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Evidence for an intestinal mechanism in hypercalciuria of spontaneously hypertensive rats.
TLDR
The adult SHR is characterized by increased Ca retention due to primary hyperabsorption, absorptive hypercalciuria, and increased bone Ca deposition, independent of sex, parathyroid hormone, and treatment of the established hypertension.
Multiple carriers for dipeptide transport: carrier-mediated transport of glycyl-L-proline in renal BBMV.
TLDR
Measurements in the presence of valinomycin and an outwardly directed K+ gradient strongly suggest that H(+)-stimulated uptake at both concentrations is electrogenic, and competitive inhibition of Gly-Pro transport was demonstrated for the dipeptides Gly-Gly and Gly-Sar.
Evidence against the role of calcium deficiency in genetic hypertension.
TLDR
Evaluating the blood pressure response in spontaneously hypertensive rats (SHR) as calcium balance was decreased by dietary restriction of calcium or increased by supplementation with magnesium or 1 alpha, 25-dihydroxycholecalciferol (calcitriol) refutes the existence of calcium deficiency at this normotensive stage and does not support the role ofcium deficiency in genetic hypertension.
Chronic DOCA treatment increases Ca absorption: role of hypercalciuria and vitamin D.
TLDR
Data best fit the hypothesis that increased Ca absorption is secondary to the calciuric effects of DOCA and high-salt diet and is mediated via the increased parathyroid hormone and 1,25-dihydroxyvitamin D3 activities.
Renal responses to calcium deprivation in young rabbits.
TLDR
There are rapidly induced, appropriate renal homeostatic adaptations to dietary Ca deprivation in the rabbit and it is suggested that increases in endogenous plasma parathyroid hormone concentration, in part, play a role in mediating these changes.
Nephrotic syndrome and acute renal failure associated with hepatitis A virus infection.
TLDR
This case report is the first English documentation associating HAV infection with immune complex mesangial proliferative glomerulonephritis associated with nephrotic syndrome.
Activation of proximal tubular Na(+)-H+ exchange by angiotensin II.
TLDR
The data indicate that the Vmax effect is caused by an apparent increase in the number (density) of active Na(+)-H+ carriers present in the luminal membrane, and the possibility that the observed kinetic change involves an exocytic mechanism was tested.
Esophageal carcinoma presenting with nephrotic syndrome: association with anti-neutrophil cytoplasmic antibody.
TLDR
A patient with an otherwise asymptomatic squamous cell carcinoma of the esophagus whose presenting manifestation was membranous glomerulonephritis and nephrotic syndrome was reported, and perinuclear anti-neutrophil cytoplasmic antibody was positive.
Carrier-mediated transport of pyroglutamyl-histidine in renal brush border membrane vesicles.
TLDR
This study demonstrates the existence of a high-affinity, low-capacity H+ cotransport system for pGlu-His in the proximal tubular luminal plasmalemma, which appears to be specific for pyroglutamyl-containing dipeptides.
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