Fetal and neonatal hydronephrosis.
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Adult↗
Biomedical subjects
A Quan
Publications and source records attributed to A Quan.
Late onset seizures, hemiparesis and blindness in hemolytic uremic syndrome.
Neurologic complications of hemolytic uremic syndrome, including seizures, usually occur early during the acute phase of the illness. We report a3-year-old girl with classic diarrhea-associated hemolytic uremic syndrome who developed late onset seizures, hemiparesis and transient blindness on the 17th hospital day, at which time her recovery was characterized by improvement in her blood pressure, serum electrolytes, renal function, hematocrit and platelet count. A CT and MR revealed brainstem and posterior parietal and occipital infarct/edema. The association of these radiologic findings within the posterior distribution along with visual loss and seizures are unique to posterior reversible encephalopathy syndrome. Within 7 days, she regained motor function and vision and had no further seizure activity. At 6 months follow-up, physical examination revealed normal motor function and vision and a repeat MR showed near resolution of the previous findings with minimal occipital lobe gliosis. This case report describes the uncommon finding of late onset seizures occurring during the recovery phase of hemolytic uremic syndrome with MR findings consistent with posterior reversible encephalopathy syndrome.
Blindness↗
Recurrence of hemolytic uremic syndrome after renal transplantation in children: a report of the North American Pediatric Renal Transplant Cooperative Study.
BACKGROUND: Hemolytic uremic syndrome (HUS) is the cause of renal failure in 2-4% of children on dialysis. After renal transplantation, HUS can recur, but recurrence rate and risk factors are controversial. METHODS: We reviewed the recurrence of HUS within the North American Pediatric Renal Transplant Cooperative Study (NAPRTCS) registry and used a separate questionnaire to ascertain additional clinical information. RESULTS: Of 68 renal allografts, HUS recurred in 6 allografts (8.8%) occurring in five patients (8.2%). Four patients had atypical HUS, whereas one patient had classic HUS. HUS recurred after transplantation in 33 days or less in all but one allograft. Outcome was poor with five of six allografts lost, despite treatment with fresh-frozen plasma or plasmapheresis. Cyclosporine had no effect on outcome or HUS recurrence. CONCLUSIONS: The risk of HUS recurrence in the allograft is 8-9% and is heightened in atypical HUS. Treatment was not effective and graft outcome was poor. Cyclosporine does not affect HUS recurrence.
Adolescent↗
Effect of prenatal dexamethasone on rat renal development.
BACKGROUND: Prenatal insults can program the developing fetus to develop diseases that manifest in later life. Dexamethasone is often administered to the developing fetus to accelerate pulmonary development. The purpose of the present study was to determine whether prenatal dexamethasone adversely affects renal development and predisposes rats to develop renal disease and hypertension in later life. METHODS: Pregnant rats were given either vehicle or two daily intraperitoneal injections of dexamethasone (0.2 mg/kg body weight) on gestational days: 11 and 12, 13 and 14, 15 and 16, 17 and 18, 19 and 20, or 20 and 21. Tail cuff blood pressure, glomerular number, and inulin clearance were measured in control and prenatal dexamethasone-treated rats when the rats were 60 to 90 days of age. RESULTS: Prenatal dexamethasone did not affect the length of gestation, the number of animals per litter, or the total body weight or kidney weight measured at one day of age. Offspring of rats administered dexamethasone on days 15 and 16 gestation had a 30% reduction in glomerular number compared with control at 60 to 70 days of age (24,236 +/- 441 vs. 30,453 +/- 579, P < 0.01). Rats receiving prenatal dexamethasone on days 17 and 18 had an approximate 20% reduction in glomeruli compared with control (P < 0.01). Offspring of rats receiving dexamethasone on days 15 and 16 gestation had systolic blood pressures at 60 to 90 days of age that were higher than any other group (P < 0.05). The glomerular filtration rate was comparable in all of the groups. CONCLUSIONS: This study shows that two daily doses of prenatal dexamethasone (0.2 mg/kg body weight) in rats do not produce intrauterine growth retardation. Adult offspring of rats that received prenatal dexamethasone during specific times of gestation have a reduced number of nephrons and hypertension.
Animals↗
Dexamethasone inhibits the binding of nuclear factors to the IL-5 promoter in human CD4 T cells.
BACKGROUND: IL-5 is produced by the T(H)2 subset of CD4(+) T lymphocytes and is necessary for the eosinophilia typical of allergic conditions. Glucocorticoids such as dexamethasone are highly effective inhibitors of eosinophilic inflammation, and one of their effects is inhibition of IL-5 gene expression. OBJECTIVE: We wished to examine the effect of dexamethasone on the binding of nuclear factors from primary human CD4(+) T lymphocytes to the RE-I and RE-II positively acting regulatory elements of the IL-5 promoter. METHODS: CD4(+) T cells, purified from PBMCs by magnetic bead separation, were activated with anti-CD3 antibody and phorbol myristate acetate. Nuclear extracts were tested in electrophoretic mobility shift assays with probes based on RE-I and RE-II. RESULTS: In extracts from activated cells, the RE-II region of the promoter formed a complex that was shown by supershift assay to contain NFATc. This complex was abolished by treatment of the cells with dexamethasone before activation and was weak or absent in unactivated cells. By contrast, binding to the RE-I region and to the GATA-3 site within RE-I was observed in resting cells and was not affected by activation or treatment with dexamethasone. CONCLUSION: Dexamethasone inhibits the inducible binding of factors to the RE-II region but does not affect the constitutive binding to the RE-I region. Characterization of such molecular effects of glucocorticoids could enable the development of specific inhibitors of IL-5 expression that lack the side effects of glucocorticoids.
Binding, Competitive↗
The renal nerve is required for regulation of proximal tubule transport by intraluminally produced ANG II.
The proximal tubule synthesizes and luminally secretes high levels of angiotensin II, which modulate proximal tubule transport independently of systemic angiotensin II. The purpose of this in vivo microperfusion study is to examine whether the renal nerves modulate the effect of intraluminal angiotensin II on proximal tubule transport. The decrement in volume reabsorption after addition of 10(-4) M luminal enalaprilat is a measure of the role of luminal angiotensin II on transport. Acute denervation decreased volume reabsorption (2.97 +/- 0.14 vs. 1.30 +/- 0.21 nl. mm(-1). min(-1), P < 0.001). Although luminal 10(-4) M enalaprilat decreased volume reabsorption in controls (2.97 +/- 0.14 vs. 1.61 +/- 0.26 nl. mm(-1). min(-1), P < 0.001), it did not after acute denervation (1.30 +/- 0.21 vs. 1.55 +/- 0.19 nl. mm(-1). min(-1)). After chronic denervation, volume reabsorption was unchanged from sham controls (2.26 +/- 0.28 vs. 2.70 +/- 0.19 nl. mm(-1). min(-1)). Addition of luminal 10(-4) M enalaprilat decreased volume reabsorption in sham control (2.70 +/- 0.19 vs. 1.60 +/- 0.10 nl. mm(-1). min(-1), P < 0.05) but not with chronic denervation (2.26 +/- 0.28 vs. 2.07 +/- 0.20 nl. mm(-1). min(-1)). Addition of 10(-8) M angiotensin II to the lumen does not affect transport due to the presence of luminal angiotensin II. However, addition of 10(-8) M angiotensin II to the tubular lumen increased the volume reabsorption after both acute (1.30 +/- 0.21 vs. 2.67 +/- 0.18 nl. mm(-1). min(-1), P < 0.05) and chronic denervation (2.26 +/- 0.28 vs. 3.57 +/- 0.44 nl. mm(-1). min(-1), P < 0.01). These data indicate that renal denervation abolished the luminal enalaprilat-sensitive component of proximal tubule transport, which is consistent with the renal nerves playing a role in the modulation of the intraluminal angiotensin II mediated component of proximal tubule transport.
Absorption↗
Impact of total body water errors on Kt/V estimates in children on peritoneal dialysis.
Determining Kt/V in peritoneal dialysis (PD) requires estimation of total body water (TBW). The Dialysis Outcomes Quality Initiative (DOQI) guidelines recommend use of the Mellits and Cheek (MC) formulas for the estimation of TBW in children. However, the MC formulas were developed from healthy children and may not apply to children on PD. Re-evaluating the MC data with additional, recent data from healthy infants has led to the development of new formulas. In addition, and as part of a prospective study of children initiating PD, the Pediatric Peritoneal Dialysis Study Consortium (PPDSC) has directly measured TBW using H2[18O]. To assess the impact of various TBW estimates, KPDt/V values prospectively collected in 24 children were calculated using H2[18O]-measured TBW (O18), MC-derived TBW (MCD), and new-formula TBW (NEW). The mean weekly KPDt/V by O18 was 2.2; by MCD, it was 2.0; and by NEW, it was 2.0. The results derived using the O18 method varied from both the MCD and the NEW results (p < 0.001). The mean deviation from the measured KPDt/V using O18 was 9.5% (maximum: 16%) using the MCD estimate and 7.8% (maximum: 18%) using the NEW formulas. Determinations of KPDt/V are significantly affected by the method of estimating TBW. The PPDSC formulas for children on PD based on the use of H2[18O] offer the most accurate means of calculating TBW and should replace formulas derived from healthy children. The use of Kt/V itself as a marker of adequacy in children will be validated only in prospective studies.
Adolescent↗
Pharmacotherapy for hypertension in women of different races.
OBJECTIVES: To assess whether the relative and absolute benefit of hypertension treatment in women varies with age or race. SEARCH STRATEGY: Literature search of studies from 1966 to 1998 using MEDLINE, reviews, and consultation with experts. SELECTION CRITERIA: Studies were eligible if they were randomized controlled trials of pharmacological treatment of primary hypertension, with cardiovascular morbidity and mortality outcomes, and with over one hundred women enrolled. DATA COLLECTION AND ANALYSIS: The pooled population included 23,000 women. Relative risks were combined for each endpoint to form summary risk ratios (RR) using meta-analytic techniques based on a random-effects model. Summary RR's were converted to numbers needed to treat (NNT). Data were dichotomized by age to approximate menopausal status (30 to 54 years, and 55 years and older), and by race (white and African American). MAIN RESULTS: In women ages 55 years or older (90% white), hypertension treatment results in a 38% risk reduction in fatal and nonfatal cerebrovascular events (95% confidence interval (CI) 27-47%, 5 year NNT 78), a 25% reduction in fatal and nonfatal cardiovascular events (95% CI 17-33%, 5 year NNT 58), and a 17% reduction in cardiovascular mortality (95% CI 3-29%, 5 year NNT 282). In women ages 30 to 54 years (79% white), hypertension treatment results in a 41% risk reduction in fatal and nonfatal cerebrovascular events (95% CI 8-63%, 5 year NNT 264), and a 27% risk reduction in fatal and nonfatal cardiovascular events (95% CI 4-44%, 5 year NNT 259). Hypertension treatment in African American women (mean age 52 years) reduced the risk of fatal and nonfatal cerebrovascular events by 53% (95% CI 29-69%, 5 year NNT 39), fatal and nonfatal cardiovascular events by 45% (95% CI 18-63%, 5 year NNT 21), fatal and nonfatal coronary events by 33% (95% CI 6-52%, 5 year NNT 48), and all cause mortality by 34% (95% CI 14-49%, 5 year NNT 32). Analyses in white women 30 to 54 years old did not show any statistically significant treatment benefit or harm. REVIEWER'S CONCLUSIONS: Hypertension treatment lowers the relative and absolute risk of cardiovascular morbidity and mortality in women ages 55 years and older, and in African American women of all ages. A greater effort should be made to increase awareness and treatment in these groups of women. Although relative risk reductions for cerebrovascular and cardiovascular events are similar for younger and older women, the NNT of younger women is at least 4 times higher. Decisions for treatment of hypertension in younger white women should be influenced by the individual patient's absolute risk of cardiovascular disease.
Adult↗
Acute impairment of relaxation by low levels of testosterone in porcine coronary arteries.
OBJECTIVES: While there are many suggested reasons for the marked gender bias in cardiovascular events, much of the available data indicate that circulating estrogens are cardioprotective. The possibility that endogenous androgens may be detrimental to the cardiovascular system has received relatively less attention. We investigated the short-term modulatory effects of various concentrations of testosterone on vascular function in isolated porcine coronary artery rings. RESULTS: The higher concentrations (> 1 microM) of testosterone relaxed U46619-contracted coronary artery rings in an endothelium-independent manner. This direct effect was insensitive to the testosterone receptor antagonists, flutamide and cyproterone acetate. Short-term exposure (20 min) to low levels of testosterone (1-100 nM), which were ineffective on their own on vascular function, significantly diminished relaxation to bradykinin and calcium ionophore A23187 but not those produced by levcromakalim and sodium nitroprusside. The inhibitory effect observed with 1 nM testosterone was only partially reversed by flutamide and cyproterone acetate and unaltered in the presence of actinomycin D and cycloheximide. CONCLUSIONS: These results demonstrate that acute treatment with testosterone, at concentrations that have no effect on their own, reduces vasorelaxation. Furthermore, they suggest that this modulatory action may be in part independent of the classical testosterone receptor since it was not completely sensitive to the anti-androgens and was not inhibited by the transcriptional and translational inhibitors. These findings support the postulation that testosterone may have unfavorable influences on vascular function.
15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
Predictive value of quantitative PCR-based viral burden analysis for eight human herpesviruses in pediatric solid organ transplant patients.
Human herpesviruses can cause significant morbidity and mortality in pediatric solid organ transplant recipients. It was hypothesized that viral burden quantification by polymerase chain reaction using an internal calibration standard could aid in distinguishing between viral disease and latency. Here we report the results of a 2-year prospective study of 27 pediatric solid organ (liver, kidney, or heart) transplant recipients in which multiple samples were analyzed for levels of all eight human herpesviruses by internal calibration standard-polymerase chain reaction. Herpes simplex viruses 1 and 2, varicella-zoster virus, and Kaposi's sarcoma-associated herpesvirus were not detected in any of these samples. Human herpesvirus types 6 and 7 were detected in half of the patients, but were present at low levels, similar to those found in reference populations. Epstein-Barr virus (EBV) and cytomegalovirus (CMV) were detected in 89% and 56% of the patients, respectively. Viral burden analysis suggested distinct patient populations for CMV, with a natural cutoff of 10,000 viral targets/ml blood strongly associated with disease. In some cases, a dramatic increase in CMV levels preceded clinical evidence of disease by several weeks. EBV viral burden was relatively high in the only patient presenting with an EBV syndrome. However, two other patients without evidence of EBV disease had single samples with high EBV burden. Rapid reduction in both EBV and CMV burden occurred with antiviral treatment. These data suggest that viral burden analysis using internal calibration standard-polymerase chain reaction for CMV, and possibly other herpesviruses, is an effective method for monitoring pediatric transplant patients for significant herpesvirus infection and response to therapy.
Adolescent↗
Acetylcholine-mediated relaxation in rat thoracic aorta is enhanced following acute exposure to physiological concentrations of 17beta-estradiol.
We investigated the effects of short-term exposure to low concentrations of 17beta-estradiol on vasorelaxation using an in vitro rat thoracic aortic ring preparation. Supraphysiological levels of 17beta-estradiol directly relaxed phenylephrine-contracted rings. Although acute incubation (20 min) with 1-100 nM of the female sex hormone did not have any significant effect on phenylephrine-contracted rings, relaxation evoked by acetylcholine was significantly potentiated. In contrast, calcium ionophore A23187-elicited endothelium-dependent relaxation as well as cromakalim- and sodium nitroprusside-mediated endothelium-independent relaxation was unchanged following the same regime with 17beta-estradiol. These results demonstrate that short-term treatment with physiologically relevant levels of 17beta-estradiol, which on their own have no effect, enhances endothelium-dependent relaxation by acetylcholine. The vascular effects observed herein may partly account for some of the improved acute vasodilatory responses reported with 17beta-estradiol on blood flow in humans.
Acetylcholine↗
Differential effects of 17beta-estradiol and testosterone on the contractile responses of porcine coronary arteries.
1. We investigated the effects of short-term exposure to physiological levels of 17beta-estradiol and testosterone on vasocontractile responses in porcine coronary artery rings. 2. Concentration-response curves to endothelin-1, 5-hydroxytryptamine, the thromboxane analogue U46619 and KCl were constructed in endothelium-intact and endothelium-disrupted artery rings. 3. Thirty minutes exposure to 17beta-estradiol (1 and 30 nM) significantly attenuated vasoconstriction to endothelin-1, 5-hydroxytryptamine and U46619. Conversely, the same concentrations of testosterone significantly potentiated responses elicited by these contractile agents. These inhibitory effects of 17beta-estradiol and enhancing actions of testosterone on contractions were endothelium-independent. KCl-mediated contractions were unaffected by the presence of either sex hormones. 4. The oestrogen receptor antagonists, tamoxifen (10 microM) and ICI 182,780 (10 microM), were unable to reverse the inhibitory influence 1 nM 17beta-estradiol had on the agonist-mediated contractile responses. Similarly, the androgen receptor antagonists, flutamide (10 microM) and cyproterone acetate (10 microM), failed to affect the potentiating activities of 1 nM testosterone. The alteration in vasoconstrictive responses observed following acute exposure to either 1 nM 17beta-estradiol and 1 nM testosterone were apparent even in the presence of the protein synthesis inhibitor cycloheximide (10 microM) and the transcription inhibitor actinomycin D (10 microM). 6. In conclusion, we report a unique type of sex hormone action on the coronary vasculature. These events occur at low nanomolar concentrations of 17beta-estradiol and testosterone, are insensitive to conventional sex hormone receptor antagonists, are not blocked by de novo protein synthesis inhibitors and have rapid time-courses that are uncharacteristic of classical genomic activities.
15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
Regulation of proximal tubule transport by endogenously produced angiotensin II.
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Angiotensin II↗
Acute vision loss in children with autosomal recessive polycystic kidney disease.
Patients with autosomal recessive polycystic kidney disease (ARPKD) often present with renal insufficiency and hypertension. We present two children with ARPKD and end-stage renal disease who developed anterior ischemic optic neuropathy and vision loss. Anterior ischemic optic neuropathy occurs rarely in children and has never been reported in children with ARPKD or end-stage renal disease. Both of our patients were chronically hypotensive and anemic, which are known risk factors for ischemic optic neuropathy.
Anemia↗
Effect of luminal angiotensin II receptor antagonists on proximal tubule transport.
The proximal tubule can endogenously synthesize and secrete luminal angiotensin II at a concentration approximately 100- to 1000-fold higher than that in the systemic circulation. We have recently shown that this endogenously produced and luminally secreted angiotensin II regulates proximal tubule volume reabsorption, which is a reflection of sodium transport within this segment. In this study, we use in vivo microperfusion of angiotensin II receptor antagonists into the lumen of the proximal tubule to examine the role of the luminal AT1 and AT2 receptor in the regulation of volume reabsorption. Systemically administered (intravenous) AT1 and AT2 receptor antagonists, acting through basolateral angiotensin II receptors, have previously been shown to inhibit proximal tubule transport. Luminal perfusion of 10(-6) mol/L Dup 753 (AT1 antagonist) and 10(-6) mol/L PD 123319 (AT2 antagonist) decreased proximal tubule volume reabsorption from 2.94 +/- 0.18 to 1.65 +/- 0.18 and 1.64 +/- 0.19 nL/mm x min, respectively, P < .01. Luminal perfusion of 10(-4) mol/L CGP 42112A, another AT2 antagonist, similarly decreased volume reabsorption to 1.32 +/- 0.36 nL/nm x min, P < .01. The inhibition of transport with AT1 and AT2 antagonist was additive, as luminal perfusion of 10(-6) mol/L Dup 753 plus 10(-6) mol/L 123319 resulted in a decrease in volume reabsorption to 0.41 +/- 0.31 nL/mm x min, P < .001 v control, P < .05 v Dup 753, and P < .01 v PD 123319. These results show that endogenously produced angiotensin II regulates proximal tubule volume transport via both luminal AT1 and AT2 receptors.
Angiotensin II↗
Acute exposure to a low level of testosterone impairs relaxation in porcine coronary arteries.
1. While the gender bias associated with coronary artery disease has been suggested to be partially accounted for by the protective effects of oestrogens, the role of testosterone remains unclear. The aim of the present study was to determine whether vasorelaxation could be affected by acute administration of testosterone with and without 17 beta-oestradiol. 2. Precontracted porcine coronary artery rings were relaxed with sodium nitroprusside (SNP), levcromakalim, bradykinin (BK) or A23187. At 1 nmol/L, testosterone impaired relaxations to BK and A23187, while the same concentration of 17 beta-oestradiol potentiated levcromakalim- and SNP-induced relaxations. The impairment of relaxation responses by testosterone was reduced in the presence of 17 beta-oestradiol, while the enhancement by 17 beta-oestradiol was decreased by testosterone. 3. We demonstrate that a low level of testosterone can impair agonist-induced relaxation, an effect that is reduced by 17 beta-oestradiol. This further supports evidence indicating a detrimental role for testosterone in coronary artery disease and suggests that circulating levels of testosterone may undermine the beneficial effects of oestrogen in women.
Animals↗
Efficacy of treating hypertension in women.
OBJECTIVE: To assess whether the relative and absolute benefit of hypertension treatment in women varies with age or race. DESIGN: Systematic review of studies from 1966 to 1998 using MEDLINE, reviews, and consultation with experts. Eleven randomized controlled trials of pharmacologic treatment of prJgiary hypertension with cardiovascular morbidity and mortality outcomes were selected, with a pooled population of 23,000 women. Relative risks were combined for each end point to form a summary risk ratio using meta-analytic techniques based on a random-effects model. Summary risk ratios were converted to numbers needed to treat (NNTs). Data were dichotomized by age to approxJgiate menopausal status (30 to 54 years, and 55 years and older), and by race (white and African American). MAIN RESULTS: In women aged 55 years or older (90% white), hypertension treatment resulted in a 38% risk reduction in fatal and nonfatal cerebrovascular events (95% confidence interval [CI] 27%, 47%; 5-year NNT 78), a 25% reduction in fatal and nonfatal cardiovascular events (95% CI 17%, 33%; 5-year NNT 58), and a 17% reduction in cardiovascular mortality (95% CI 3%, 29%; 5-year NNT 282). In women aged 30 to 54 years (79% white), hypertension treatment resulted in a 41% risk reduction in fatal and nonfatal cerebrovascular events (95% CI 8%, 63%; 5-year NNT 264), and a 27% risk reduction in fatal and nonfatal cardiovascular events (95% CI 4%, 44%; 5-year NNT 259). Hypertension treatment in African-American women (mean age, 52 years) reduced the risk of fatal and nonfatal cerebrovascular events by 53% (95% CI 29%, 69%; 5-year NNT 39), fatal and nonfatal cardiovascular events by 45% (95% CI 18%, 63%; 5-year NNT 21), fatal and nonfatal coronary events by 33% (95% CI 6%, 52%; 5-year NNT 48), and all-cause mortality by 34% (95% CI 14%, 49%; 5-year NNT 32). Analyses in white women aged 30 to 54 years did not show any statistically significant treatment benefit or harm. CONCLUSIONS: Hypertension treatment lowers the relative and absolute risk of cardiovascular morbidity and mortality in women aged 55 years and older and in African-American women of all ages. A greater effort should be made to increase awareness and treatment in these groups of women. Although relative risk reductions for cerebrovascular and cardiovascular events are sJgiilar for younger and older women, the NNT of younger women is at least 4 tJgies higher. Decisions about treatment of hypertension in younger white women should be influenced by the individual patient's absolute risk of cardiovascular disease.
Adult↗
Endogenous angiotensin II modulates rat proximal tubule transport with acute changes in extracellular volume.
In the present study, we examined whether the effect of endogenously produced angiotensin II on proximal tubule transport in the male Sprague-Dawley rat is regulated by acute changes in extracellular volume. We measured the magnitude of endogenous angiotensin II-mediated stimulation of transport by sequentially perfusing proximal tubules in vivo, first with an ultrafiltrate-like solution, then by reperfusion of the same tubule with an ultrafiltrate-like solution containing 10(-8) M losartan (angiotensin II receptor antagonist). During volume contraction, 10(-8) M losartan decreased volume reabsorption from 4.20 +/- 0.50 to 1.70 +/- 0.30 nl . mm-1 . min-1 (P < 0.05), a decrease of 58.0 +/- 7.0%. In contrast, after acute volume expansion, 10(-8) M losartan decreased volume reabsorption from 1.84 +/- 0.20 to 1.31 +/- 0.20 nl . mm-1 . min-1 (P < 0.05), a decrease of 29.6 +/- 9.0%. In hydropenic rats, addition of exogenous luminal angiotensin II had no effect on transport. However, in volume-expanded rats, addition of 10(-8) M angiotensin II increased volume reabsorption from 2.10 +/- 0.34 to 4. 38 +/- 0.59 nl . mm-1 . min-1 (P < 0.005). These data are consistent with endogenously produced angiotensin II augmenting proximal tubule transport to a greater degree during volume contraction than after volume expansion.
Absorption↗