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The regulation of aquaporin-2 (AQP2) water channel excretion in the collecting duct depends mainly on the action of vasopressin (AVP). Recently, however, other regulatory factors have been identified: atrial natriuretic factor, oxytocin and prostaglandins. In healthy volunteers (5 males, 5 females; mean age 23 ± 3 years) we therefore evaluated the effect of a stable analogue of prostacyclin-2 (PGI[sub 2] ), iloprost, on renal function and on the urinary excretion of AQP2 (U-AQP2). After 6 h of iloprost infusion, U-AQP2 increased from 0.8 ± 0.15 to 1.8 ± 0.2 pmol/mg creatinine (p < 0.001), while the urinary flow rate increased from 1.4 ± 0.2 to 1.8 ± 4 (p < 0.01). No significant change was found in the AVP serum concentration, with a basal value of 3.17 ± 0.12 vs. 3.15 ± 0.12 pg/ml after 6 h of prostacyclin infusion. All the values returned to pre-study levels after a recovery period of 6 h. In conclusion, the PGI[sub 2] analogue, iloprost, can induce U-AQP2 excretion independent of AVP.Copyright © 2002 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

The article analyzes potential non-lipid-lowering uses of statins in the kidney. A crucial factor in normal tissue turnover in adult humans is the maintenance of a constant number of cells forming the tissue. This ensures cell renewal and regulates the delicate balance between cellular proliferation and death or apoptosis. In diseases ranging from glomerulonephritis to hypertension, renal damage frequently leads to cellular proliferation, that triggers a chronic mechanism which can cause permanent loss of renal function. Statins can influence this balance. Cholesterol, an essential component in the cellular membrane, is required for cell proliferation. By playing a part in the uptake of lipids in glomeruli, macrophages may also play a decisive role in lipid induced glomerulosclerosis. In conclusion, lovastatins, such as all lipophilic statins, can trigger apoptosis in cultures of smooth muscle cells of rats and humans. As confirmed by findings, fluvastatin has a pro-apoptotic effect both on cultured human smooth muscle cells, and on cultured vero monkey renal cells. As suggested by findings, and considering the marked effect that statins have on cell proliferation, apoptosis and cell cycle progression, and on the basis of in vivo and in vitro evidence, these drugs might be used for a wide range of proliferative diseases, like progressive glomerulonephritis, ischemic nephropathy, chronic nephropathy following transplantation and polycystic disease.

The effect of a static magnetic field (MF) of 0.5 mT of intensity on the cell proliferation/cell death balance was investigated in renal cells (VERO) and cortical astrocyte cultures from rats. Magnetic stimulation was delivered by magnetic disks at known intensities. The percentage of apoptotic and necrotic cells was evaluated using flow cytometry and morphological analysis following Hoechst chromatin staining. An index of cell proliferation was determined using sulfonated tetrazolium (WST-1). Control cultures were prepared without exposure to MFs. After 2, 4 and 6 days of exposure to a MF, we observed a gradual decrease in apoptosis and proliferation and a gradual increase in cells with a necrotic morphology with respect to the control group. In astrocyte cultures, over a 6-day exposure period. A gradual increase was observed in apoptotic, proliferating, and necrotic cells. Our findings suggest that the effect of exposure to MFs varies, depending on the cell type; MFs may also have a nephropathogenic effect. Copyright © 2001 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Many previous studies have shown that aquaporin-2 (AQP2), the vasopressin-regulated water channel, is excreted in the urine and that the excretion increases in response to vasopressin. Moreover, recently a close correlation between AQP2 excretion in urine and kidney AQP2 expression has been demonstrated, showing that urinary excretion of AQP2 is a reliable indicator for AQP-2 function. As head-out water immersion causes an expansion in the central vascular volume equal to that induced by 2 liters of saline, without modifying plasma composition, we used immersion in water to evaluate if the response to acute expansion of the central vascular volume could involve vasporessin (AVP) and AQP2. In healthy subjects, concentrations of plasma atrial natriuretic factor (ANF) and AVP, and urinary AQP2 were measured during a 2-hour immersion period. In all subjects, immersion caused a prompt and marked increase in immunoreactive ANF (23.0 ± 2.12 pg/ml at second hour vs. 2.17 ± 0.42 pg/ml at baseline) and in urinary excretion of AQP2 (23.9 ± 2.69 pmol/mg creatinine at second hour vs. 4.42 ± 0.14 pmol/mg creatinine at baseline), while a significant decrease was found in plasma AVP. Recovery was associated with a prompt return to pre-study levels. These findings demonstrate that heat-out water immersion stimulates urinary excretion of AQP2 in absence of an increase in plasma AVP.Copyright © 2000 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Focuses on hemodynamic effects of recombinant human erythropoietin. Role of kidney in producing erythropoietin; Impact of erythropoietin on erythroid cells; Overview of the study conducted to show how human erythropoietin therapy induces hypertension or aggravates pre-existing hypertension.

Presents a letter to the editor about an increase of serum levels by administration of erythropoietin.