The literature on hydronatriuresis control processes operating at the level of individual renal functional units and of the organ as a whole is analysed. 1) Elementary sodium salt and water tubular transport mechanisms. In converting the filtrate into urine, the kidney expends metabolic energy: this is used in the (active) transport of sodium salts; (passive) transport of water takes place along the osmotic gradients created by salt transfer. The proximal tubules reabsorb the sodium bic-rbonate actively. The reabsorption of the osmitic equivalent of water has the effect of concentrating NaCl in the tubular fluid. An important role in the reabsorption of NaCl is played by passive diffusion from the lumen to the interstitial fluid; the remainder is transferred actively, perhaps by an electrically neutral pump. With respect to the other nephronic segments, the proximal tubule has a relatively high passive permeability to water and salts: active transport here must not surmount high friction resistances nor take place against important concentration gradients. The low permeability of the distal nephron, on the other hand, increases the energy cost of salt transport; for the same reason, important electrochemical gradients are created and the composition of tubular fluid is drastically altered. 2) Elementary mechanisms of tubular potassium transport. Potassium is reabsorbed actively along the whole nephron by a luminal pump. The proximal tubules and Henle loops promote practically complete absorption of filtrated potassium. The distal tubules and collectors have the two-fold capacity of secreting and reabsorbing cation: the quantity of potassium excreted with the urine depends on the degree of excess of the secretion process. At distal tubular level, potassium secretion is a passive phenomenon dependent on the favourable transluminal gradient of the cation's electrochemical potential. 3) Renal function and volume homoeostasis of extracellular fluid. The organism's sodium content is largely controlled by renal excretion of sodium; homoeostasis of the sodium mass guarantees volume homoeostasis of the extracellular fluid through thirst and osmotic secretion of ADH. Extracellular fluid volume errors are picked up by the organism to the extent to which they translate themselves into pressure variations in the low pressure vascular system or into variations in haematic constituent concentration within the vascular sector, produced with velocities independent, at least in the short term, of the volume of extracellular fluid. In control of natriuria are the glomerular filtrate, intrarenal distribution of blood flow and tubular reabsorption of sodium; in its turn, the latter is subject to nervous and hormonal influences and influences from the physical environment surrounding the nephrons...

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PubMed1974

[Angiotensin II: its possible role in homeostasis of extracellar fluid volume].

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Aldosterone↗

PubMedDate not supplied

Association of cyclosporine and 311 nM UVB in the treatment of moderate to severe forms of psoriasis: a new strategic approach.

Psoriasis is a T-lymphocyte mediated autoimmune disease. The response to therapies targeting T-lymphocytes suggest that the latter is a key cell in the pathogenesis of the disease. Cyclosporine (CsA) inhibits the proliferation and the IL-2 dependent expansion of T-lymphocytes. Ultraviolet radiation is an effective treatment for psoriasis. Several studies have demonstrated a significant improvement of the therapeutic response when narrow-band radiation is issued by TL-01 fluorescent lamp compared to broad- band UVB issued by other fluorescent sources. The effects of UVB on the immune system appear to be limited to the cell-mediated compartment of the immune response. In order to reduce the cumulative dose of UVB and limit the toxicity of drugs in the therapy of psoriasis, phototherapy with UVB has been used as treatment in association with other standard therapies. The purpose of the study is to evaluate, in patients with moderate to severe psoriasis a combined therapy with Cyclosporine A and 311 nm UVB phototherapy.

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Disseminated granuloma annulare: efficacy of cyclosporine therapy.

Granuloma annulare is an anatomo-clinical entity that is frequently encountered in everyday dermatological practice. We report our experience regarding 4 patients with disseminated granuloma annulare. Each patient was treated with a cycle of cyclosporine therapy for six weeks. A cycle of systemic cyclosporine therapy was started at a dose of 4 mg/kg/day for four weeks, subsequently reduced by 0.5 mg/kg/day every two weeks. The clinical picture more or less completely resolved within three weeks in all of the patients, and there were no relapses during the dose-tapering period or the following 12 months. Cyclosporine was optimally tolerated by all four patients, none of whom experienced any therapy-related side effects. Cyclosporine is a valid therapeutic option for the treatment of disseminated granuloma annulare, although we recommend its use in a protected hospital environment that facilitates patient monitoring.

Cyclosporine↗

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[Dopamine, catecholamine receptors, and neurohumoral regulation of renal function].

Were studied in healthy human subjects under conditions of hydro-saline retention the intrarenal mechanism underlying the hydronatriuretic effect of Dopamine (DA) and the changes in DA renal effects induced by Sulpiride (S). DA was infused i.v. in a subpressor dose (0,1 microgram/kg . min) during induced hypotonic polyuria. In each experiment four clearance periods of 15 min were performed; DA was administered during the second and third clearance periods. The glomerular filtration rate and renal effective plasma flow were estimated as endogenous creatinine and PAH clearances, respectively. Tubular sodium and potassium reabsorptions were also determined. 1) In the state of hydro-saline retention, renal arteriolar (mainly preglomerular) vasodilation was produced by DA. Moreover, both sodium isosmotic reabsorption as a percentage of sodium filtered load and sodium anisosmotic reabsorption as a percentage of sodium distal load were inhibited. These tubular inhibitions were found to be correlated with the haemodynamic effects of DA. 2) Sulpiride treatment (4,4 mg/kg . day given orally for two days prior to the experiment and 100 mg i.m. 40 min before DA infusion) caused (a) an increase in the hydro-natriuretic response to hydration during control clearance and (b) a decrease in DA haemodynamic effects. An interpretation is proposed accounting for these DA effects as well as for dependence of DA renal effects on the extracellular fluid volume.

Adult↗

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[Extrinsic catecholaminergic control of the renal function during water and salt depletion].

Renal function was studied by means of the clearance method in the healthy subject during hypotonic polyuria induced in initial depletion conditions with or without adrenolytic treatment. Three experiments were performed: a) 19 in water-salt depletion; b) 9 in depletion associated with (+/-)-propranolol; c) 9 in depletion associated with prazosin. 15' clearance periods were carried out during control, dopamine infusion in a subpressor dose (0.1 microgram x kg-1 x min-1) and after suspension, respectively. PAH and endogenous creatinine clearance was also determined, Propranolol made no significant difference to renal function by comparison with simple depletion, whereas the more intense depletive effect of prazosin lead to a significant reduction in renal plasma flow and the glomerular filtration rate. Isosmotic and anisosmotic reabsorption of sodium (in % of the respective loads) was inhibited despite reduction of the filtrate and of the distal sodium load. Dopamine was ineffective as a vasodilator and natriuretic in water and salt depletion, while it displayed significant sodium-retaining properties. Pretreatment with propranolol and prazosin allowed dopamine to show vasodilator and hydrosaluretic effects during depletion. These results are in line with the view that the renal vasal and tubular alpha-adrenergic receptors make a significant contribution to the water and salt conservation associated with volume depletion, and that dopamine influences renal function under these experimental conditions probably by activating prejunctional beta-adrenergic receptors of noradrenergic nerve endings.

Adult↗

PubMedDate not supplied

[Dopamine as a regulator of natriuresis. Experimental bases and their implications].

Renal effects of dopamine (DA) infused i.v. in a subpressor dose (0.1 microgram. kg.-1 min-1) were investigated in healthy human subjects during steady hypotonic polyuria. In each experiment four clearance (cl.) periods of 15 min were performed; DA was administered during the second and the third cl. periods. The glomerular filtration rate and renal effective plasma flow were estimated as endogenous creatinine and PAH clearances. Moreover the following variables were evaluated: a) sodium total and sodium isosmotic reabsorption as a % of sodium filtered load (s.f.l.); b) sodium anisosmotic reabsorption as a % of sodium distal load (s.d.l.); c) total renal vascular resistance (RT), arteriolar afferent (RA) and efferent (RE) resistances. Three groups of experiments were performed: A) in hydro-saline retention by DOCA pretreatment (24 subjects); B) in hydro-saline depletion by natriuretic pretreatment (20 subjects); C) in hydro-saline depletion and beta-adrenergic blockade induced by natriuretic and propranolol pretreatments (9 subjects). In A experimental condition DA significantly increased renal plasma flow, glomerular filtration rate, urinary flow, urine sodium concentration and osmolarity; on the contrary DA significantly decreased RT, RA, sodium total and isosmotic reabsorption, % of s.f.l., and sodium anisosmotic reabsorption, % of s.d.l. In B condition no significant changes were observed during DA infusion in either haemodynamic parameters or urinary flow; on the other hand DA significantly blunted urinary osmolarity, urinary sodium concentration and sodium excretion rate suggesting an increased sodium anisosmotic reabsorption (% of s.d.l.). In C condition the vasodilating and hydrosaluretic effects of DA were restored. Our results suggest that DA activates, besides "dopaminic" vascular receptors, the presynaptic facilitory beta-adrenergic receptors in renal adrenergic pathways. Thus the renal action of DA depends on renal adrenergic activity.

Adult↗

PubMedDate not supplied

Studies on renal function in healthy women with different degrees of induced potassium depletion. 1) Hormonal changes relevant to salt and water balance.

In healthy women we have studied the effects of potassium depletions of different degrees on the generation of some bioregulators of hydro-saline balance. The study has been performed on 20 women in normal potassium balance (N group) and 20 women submitted to potassium depletive treatment by dietary and pharmacological means. On the basis of different patterns of treatment we have obtained three groups i.e. KD1 (n = 8), KD2 (n = 6) and KD3 (n = 6) with potassium cumulative deficit of 160 +/- 43, 198 +/- 22 and 214 +/- 54 mmol, respectively. The renal function was assessed by the clearance method during induced hypotonic polyuria and subsequent moderate antidiuresis induced by low dose infusion of lysine-8-vasopressin. The urinary PGE2, 6-keto-PGF1 (6KPGF) and TxB2 were determined by the RIA method. Moreover, the basal PRA and urinary aldosterone were determined before the renal functional exploration. The data obtained in both KD2 and KD3 groups where renal hypokalemic dysfunctions occurred--indicate that hypokalemia stimulated renin secretion and inhibited the reactivity of renal prostanoid production to the polyuric stimulus. However, in the KD3 group--where the circulating levels of renin, and probably of angiotensin II were the highest--the hypokalemic depression of the synthesis of 6KPGF and TxB2 precursors was attenuated while the synthesis of PGE2 was still inhibited.

Adult↗

PubMedDate not supplied

Responses of the renal prostanoids to a short-term depletion of sodium or potassium in healthy women.

The short-term effects of extracellular fluid volume depletion on the generation of some bioregulators of the renal function have been studied in healthy women. Eight subjects (SD group) were submitted to a low NaCl dietary intake and natriuretic treatment. At the end of the treatment (6 days) a cumulative sodium deficit of 381 +/- 55 mmol (mean +/- SEM) and a body weight variation of -2.1 +/- 0.28 kg were estimated. The renal function was explored by clearance method during hypotonic polyuria induced by oral water load and subsequent antidiuresis induced by low-dose infusion of lysine-8-vasopressin. The basal values of plasma renin activity were determined just before the water load as well as the urinary aldosterone excretion of the foregoing 24 hours was. During the renal functional exploration the urinary concentrations of PGE2, 6-keto-PGF1 alpha (6KPGF) and TxB2 were determined by RIA method. We report also, as comparison terms, the results obtained either in potassium depletion (KD group, n = 12) or in normal sodium and potassium balance (N group, n = 20). 1) In the SD vs N group-besides the increase in renin and aldosterone secretion-the behaviour of urinary prostanoids is consistent with a stimulation of the renal synthesis of PGI2 and TxA2 as well as of PGE2, at least as a trend. 2) In the KD vs N group an increase in renin secretion occurred while the urinary aldosterone was not significantly decreased. The urinary prostanoid data suggest an inhibition of the renal synthesis of PGE2 and PGI2. All three urinary prostanoids were significantly lower in the KD as compared to the SD group. Thus, in salt depletion the renal prostanoid synthesis was enhanced while it was depressed in potassium depletion, despite the increased renin secretion.

Adult↗

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Interactions between acute effect of angiotensin converting enzyme inhibition and salt balance on the renal function and urinary prostanoids. Studies in healthy women.

The acute effects of angiotensin converting enzyme inhibition on the renal function and urinary prostanoids were studied. Healthy women were studied in both sodium depletion (n = 8) and normal balance of sodium and potassium (n = 6). Each woman underwent paired renal functional explorations (by the clearance method during hypotonic polyuria and subsequent antidiuresis) in the absence and in the presence of enalapril. In both experimental conditions enalapril failed to affect urinary prostanoid excretions. Only in the presence of hyperreninemia induced by salt depletion, enalapril was effective in inducing renal tubular effects only partly consistent with a depressed activity of angiotensin-aldosterone system. Specifically, in sodium depletion enalapril treatment promoted a decreasing trend in urinary salt excretion, dependent in turn on selective stimulation of the distal tubule NaCl transport. Furthermore, plasma potassium concentration was reduced despite the concomitant decrease in urinary potassium excretion.

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