1.day-1 ip) or vehicle for 3 wk. Dahl salt-resistant (DR) rats were controls. As observed previously, the slope of the pressure-natriuresis relationship was greater (P < 0.05) in L-arginine-treated DS rats than vehicle DS rats and not different from DR rats. The slope of the relationship between renal perfusion pressure and RIHP was greater (P < 0.05) in DR rats than vehicle DS rats. In L-arginine-treated DS rats the slope of this relationship was greater (P < 0.05) than that in vehicle DS rats and not different from DR rats. Removal of the renal capsule blunted the pressure-natriuresis relationship in L-arginine-treated DS rats but had no effect in vehicle DS rats. Thus L-arginine improves transmission of perfusion pressure into the renal interstitium in DS rats and may contribute to the improved pressure-natriuresis response.

Blood flow-dependent changes in renal interstitial guanosine 3′,5′-cyclic monophosphate in rabbits

2002 ◽  
Vol 282 (2) ◽  
pp. F238-F244 ◽  
Author(s):  
Akira Nishiyama ◽  
Shoji Kimura ◽  
Toshiki Fukui ◽  
Matlubur Rahman ◽  
Hirohito Yoneyama ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Perfusion Pressure ◽  
Ambient Pressure ◽  
Renal Perfusion ◽  
Cyclic Monophosphate ◽  
Renal Perfusion Pressure ◽  
Highly Correlated ◽  
Acute Changes ◽  
Oxide Synthase

We examined responses of renal interstitial guanosine 3′,5′-cyclic monophosphate (cGMP) to changes in renal perfusion pressure (RPP) within and below the range of renal blood flow (RBF) autoregulation. A microdialysis method was used to monitor renal cortical and medullary interstitial cGMP levels in anesthetized rabbits. RPP was reduced in two steps: from ambient pressure (89 ± 3 mmHg) to 70 ± 2 mmHg ( step 1) and then to 48 ± 3 mmHg ( step 2). RBF was maintained in step 1 but was significantly decreased in step 2 from 2.94 ± 0.23 to 1.47 ± 0.08 ml · min−1 · g−1. Basal interstitial concentrations of cGMP were significantly lower in the cortex than in the medulla (12.1 ± 1.4 and 19.9 ± 0.4 nmol/l, respectively). Cortical and medullary cGMP did not change in step 1 but were significantly decreased in step 2, with significantly less reduction in cGMP concentrations in the medulla than in the cortex (−25 ± 3 and −44 ± 3%, respectively). Over this pressure range, changes in cortical and medullary cGMP were highly correlated with changes in RBF ( r= 0.94, P < 0.005 for cortex; r = 0.82, P < 0.01 for medulla). Renal interstitial nitrate/nitrite was not changed in step 1 but was significantly decreased in step 2 (−38 ± 2% in cortex and −20 ± 2% in medulla). Nitric oxide synthase inhibition with N G-nitro-l-arginine methyl ester (l-NAME, 30 mg/kg bolus, 50 mg · kg−1 · h−1 iv infusion) significantly decreased RBF (by −46 ± 4%) and interstitial concentrations of cGMP (−27 ± 4% in cortex and −22 ± 4% in medulla, respectively). During l-NAME treatment, renal interstitial concentrations of cGMP in the cortex and medulla were similarly not altered in step 1. However, l-NAME significantly attenuated cGMP responses to a reduction in RPP in step 2. These results indicate that acute changes in RBF result in alterations in nitric oxide-dependent renal interstitial cGMP levels, with differential effects in the medulla compared with the cortex.

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