Bicarbonate reabsorption in the papillary collecting duct of rats

1981 ◽  
Vol 389 (3) ◽  
pp. 271-275 ◽  
Author(s):  
K. J. Ullrich ◽  
F. Papavassiliou
1983 ◽  
Vol 245 (5) ◽  
pp. F535-F544
Author(s):  
T. D. DuBose

DuBose, Thomas D., Jr. Application of the disequilibrium pH method to investigate the mechanism of urinary acidification. Am. J. Physiol. 245 (Renal Fluid Electrolyte Physiol. 14): F535-F544, 1983.--The cellular mechanism of renal bicarbonate reabsorption has been debated for four decades. Recent technological advances have allowed distinction between primary bicarbonate reabsorption and a proton secretory mechanism. The disequilibrium pH method has been applied widely for this purpose and has supported the latter hypothesis uniformly. The demonstration of elevated values for PCO2 in tubular and vascular structures of the renal cortex has not altered this view. Indeed, by employing a newly developed method for measurement of equilibrium pH in vivo that permits contact with the environment within the tubule lumen to continue, we demonstrated an acid disequilibrium pH in the proximal tubule after carbonic anhydrase inhibition equal to -0.68 pH units. A spontaneous disequilibrium pH was not present in the distal tubule during control conditions or during metabolic alkalosis but was demonstrated during combined respiratory acidosis-metabolic alkalosis. This finding agrees qualitatively with observed rates of bicarbonate reabsorption in the perfused distal tubule in vivo. With use of similar techniques, an acid disequilibrium pH in conjunction with elevated values for PCO2 was observed in the papillary collecting duct. Thus, proton secretion appears to be the predominant mechanism of bicarbonate reabsorption in superficial nephrons and explains, as well, the means by which the urine-to-blood PCO2 gradient in alkaline urine is established.


1993 ◽  
Vol 264 (2) ◽  
pp. F267-F273
Author(s):  
H. Saxenhofer ◽  
W. R. Fitzgibbon ◽  
R. V. Paul

Urodilatin (URO) [ANP-(95-126)] is an analogue of atrial natriuretic peptide (alpha-ANP) [ANP-(99-126)] that was first isolated from human urine. In rat mesangial cells, URO competed with high affinity for non-guanylate cyclase-coupled ANPR-C receptors [concentration at which 50% labeled ligand is displaced (IC50) approximately 70 pM], but with lesser affinity to the guanylate cyclase-linked ANPR-A receptors (IC50 approximately 800 pM). alpha-ANP bound to both receptors with similar affinity [dissociation constant (Kd) approximately 150 pM]. In papillary collecting duct homogenates, which possess only ANPR-A receptors, the apparent Kd value averaged 229 pM for alpha-ANP and 2.7 nM for URO. Intravenous URO was at least as potent and effective as alpha-ANP in inducing diuresis and natriuresis in anesthetized rats, but URO was approximately 10-fold less potent in stimulating guanosine 3',5'-cyclic monophosphate generation in mesangial and inner medullary collecting duct cells. We conclude that URO has a lesser affinity than alpha-ANP for guanylate cyclase-coupled ANP receptors in the kidney and that the relative natriuretic potency of URO in vivo cannot be directly attributed to its binding characteristics with ANPR-A receptors.


1988 ◽  
Vol 254 (4) ◽  
pp. F477-F483 ◽  
Author(s):  
A. van de Stolpe ◽  
R. L. Jamison

Micropuncture collections were obtained from the terminal collecting duct (CD) at base and tip of the renal papilla of the rat. Group 1 was studied before and during infusion with atrial natriuretic peptide (ANP), group 2 was administered the vehicle only, and group 3 received acetazolamide to increase sodium delivery to the base to a similar extent as after ANP. ANP caused a decrease in blood pressure, a slight increase in GFR, natriuresis, and diuresis. Sodium delivery to the collecting duct at the base of the papilla increased. Between base and tip, sodium reabsorption was inhibited. Tubule fluid sodium concentration (TFNa) was increased at the base and remained high at the tip; in contrast TFNa fell between base and tip in control and acetazolamide groups. After acetazolamide, sodium reabsorption in the terminal CD was not inhibited. These results demonstrate that in vivo ANP 1) increases the delivery of sodium to the terminal CD and 2) inhibits sodium reabsorption in the terminal CD. The findings for chloride were similar to those for sodium. ANP also increased delivery of H2O, K, Ca, and Mg to the CD at the papillary base but did not significantly affect their transport by the terminal CD.


Author(s):  
Carsten A. Wagner ◽  
Olivier Devuyst

The kidney is central to acid–base homeostasis. Major processes are reabsorption of filtered bicarbonate, de novo synthesis of bicarbonate from ammoniagenesis, and net excretion of protons. The latter requires buffers such as ammonium, phosphate, citrate and other bases binding protons (so-called titratable acids). The proximal tubule is the major site of bicarbonate reabsorption and only site of ammoniagenesis. The thick ascending limb and the distal convoluted tubule handle ammonia/ammonium and complete bicarbonate reabsorption. The collecting duct system excretes protons and ammonium, but may switch to net bicarbonate secretion. The kidney displays a great plasticity to adapt acid or bicarbonate excretion. Angiotensin II, aldosterone and endothelin are involved in regulating these processes, and they induce morphological changes along the nephron. Inborn and acquired disorders of renal acid–base handling are caused by mutations in acid–base transport proteins or by dysregulation of adaptive mechanisms.


1982 ◽  
Vol 242 (6) ◽  
pp. F657-F663
Author(s):  
J. P. Pennell ◽  
J. J. Bourgoignie

Water transport by terminal papillary collecting ducts was examined by micropuncture of the renal papilla in 15 rats with a solitary remnant kidney (RK) and in 27 normal rats, 10 of which had undergone sham operation. Before papillary exposure, urinary osmolality was significantly (P less than 0.001) lower in RK rats (685 vs. 1,722 mosmol/kg H2O in normal rats). After papillary exposure, urinary osmolality decreased by 50% in normal rats but did not change in RK rats. In RK rats, a greater percentage of filtered water was delivered to (5.74% vs. 2.29% in normal rats, P less than 0.001) and reabsorbed by (1.94% vs. 0.94% in normal rats, P less than 0.005) the terminal millimeter of papillary collecting ducts. Fractional water reabsorption by terminal papillary collecting ducts correlated directly (r = 0.83, P less than 0.001) with fractional water delivery, suggesting load dependence of water reabsorption. Estimated absolute water reabsorption by terminal collecting ducts was equivalent for remnant and normal kidneys and increased two-to fourfold in remnant kidneys when analyzed per functioning papillary collecting duct. There was an inverse relationship between urinary osmolality and fractional water delivery to papillary collecting ducts (r = 0.65, P less than 0.001). Although the data do not exclude functional alterations of papillary collecting ducts, the events underlying the reduction of urinary osmolality in remnant kidneys appear to involve physiological processes based on a high delivery and reabsorption of water.


1985 ◽  
Vol 248 (2) ◽  
pp. F219-F227 ◽  
Author(s):  
E. Higashihara ◽  
J. P. Kokko

Recent studies have suggested that potassium, like urea, undergoes medullary recycling. The present cortical and papillary micropuncture studies were designed to confirm the existence of medullary potassium recycling and to determine whether acute infusions of aldosterone affected this phenomenon. Thus, nephron segmental analysis of potassium and sodium transport was conducted in adrenalectomized Munich-Wistar rats and similarly prepared rats that received aldosterone acutely to achieve physiological blood levels. The clearance results demonstrated that aldosterone has an acute antinatriuretic and a kaliuretic effect, whereas the micropuncture studies demonstrated that 1) aldosterone increases potassium secretion between early and late distal tubule punctures; 2) aldosterone causes an increase in delivery of potassium to the papillary collecting duct; 3) aldosterone does not increase potassium secretion across the papillary collecting duct; and 4) aldosterone significantly increases medullary potassium recycling as evidenced by increased quantities of potassium present at the bend of the loop of Henle in response to aldosterone infusions. Thus, the studies confirm the existence of potassium recycling and suggest that this phenomenon is a feedback system that, in part, regulates urinary potassium excretion.


1989 ◽  
Vol 36 (2) ◽  
pp. 201-209 ◽  
Author(s):  
Clemens Grupp ◽  
Iris Pavenstädt-Grupp ◽  
R. Willi Grunewald ◽  
Christopher Bevan ◽  
John B. Stokes ◽  
...  

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