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M Cacciari

Publications and source records attributed to M Cacciari.

At least 73 records · Page 4Linked to original sources
PubMed1980

[Suppression, by beta-adrenergic receptor blockade, of the sympathomimetic component of dopamine renal action in water-saline depletion].

The effects of beta-adrenergic receptor blockade on the renal action of Dopamine (DA) in hydro-saline depletion were investigated in 9 healthy subjects. The beta-adrenergic blocking treatment was performed (Propranolol hydrochloride 2.4 mg/kg b.w. per day) during the 2 days preceding the renal function studies. For other experimental details, see our previous Note (11). In the presence of beta-adrenergic blockade DA effects in hydro-saline depletion consisted of: a) an increase in both RPF and GFR; b) a decrease in sodium abnormally isoosmotic reabsorption as % of sodium distal load; c) an increase in both sodium and osmolar clearances; d) an increase in free water clearance higher than that observed in the absence of blocking treatment. Therefore, the sympathomimetic effects of DA in hydro-saline depletion appear to be suppressed by beta-adrenergic blockade. It is suggested that such sympathomimetic action of DA may be mediated by beta-presynaptic receptors of noradrenergic nerve endings.

Adrenergic beta-Antagonists↗
PubMed1980

[Sympathomimetic component of dopamine renal action in water-saline depletion].

In 20 healthy subjects hydro-saline depletion was achieved by a 4-day natriuretic treatment associated with hypo-saline diet. Dopamine (DA) was infused in subpressor dose (.1 microgram . kg-1 . min-1) during sustained hypotonic polyuria induced by 5% glucose infusion. Four 15-min clearance periods were performed. DA was infused during the 2nd and the 3rd period. The effective renal plasma flow (RPF) as well as the glomerular filtration rate (GFR) were calculated by PAH and creatinine clearances, respectively. In our experimental conditions DA produced: a) an increase in the abnormally isoosmotic sodium reabsorption as % of sodium distal load; b) a decrease in both sodium and osmolar clearance; c) an early increase in free water clearance. RPF and GFR decreased not significantly. The present results indicate that DA in hydro-saline depletion helps to preserve the extracellular fluid volume in minimizing the salt and water loss associated with hypotonic polyuria. These effects on sodium excretion may be related to sympathomimetic properties acquired by DA in this experimental condition.

Creatinine↗
PubMed1980

[Dopamine and renal homeostatic control of osmolarity and extracellular fluid volume in initial conditions of hydro-saline depletion and retention. I. Renal functional parameters].

Renal effects of dopamine (DA) infusion (0,1 micrograms.kg-1.min-1) in healthy human subject are strongly dependent on the basal condition of the extra-cellular fluid volume. The renal vasodilation and the inhibition of isosmotic sodium reabsorption (as % of sodium filtered load) induced by DA in hydro-saline retention are highly blunted in hydro-saline depletion. Moreover the inhibitory effect on anisosmotic sodium reabsorption (as % of sodium distal load), observed in hydro-saline retention, is reversed in hydro-saline depletion. Thus, DA is likely to behave as a sodium excretion regulator.

Adult↗
PubMed1980

[Dopamine and renal homeostatic control of osmolarity and extracellular fluid volume in initial conditions of hydro-saline depletion and retention. II. Relationship between the renal functional parameters].

In hydro-saline depletion dopamine (DA) infusion (0,1 microgram.kg-1.min-1) elicits different renal effects than it does in hydro-saline retention. It is suggested that in hydro-saline depletion DA activates, besides vasal DA receptors, also vasal and tubular adrenergic receptors. Such adrenergic activation, either direct or presynaptically mediated, can account for both the decrease in the hyperemic response and the increase in the anisosmotic sodium reabsorption.

Adult↗
PubMed1980

[Sulpiride and renal action of dopamine in hydro-saline depletion in humans].

The effect of sulpiride (racemic form) pretreatment on renal action of dopamine (DA) has been investigated in 8 hydro-saline depleted human subjects. Two studies were carried out in the presence and in the absence of sulpiride, respectively. DA was infused in a subpressor dose (0,1 microgram.kg-1 . min-1) during induced hypotonic polyuria. The experimental results suggest that tubular DA effects are enhanced whilst glomerular DA effects are reversed by the presence of sulpiride.

Adult↗
PubMed1979

[Dopamine hydro-natriuresis. - II) Interactions of dopamine and expansion of extracellular liquid volume].

We have observed that in the presence of salt retention (DOCA pretreatment) dopamine (DA) promoted a hydro-natriuretic effect; in contrast in salt depletion (natriuretic pretreatment) the changes in sodium tubular reabsorption and in urinary flow were non significant. The present study was designed to identify the possible mechanisms underlying the hydro-natriuretic effect. DA was infused at a subpressor rate (0,1 microgram/kg . min) during induced hypotonic polyuria. 19 healthy human subjects at different degree of salt retention were studied. The results demonstrate that the tubular inhibitory effects produced by DA on the % sodium reabsorptions (total as % of sodium filtered load, anisosmotic as % of sodium distal load) are the higher the lower are the control values of these reabsorptions. Hence DA appears to act by enhancing the inhibitory tubular response elicited by salt retention. Moreover these inhibitory effects are positively related with the simultaneous DA-induced haemodynamic effects. This suggests that the decrease in sodium reabsorptions during DA infusion is haemodynamically mediated.

Adult↗
PubMed1979

[Sulpiride and the effect of dopamine on the kidney in human salt retention].

Experiments were performed to investigate the renal interaction between dopamine (DA) and sulpiride (S), an antagonistic drug for the central dopaminic receptors. DA was infused at a subpressor rate (0,1 microgram/kg . min) during induced hypotonic polyuria. In 8 healthy subjects in a condition of salt retention (DOCA pretreatment) two successive studies were carried out in the presence and in the absence of S. The drug treatment was started two days before the experiment. BOth the renal response to hydration and the renal effects of DA are modified by S treatment. 1) S enhances the hydro-saluretic effect produced by hydration. 2) During the early period of DA infusion, S counteracts the increase DA-induced in renal plasma flow. However the inhibitory tubular effects and the increase in the hydro-saluresis produced by DA are not significantly different from those observed in the absence of the drug.

Adult↗
PubMed1975

[Physiological basis of homeostasis of the extracellular fluid volume].

Renal, glomerular and tubular, factors responsible for the volume control of extracellular liquid were examined. The part played by angiotensin II in mediating the compensation of this liquid losses was studied in patients with spontaneous polyuria due to diencephalo-posthypophyseal diabetes insipidus or psychogenic polydipsia and healthy subjects with induced hypotonic polyuria. It was noted that: 1) acute expansion elicited a natriuretic response and increased distal sodium load, due to an increase in filtrate and relative inhibition of proximal reabsorption, or proximal inhibition if the filtrate was unchanged. The efficiency of distal sodium transport was often unchanged. 2) Return to sodium balance parity during prolonged expansion of volume, was accomplished by varying renal means, in accordance with the experimental model employed. Distal reabsorption was essentially depressed during prolonged saline load (secondary hypoaldosteronism). When protracted mineralcorticoid treatment was used, however, distal reabsorption was high, even in the escape stage, and its saturation required marked augmentation of the sodium load reaching the distal tubules. 3) Depletion of volume caused by protracted natriuretic treatment in spontaneous polyuria reduced both diuresis and sodium excretion. This resistance to the natriuretic effect of the drug followed intrarenal compensation that reduced the distal sodium load and encouraged reabsorption in some distal sites (secondary hyperaldosteronism). 4) Infusion of angiotensin II in sub- or pauci-pressor doses causes an isosmotic sodium saving, since it reduced the glomerular filtrate and increases the fraction of filtrate reabsorbed by the proximal tubules; the tubular effect is likely secondary to increased vascular, especially postglomerular resistance. In the healthy subject, angiotensin II leads to antidiuresis referable, on account of its intensity and longer time cycle, to ADH release angiotensin-dependent.

Angiotensin II↗