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C R Caflisch

Publications and source records attributed to C R Caflisch.

At least 19 recordsLinked to original sources
PubMed2000

Human intestinal epithelial cells express a novel receptor for IgA.

Binding and transport of polymeric Igs (pIgA and IgM) across epithelia is mediated by the polymeric Ig receptor (pIgR), which is expressed on the basolateral surface of secretory epithelial cells. Although an Fc receptor for IgA (FcalphaR) has been identified on myeloid cells and some cultured mesangial cells, the expression of an FcalphaR on epithelial cells has not been described. In this study, binding of IgA to a human epithelial line, HT-29/19A, with features of differentiated colonic epithelial cells, was examined. Radiolabeled monomeric IgA (mIgA) showed a dose-dependent, saturable, and cation-independent binding to confluent monolayers of HT-29/19A cells. Excess of unlabeled mIgA, but not IgG or IgM, competed for the mIgA binding, indicating that the binding was IgA isotype-specific and was not mediated by the pIgR. The lack of competition by asialoorosomucoid and the lack of requirement for divalent cations excluded the possibility that IgA binding to HT-29/19A cells was due to the asialoglycoprotein receptor or beta-1, 4-galactosyltransferase, previously described on HT-29 cells. Moreover, the FcalphaR (CD89) protein and message were undetectable in HT-29/19A cells. FACS analysis of IgA binding demonstrated two discrete populations of HT-29/19 cells, which bound different amounts of mIgA. IgA binding to other colon carcinoma cell lines was also demonstrated by FACS analysis, suggesting that an IgA receptor, distinct from the pIgR, asialoglycoprotein receptor, galactosyltransferase, and CD89 is constitutively expressed on cultured human enterocytes. The function of this novel IgA receptor in mucosal immunity remains to be elucidated.

Antibody Specificity↗
PubMed1998

IgA induced activation of human mesangial cells: independent of FcalphaR1 (CD 89).

BACKGROUND: IgA nephropathy (IgAN) is characterized by deposition of polymers of IgA1 in the mesangium, accumulation of mesangial matrix and mesangial cell proliferation. Activation of the mesangial cell by IgA, via an IgA receptor, may be an initiating event in the pathology of IgAN. METHODS: We examined the ability of radiolabeled, normal serum IgA1 to bind human mesangial cells (HMC). Activation of HMC by monomeric (mIgA1) and heat aggregated IgA1 (AIgA1) was compared by Northern analysis of c-jun expression. The expression of FcalphaR1 (CD89) mRNA on our cultured mesangial cells was also assessed by Northern analysis, reverse transcription-polymerase chain reaction (RT-PCR) and flow cytometry. RESULTS: 125I-mIgA1 and 125I-AIgA1 bound to HMC in a dose-dependent, saturable manner with similar affinities. There were 1.2 x 10(6) binding sites per cell, with an affinity constant of 2.3 x 10(6) M(-1). AIgA1 induced c-jun expression in a time and dose-dependent manner (2.4-fold above baseline after 60 min exposure to AIgA1 200 microg/ml) while mIgA1 had no effect on c-jun expression. No message for CD 89 was detectable in quiescent or AIgA1 stimulated HMC by Northern analysis or RT-PCR using several primer sequences based on the sequence of U937 FcalphaR cDNA. Flow cytometry on the mesangial cells, using My 43, a monoclonal antibody to FcalphaR1 confirmed that CD 89 was not present on the cell. CONCLUSION: These results demonstrate that HMC bind mIgA1 and AIgA1 with similar affinity. However, activation of HMC requires an aggregated form of IgA1. These processes are independent of FcalphaR1, suggesting the presence of a new IgA receptor on mesangial cells.

Antigens, CD↗
PubMed1995

Prostaglandin E2 regulation of ion transport is absent in medullary thick ascending limbs from SHR.

Regulation of HCO3- and Cl- absorption by arginine vasopressin (AVP) and prostaglandin E2 (PGE2) was examined in isolated, perfused medullary thick ascending limbs (MTAL) from 4- to 7-wk-old spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats. AVP inhibited HCO3- absorption by 50% at 10(-10) M and by 25% at 2 x 10(-12) M in MTAL from both WKY and SHR. Cholera toxin (10(-9) M) or forskolin (10(-6) M) in the bath also inhibited HCO3- absorption by 50% in the SHR. In MTAL from WKY, PGE2 (10(-6) M in the bath) increased HCO3- absorption from 7.1 +/- 0.4 to 12.0 +/- 0.4 pmol.min-1.mm-1 (P < 0.005) and decreased Cl- absorption from 65 +/- 7 to 47 +/- 6 pmol.min-1.mm-1 (P < 0.001) in the presence of 10(-10) M AVP. Under the same conditions, PGE2 had no effect on HCO3- or Cl- absorption in MTAL from SHR. PGE2 also reversed submaximal inhibition of HCO3- absorption by 2 x 10(-12) M AVP in WKY but not in SHR. With 10(-10) M AVP in the bath, phorbol 12-myristate 13-acetate (10(-6) M in the bath) increased HCO3- absorption from 6.6 +/- 0.5 to 12.3 +/- 0.4 pmol.min-1.mm-1 in MTAL from WKY and from 7.6 +/- 0.7 to 12.6 +/- 1.2 pmol.min-1.mm-1 in MTAL from SHR (P < 0.005). These results demonstrate that 1) the effects of PGE2 to stimulate HCO3- absorption and inhibit Cl- absorption in the presence of AVP are absent in MTAL from SHR, 2) the defect may involve an inability of PGE2 to stimulate protein kinase C, and 3) regulation of HCO3- absorption by AVP via adenosine 3',5'-cyclic monophosphate is similar in MTAL from WKY and SHR. The lack of PGE2 inhibition of NaCl absorption in the MTAL may contribute to renal salt retention during the development of hypertension in the SHR.

Absorption↗
PubMed1994

Effect of orally administered cadmium on in situ pH, PCO2, and bicarbonate concentration in rat testis and epididymis.

Acute injections of high doses of cadmium (Cd) induce marked testicular necrosis. However, the effects of low-dose oral Cd exposure, on a chronic basis, are not well documented. The present investigation was designed to examine the effects of such exposure on in situ pH, PCO2, and bicarbonate concentration ([HCO3-]) in the rat testis and epididymis, plasma testosterone levels, and testis and epididymis weights. Male Sprague-Dawley rats were exposed to 50 or 100 ppm Cd for 40 d. Oral administration of 50 or 100 ppm Cd was associated with significant alkalinization of luminal fluid in seminiferous tubules (ST) but did not alter in situ pH values in proximal caput (PCP), middle caput (MCP), or proximal cauda epididymidis (PCD). The in situ PCO2 values in ST, PCP, MCP, and PCD of control animals were indistinguishable from each other and from values after Cd exposure, and all values were significantly higher than system arterial blood (SAB) PCO2. Oral Cd exposure at 50 or 100 ppm did not change the values for bicarbonate in SAB, PCP, or MCP but increased markedly the value in ST. Plasma testosterone levels and testis and epididymis weights were not altered after oral cadmium administration. These findings suggest that, at the doses employed in this study, Cd exposure may result in subtle alterations in the blood-testis barrier and subsequent impairment of acid-base pathways. Furthermore, the traditional view of Cd-related testicular insult based on acute injection protocols needs to be reevaluated in terms of environmental relevance.

Administration, Oral↗
PubMed1994

Cloning of the alpha-subunit of GS protein from spontaneously hypertensive rats.

Enhanced sodium reabsorption by the kidney has a significant role in the development of genetic hypertension. In the spontaneously hypertensive rat (SHR) model of genetic hypertension, the enhanced sodium reabsorption likely arises from abnormal hormonal regulation of tubular transport. Since hormonal signaling pathways are coupled frequently via GTP binding proteins, one explanation for hormonal abnormalities in SHR would be a defect in a GTP binding protein or proteins. Recent work has suggested that the regulation of Na+,K(+)-ATPase activity by cholera toxin-sensitive GTP binding proteins is abnormal in SHR. The purpose of the present studies was to clone the alpha S-subunit, which is the subunit ADP ribosylated by cholera toxin, of GS protein to determine whether it is abnormal in SHR. Reverse transcription-polymerase chain reaction was able to detect mRNA for alpha S in both Wistar-Kyoto (WKY) rats and SHR. Northern analysis indicated that equivalent amounts of alpha S mRNA were present in WKY rats and SHR. S1 nuclease analysis demonstrated that there was no difference in the amount of alpha S short and long forms between WKY rats and SHR. Subcloning and sequencing of polymerase chain reaction products from WKY rats and SHR indicated that the alpha S forms present in renal cortex were identical. ADP ribosylation studies with cholera toxin demonstrated the presence of equivalent amounts of alpha S protein in WKY rats and SHR. Taken together, these results suggest that the abnormal regulation of Na+,K(+)-ATPase activity by a cholera toxin-sensitive pathway in SHR does not arise from a defect in the alpha S subunit.

Adenosine Diphosphate Ribose↗
PubMed1992

Acidification of testicular and epididymal fluids in the rat after surgically-induced varicocele.

Experimental left varicocele (ELV) in adult rats produces a bilateral increase in testicular blood-flow and temperature which may alter the intraluminal environment in which sperm mature. The purpose of the present study was to evaluate the effect of ELV on the in-situ pH, PCO2 and bicarbonate concentration ([HCO3-]) in seminiferous tubules (ST), initial segment (IS), proximal caput (PCP), middle caput (MCP), middle corpus (MCR), and proximal cauda epididymidis (PCD) of the rat employing pH and PCO2 microelectrodes. Adult male rats with ELV or sham-surgeries (control) were studied after 30 days. Relative to controls, ELV significantly reduced the in-situ PCO2 in the testicular artery, ST, IS, PCP, MCP, MCR and PCD. In spite of this reduction, all values remained significantly higher than the systemic arterial blood PCO2. Values for in-situ pH in ST, IS, PCP, MCP, MCR, and PCD of control rats were significantly more acidic than systemic arterial blood. Furthermore, ELV decreased the pH in ST, IS, PCP, and MCP when compared to control values. The calculated [HCO3-] in ST from control animals was less than half that in systemic arterial blood and was reduced further in IS, PCP, and MCP. Varicocele did not change the [HCO3-] in systemic arterial blood but reduced markedly the values in ST, IS, PCP, and MCP. These alterations in the in-situ pH, PCO2, and [HCO3-] in structures of the rat testis and epididymis may play a role in the anti-spermatic effect of ELV.

Animals↗
PubMed1991

Cadmium-induced changes in luminal fluid pH in testis and epididymis of the rat in vivo.

The effects of a single low subcutaneous dose of cadmium chloride (CdCl2) (2.7 mg/kg body weight) on in situ pH in the rat testis and epididymis, plasma testosterone, and testis and epididymis weights were investigated in this study. Values for in situ pH in seminiferous tubules (6.97 +/- 0.01), proximal caput (6.62 +/- 0.01), middle caput (6.59 +/- 0.01), and proximal cauda epididymidis (6.84 +/- 0.01) of sham-treated rats were significantly more acid than systemic arterial blood pH (7.41 +/- 0.01). Cadmium (Cd) administration was associated with significant alkalinization of luminal fluid in seminiferous tubules (7.17 +/- 0.02) and in proximal (7.02 +/- 0.04) and middle caput (6.99 +/- 0.03), but not in proximal cauda epididymidis (6.88 +/- 0.02), after 1 d. Eleven days after Cd administration, marked alkalinization of luminal fluid was observed in all segments studied including proximal cauda epididymidis (7.21 +/- 0.02). Plasma testosterone concentration in sham-treated rats was 1.93 +/- 0.30 ng/ml and was reduced significantly after 1 d (0.56 +/- 0.06 ng/ml) and persisted after 11 d postexposure (0.57 +/- 0.07 ng/ml). Testis and epididymis weights were not altered 1 d after Cd exposure but were significantly reduced after 11 d. These studies suggest that the alkalization observed in luminal fluid of seminiferous tubules and epididymal duct of the rat after subcutaneous CdCl2 administration may be the result of structural degeneration of the testis associated with inhibition of Leydig-cell androgen production.

Animals↗
PubMed1990

Effect of vasectomy on in situ pH in rat testis and epididymis.

The effect of bilateral vasectomy on in situ pH in seminiferous tubules, initial segments, proximal caput, middle corpus and proximal cauda epididymides of the rat has been studied employing in vivo microelectrode techniques. After bilateral vasectomy of four weeks duration, a significant increase in acidity of luminal fluid in the initial segments of the caput epididymides was observed. By eight weeks post vasectomy, luminal pH in the initial segments was significantly more acid as compared to sham-operated control animals or four weeks vasectomy while, in contrast, luminal pH in the proximal cauda epididymides was significantly more alkaline. The alteration of luminal fluid pH in the initial segments and proximal cauda epididymides after bilateral vasectomy may be the result of impairment of acid-base, as well as water transport pathways.

Animals↗
PubMed1990

Effect of alpha-chlorohydrin on in situ pH in rat testis and epididymis.

The effect of the male contraceptive, alpha-chlorohydrin, on in situ pH in seminiferous tubules and epididymal duct of the rat has been studied employing in vivo microelectrode techniques. After eight days of low-dose alpha-chlorohydrin administration (15mg/kg/day), a significant increase in acidity of luminal fluid in seminiferous tubules, proximal caput, middle caput, and proximal cauda epididymidis was observed. Increased acidity in the testis and epididymis may play an important role in the antifertility effect of alpha-chlorohydrin.

Animals↗
PubMed1990

Direct evaluation of acidification by rat testis and epididymis: role of carbonic anhydrase.

The present experiments have employed microelectrode techniques (pH and PCO2) and microcalorimetry (total CO2 concentration) to define parameters of acidification in specific structures of the rat testis and epididymis during control conditions and after administration of the carbonic anhydrase inhibitor acetazolamide (20 or 50 mg/kg). Values for in situ pH during control conditions in seminiferous tubules (ST; 6.96 +/- 0.01), proximal caput (PCP; 6.62 +/- 0.01), middle caput (MCP; 6.59 +/- 0.01), middle corpus (MCR; 7.10 +/- 0.02), and proximal cauda epididymidis (PCD; 6.85 +/- 0.01) were significantly more acidic than in testicular artery (TA; 7.36 +/- 0.01) or systemic arterial blood (SAB; 7.40 +/- 0.01) and did not change significantly after acetazolamide. In situ partial pressure of CO2 (PCO2) in TA (52.2 +/- 0.6 mmHg), ST (52.3 +/- 0.4 mmHg), PCP (52.9 +/- 0.4 mmHg), MCP (53.0 +/- 0.7 mmHg), MCR (53.4 +/- 0.4 mmHg), and PCD (52.4 +/- 0.4 mmHg) were indistinguishable from each other, but all values were significantly higher than SAB PCO2 (39.2 +/- 0.5 mmHg). Acetazolamide increased in situ PCO2 significantly in all structures except the MCR. The total CO2 concentration in normal ST fluid (10.7 +/- 0.5 mM) was significantly higher than in "primary" fluid (6.9 +/- 0.3 mM), and both values were well below TA (26.9 +/- 1.3 mM) or SAB (24.6 +/- 0.4 mM) total CO2 concentrations. In the epididymis, total CO2 concentrations were indistinguishable and not different from the value in primary fluid.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetazolamide↗
PubMed1988

Effect of selective aldosterone deficiency on acidification in nephron segments of the rat inner medulla.

Mineralocorticoid plays a role in urinary acidification and acid-base balance, but the response of the inner medulla to aldosterone has not been elucidated. A model of selective aldosterone deficiency (SAD) with hyperkalemia and hyperchloremic metabolic acidosis was employed to assess segmental acidification by measuring in situ pH, titratable acidity (TA) and total ammonia (Am). Hydrogen ion secretion was also examined as a function of the increment in in situ PCO2 in the collecting duct during bicarbonate loading. SAD rats were compared to ADX controls that received adrenalectomy and chronic replacement of gluco- and mineralocorticoid and to rats with chronic metabolic acidosis induced by oral NH4Cl (CMA). Both fractional and absolute delivery of Am to the loop of Henle was lower in SAD vs. CMA rats (1.34 to 3.63 mM, P less than 0.01). Delivery of Am to the base and tip collecting duct (BCD and TCD) was also markedly lower in SAD (1.50 vs. 0.52 and 1.77 vs. 0.47 mM, respectively, P less than 0.01). Net addition of Am and net acid between BCD and TCD, observed in CMA rats, was not observed in SAD despite equivalent degrees of systemic metabolic acidosis. Similarly, the concentration gradient favoring transfer of NH3 between loop of Henle and CD was reduced in SAD. During bicarbonate loading the increment in PCO2 at BCD, TCD and in final urine was significantly lower in SAD rats than in adrenal intact bicarbonate-loaded rats. Therefore, the acidification defect in this model of SAD appears to be a result of a decrease in ammonia production and delivery to the loop of Henle, impaired transfer from loop to collecting duct and reduction in the rate of H+ secretion by the collecting duct.

Acid-Base Equilibrium↗
PubMed1987

Transepithelial ammonia concentration gradients in inner medulla of the rat.

Transport of NH3 from loops of Henle to medullary collecting ducts has been proposed to play an important role in renal ammonia excretion. To determine whether transepithelial ammonia concentration gradients capable of driving this transport are present in the inner medulla, micropuncture experiments were performed in control rats and in rats with chronic metabolic acidosis. In situ pH and total ammonia concentrations were measured to calculate NH3 concentrations ([NH3]) for base and tip collecting duct, loop of Henle, and vasa recta. In control and acidotic rats, [NH3] in the loop of Henle was significantly greater than [NH3] in the collecting ducts. [NH3] did not differ in loop of Henle and adjacent vasa recta in either group of rats, indicating that NH3 concentration gradients between loop and collecting duct represent NH3 gradients that are present between medullary interstitium and collecting duct. During acidosis, an increase in collecting duct ammonia secretion was associated with an increase in the NH3 concentration difference between loop of Henle and collecting duct but occurred in the absence of a fall in collecting duct pH. The NH3 concentration gradient favoring diffusion of NH3 into the collecting ducts increased during acidosis because [NH3] in the loop of Henle and medullary interstitium increased more than [NH3] in the collecting duct. These findings indicate that transport processes involved in medullary ammonia accumulation play an important role in regulating ammonia secretion into the inner medullary collecting duct in vivo and that a fall in inner medullary collecting duct pH is not necessarily required for ammonia secretion by this segment to increase during chronic metabolic acidosis.

Acidosis↗
PubMed1985

Validation of the difference in urine and blood carbon dioxide tension during bicarbonate loading as an index of distal nephron acidification in experimental models of distal renal tubular acidosis.

Recent classifications of the several pathophysiologic types of distal renal tubular acidosis (secretory, voltage dependent, and gradient) have been based on the response of acidification parameters to a series of provocative maneuvers in vivo and in vitro. A reduction in the difference in urine and blood CO2 tension during bicarbonate loading (U-B pCO2 gradient), a widely applied parameter, has been employed as an index of reduced distal nephron proton secretion. This study was designed to test the validity of the U-B pCO2 gradient in a variety of experimental models of distal renal tubular acidosis by measuring and comparing disequilibrium pH (a direct technique to detect H+ secretion in situ) with the pCO2 in the papillary collecting duct of the rat in vivo during bicarbonate loading. Chronic amiloride, lithium chloride, and amphotericin-B administration, and the post-obstructed kidney models were employed. Amiloride resulted in an acidification defect which did not respond to sulfate infusion (urine pH = 6.15 +/- 0.08), and was associated with an obliteration of the acid disequilibrium pH (-0.26 +/- 0.05- -0.08 +/- 0.03) and reduction in papillary pCO2 (116.9 +/- 3.2 - 66.9 +/- 2.5 mmHg). The defect induced by lithium administration responded to Na2SO4 (urine pH = 5.21 +/- 0.06) but was similar to amiloride with respect to the observed reduction in disequilibrium pH (-0.04 +/- 0.02) and pCO2 (90.3 +/- 3.0 mmHg). The post-obstructed kidney model was characterized by an abnormally alkaline urine pH unresponsive to sulfate (6.59 +/- 0.06) and a reduction in disequilibrium pH (+0.02 +/- 0.06) and pCO2 (77.6 +/- 3.6 mmHg). Amphotericin-B resulted in a gradient defect as characterized by excretion of an acid urine after infusion of sodium sulfate (5.13 +/- 0.06). Unlike other models, however, amphotericin-B was associated with a significant acid disequilibrium pH (-0.11 +/- 0.05) and an appropriately elevated urine pCO2 (119.8 +/- 6.4 mmHg) which did not differ from the respective values in control rats. Thus, these findings support the use of the U-B pCO2 as a reliable means of demonstrating impaired distal nephron proton secretion in secretory and voltage-dependent forms of distal renal tubular acidosis (RTA) and supports the view that proton secretion is not impaired in gradient forms of distal RTA.

Absorption↗
PubMed1984

Role of metabolic CO2 production in the generation of elevated renal cortical PCO2.

Several possible explanations for the elevated CO2 tension observed in structures of the renal cortex have been proposed. The present study was designed to investigate the contribution of renal metabolic CO2 production and removal and the role of incomplete equilibration of the CO2 added to peritubular plasma in an environment devoid of carbonic anhydrase. PCO2 was measured in vivo with PCO2 microelectrodes in early (EP) and late proximal (LP) tubules and stellate vessels (SV) during control conditions and after hyperoncotic albumin, aortic constriction, vanadate, rotenone, or 2,4-dinitrophenol (2,4-DNP) per renal artery, and carbonic anhydrase infusion. In all groups values for PCO2 in EP, LP, and SV sites were indistinguishable but significantly higher than systemic arterial PCO2. PCO2 increased to 71.4 +/- 1.4 mmHg with hyperoncotic albumin and to 87.0 +/- 1.8 mmHg after 2,4-DNP (P less than 0.001). During aortic constriction, vanadate infusion, and rotenone per renal artery, PCO2 fell to 53.7 +/- 0.9, 55.2 +/- 2.5, and 57.3 +/- 1.3, respectively (P less than 0.001). Renal O2 consumption decreased significantly after rotenone (-38.1 +/- 5.6 to -13.3 +/- 2.7 mumol X min-1 X kg-1) and increased significantly after 2,4-DNP (-35.7 +/- 5.9 to -75.9 +/- 6.9 mumol X min-1 X kg-1). These findings demonstrate that renal energy utilization and metabolic CO2 production represents an important source of renal cortical PCO2. Carbonic anhydrase infusion resulted in a decrease in PCO2 to 58.2 +/- 1.2 mmHg (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1982

PCO2 measurements in surface proximal tubules and peritubular capillaries of the rat kidney.

PCO2 was measured in surface proximal tubules and peritubular capillaries in the rat under normal acid-base conditions and in three settings with decreased HCO3(-) reabsorption: benzolamide administration, respiratory alkalosis, and metabolic acidosis. Under normal conditions, PCO2 in the early proximal tubule (EP) was 10.5 mmHg higher than PaCO2 (P less than 0.001) and 3-4 mmHg higher than late proximal (LP) and peritubular capillary (PC) PCO2 (P less than 0.001). PCO2 in LP and PC was 7 mmHg higher than PaCO2 (P less than 0.001). Benzolamide (3 mg/kg) had no effect on the difference between PC and arterial PCO2 or between EP and PC PCO2. Increasing benzolamide to 8 mg/kg increased PCO2 in the surface structures relative to arterial PCO2 by 3-5 mmHg (P less than 0.01). Metabolic acidosis did not alter the relationships between cortical and arterial PCO2. By contrast, respiratory alkalosis decreased cortical PCO2 relative to PaCO2 by over 50%. Nonetheless, EP PCO2 was still higher than LP or PC PCO2 (P less than 0.01). Thus, reducing HCO3(-) reabsorption does not obliterate the difference between EP and LP or PC PCO2 nor does it invariably reduce PCO2 in the surface structures of the kidney relative to arterial PCO2.

Animals↗
PubMed1981

Dissociation of saline-induced natriuresis from urea washout in the rat.

Medullary urea washout has been postulated to play a major role in the natriuretic response to volume expansion (VE). To examine this hypothesis, renal tissue solute composition was measured in a natriuretic and nonnatriuretic model of VE. Renal tissue composition was analyzed during hydropenia, acute VE, acute VE with renal artery pressure reduced to 70 mmHg at the onset of saline loading (immediate clamping), and acute VE with renal artery pressure reduced to 70 mmHg after 45 min of saline loading (delayed clamping). Immediate clamping, a nonnatriuretic model of VE, prevented VE-induced urea washout and the increase in sodium and water content in the cortex and outer medulla. Delayed clamping, a natriuretic model of VE, produced a pattern of tissue composition very similar to immediate clamping. Tissue urea content was not significantly different in the two protocols and only minor differences in sodium and water content were noted. Thus, under these experimental conditions, VE-induced natriuresis can be dissociated from medullary urea washout, and other mechanisms must be invoked to explain the increased sodium excretion.

Animals↗
PubMed1980

Effect of benzolamide on pH in the proximal tubules and peritubular capillaries of the rat kidney.

The influence of carbonic anhydrase inhibition with benzolamide on proximal tubular and peritubular capillary pH was evaluated in the rat using a glass-membrane pH microelectrode. Control peritubular capillary pH, 7.38 +/- .02 (N=11), was significantly lower than control arterial pH, 7.44 +/- .01, p < .05. Early proximal tubular pH, 7.20 +/- .02 (N = 17), was more alkaline than late proximal tubular pH, 6.74 +/- .06 (N = 13), p < .001; pH at both sites was more acid than in the peritubular capillary, p < .001. Benzolamide treatment had no detectable effect on arterial or peritubular capillary pH, but reduced early proximal tubular pH by 0.54 pH units, to 6.66 +/- .04 (N = 13), p < .001. Late proximal pH also fell slightly to 6.57 +/- .03 (N = 14), p < .02. The results support previous observations indicating that benzolamide treatment decreases early proximal tubular pH dramatically, and provide further evidence that HCO3- reabsorption is accomplished by hydrogen ion secretion in the proximal tubule.

Animals↗