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Biomedical subjects

M Cacciari

Publications and source records attributed to M Cacciari.

At least 19 recordsLinked to original sources
PubMed2000

Renal synthesis of prostacyclin and thromboxane in healthy women: differential effects of a short-term saline loading.

It is accepted that the urinary excretions of the stable metabolites of prostaglandin (PG)I2 and thromboxane(Tx) A2, 6-keto-PGF1alpha (6KPGF) and TxB2 respectively, provide an accurate estimate of both basal and stimulated renal synthesis of their precursors. The excretory profile of these metabolites has been evaluated in healthy women submitted to a short-term expansion in extracellular fluid volume. Salt retention (SR group, n=6) was induced by physiological saline (0.9% NaCl) i.v. infusions (2 L per day) over a period of 2 days. On the third day the increase in body weight was 0.92 +/- 0.27 kg (P<0.05). The results of the study have been compared to those previously obtained in normal balance of sodium and potassium (N group, n=20) and in induced salt depletion (SD group, n=14). A common study protocol was used. Basal values of plasma renin activity (PRA) and urinary aldosterone excretion were determined. Renal functional exploration [clearance (cl.) method] was performed during hypotonic polyuria (induced by oral water load) and subsequent moderate antidiuresis (induced by low-dose infusion of an antidiuretic hormone analogue). Urinary 6KPGF and TxB2 concentrations were estimated by RIA method and their urinary excretions were determined at both high and low urinary flow rates. The linear regressions of the urinary metabolite excretions vs. urinary flow rate were estimated by using the data obtained in both hypotonic polyuria and antidiuresis. Salt retention (SR vs. N group) was effective in decreasing the basal values of plasma renin activity and urinary aldosterone excretion. Moreover, during hypotonic polyuria it was effective in increasing the absolute and fractional excretions of sodium and chloride, in the absence of significant variations in mean arterial pressure and creatinine cl. Regarding urinary prostanoid excretions the following results were obtained. 1. Comparative data for hypotonic polyuria. In the SR vs. N group, the urinary excretion of 6KPGF was significantly higher, whereas that of TxB2 was not significantly different. In the SR vs. SD group, the urinary excretion of 6KPGF was not significantly different, whereas that of TxB2 was significantly lower. 2. Comparative data for the regression lines of the urinary prostanoid excretions vs. diuresis. In the SR vs. N group, the regression line slope for 6KPGF excretion was significantly higher, whereas that for TxB2 excretion was not significantly different. In the SR vs. SD group, the regression line slope for 6KPGF excretion was not significantly different, whereas that for TxB2 excretion was significantly lower. 3. Correlative data in the SR group during hypotonic polyuria. The plasma chloride concentration was positively correlated with urinary flow rate, absolute and fractional chloride excretions, and 6KPGF excretion but not with TxB2 excretion. In conclusion, functionally effective salt retention in healthy women induces a selective stimulation of renal synthesis of prostacyclin, unlike salt depletion, in which the synthesis of both PGI2 and TxA2 is upregulated.

6-Ketoprostaglandin F1 alpha↗
PubMed1999

Renal prostanoids: physiological relevance in healthy salt-depleted women.

The effective role played by prostanoids in the control of renal function has been investigated in healthy women with salt depletion. Salt depletion (SD2 group, n = 6) was induced by low sodium chloride dietary intake (< or = 60 mmol per day) and combined treatment with natriuretic and potassium-sparing drugs. At the end of the depletive treatment, the cumulative sodium deficit was 513 +/- 56 mmol. The renal function and urinary excretions of prostaglandin (PG) E2, 6-keto-PGF1 alpha (6KPGF) and thromboxane (Tx) B2 were evaluated during hypotonic polyuria. The basal values of plasma sodium and potassium concentrations, plasma renin activity (PRA) and urinary aldosterone excretion were determined before the induction of hypotonic polyuria. Paired studies were performed in the absence (control) and presence of indomethacin both in the SD2 group and in a previously studied group (N2, n = 6) of healthy women in normal sodium and potassium balance. Women in normal balance received 100 mg i.m. of indomethacin, salt-depleted women received only 50 mg (because 100 mg of the drug produced a prolonged anuria). In the SD2 vs. N2 group in the absence of treatment the following significant differences were found: (a) higher basal values of PRA and urinary aldosterone excretion; (b) higher urinary excretions of 6KPGF and TxB2 but not of PGE2; (c) lower values of urinary flow rate, creatinine clearance, absolute and fractional excretions of sodium and chloride, plasma osmolality and plasma electrolyte concentrations. The effects of the indomethacin have been assessed as percentage variations by using paired data for each experimental group. In the SD2 vs. N2 group the reduction in urinary excretions of 6KPGF, TxB2 and potassium as well as in creatinine clearance were not significantly different. On the other hand, the following were significantly different: (a) the lower reduction in PGE2 excretion; (b) the higher reduction in urinary flow rate and in CH2O; (c) the reductions in absolute and fractional excretions of sodium and chloride, and the increase in plasma potassium concentration, significant in the SD2 group but not in the N2 group. The data suggest that: (1) when stimulated by salt depletion the renal biosynthetic pathways of PGI2 and TxA2 showed greater sensitivity to indomethacin inhibition; (2) the effects of the neurohormonal systems activated by salt depletion were either modulated or mediated by renal prostanoids.

Adult↗
PubMed1999

Renal function and urinary prostanoid excretions in salt-depleted women: comparative effects of enalapril and indomethacin treatments.

The acute effects on urinary prostanoid excretion and on renal function induced by pharmacological inhibition of either the angiotensin-converting enzyme or of the cyclooxygenase system, respectively, have been studied in healthy salt-depleted women. Two experimental groups were studied during salt depletion, SD1 (n=8) and SD2 (n=6). Salt depletion was obtained by combining a low sodium chloride dietary intake (< or =60 mmol per day) with natriuretic and potassium sparing treatment. Paired studies were performed in the absence and in the presence of enalapril (SD1 group) or indomethacin (SD2 group). In both paired studies renal function was estimated by the clearance (cl.) method and the urinary concentrations of PGE2, 6-keto-PGF1alpha and TXB2 were estimated by RIA during sustained hypotonic polyuria (induced by oral water load). Enalapril did not influence urinary excretion of prostanoids. Its main significant effects were: (a) a reduction in mean arterial pressure (MAP); (b) an increase in free-water cl. (C(H2O)) and a reduction in osmolar cl. (Cosm); (c) a reduction in the absolute and fractional urinary excretions of sodium and chloride; and (d) a reduction in both the plasma concentration and urinary excretion of potassium. The urinary flow rate and the creatinine cl. were not significantly affected. Indomethacin reduced urinary excretion of prostanoids and in addition it produced the following significant effects: (a) a reduction in urinary flow rate, C(H2O) and Cosm values, and in absolute and fractional urinary excretions of sodium and chloride; and (b) an increase in plasma potassium concentration. MAP, creatinine cl. and urinary potassium excretion were not significantly affected. With regard to the main parameters, both enalapril and indomethacin exerted similar effects on urinary sodium and chloride excretion but opposite effects on C(H2O) and plasma potassium concentration. In conclusion, after enalapril in a salt-depleted state, the functional expression of acute angiotensin II deprivation was partially masked by the activation of a homeostatic system responsible both for improvement in renal salt conservation and for facilitated cellular potassium uptake. After indomethacin in the same setting, the results were consistent with a differential role of prostanoids in modulating or mediating the activities of neuro-hormonal agonists.

6-Ketoprostaglandin F1 alpha↗
PubMed1998

Effects of experimental salt depletion on urinary prostanoid excretions in normal women.

The effects of moderate salt depletion on urinary excretions of prostanoids (PG)E2, 6-keto-PGF1alpha (6KPGF) and thromboxane (TX)B2 have been investigated in healthy women (SD group, n = 14). Salt depletion was obtained by combining a low sodium chloride dietary intake (< 60 mmol per day) with natriuretic and potassium sparing treatment. At the end of the treatment, the cumulative sodium deficit was 438 +/- 42 mmol (mean +/- SEM). Plasma renin activity (PRA) and urinary aldosterone excretion were determined in basal conditions. Renal functional exploration was performed during hypotonic polyuria (by oral water load) and subsequent moderate antidiuresis (by low dose infusion of an antidiuretic hormone analogue). In both phases, renal function was estimated by the clearance (cl.) method and the urinary concentrations of PGE2, 6KPGF and TXB2 by RIA method. The control group was composed of 20 healthy women in normal sodium and potassium balance (N group). Salt depletion was effective in increasing the basal values of plasma renin activity (PRA) and urinary aldosterone excretion. Moreover, it was effective in inducing the following during polyuria: (a) a depression of the diuretic response to water load in presence of a reduction in plasma osmolality; (b) a reduction in creatinine cl. in the absence of significant changes in mean arterial pressure; (c) an increase in the fractional reabsorption of sodium and chloride, in particular at the level of the diluting segments. Both in polyuria and in antidiuresis, the excretions of 6KPGF and TXB2 were higher in the SD vs. N group, while the excretion of PGE2 was not significantly different. In SD and N pooled groups, significant positive correlations were shown between basal PRA and urinary excretions during polyuria of 6KGPF and TXB2, (but not of PGE2) as well as between the excretions of the two metabolites. In conclusion, functionally effective salt depletion induces in healthy women a stimulation of renal synthesis of both prostacyclin and thromboxane. The excretory data do not give evidence of a similar effect on PGE2 synthesis.

6-Ketoprostaglandin F1 alpha↗
PubMed1996

Effective role of the renin-angiotensin system in the control of prostanoid synthesis and renal function in healthy women with moderate salt depletion.

The interaction between moderate salt depletion and urinary excretions of prostanoids (PGE2,6-keto-PGF1 alpha and TxB2), as well as the effective role of the activated renin-angiotensin system (RAS), in the control of renal function and urinary prostanoid excretions have been investigated in healthy women. Salt depletion (SD, n = 8) was induced by low sodium chloride dietary intake (< or = 60 mmol per day) and combined treatment with natriuretic and potassium sparing drugs. The cumulative sodium deficit was 381 +/- 55 mmol. The renal function and urinary excretion of prostanoids were evaluated during hypotonic polyuria (oral water load) and subsequent moderate antidiuresis (lysine-8-vasopressin (LVP) low-dose infusion). Basal plasma renin activity (PRA) and urinary aldosterone excretion were determined, before the water load, in both the SD group and control studies in normal balance of sodium and potassium (N, n = 20). Paired studies were performed in the absence and in the presence of enalapril in the same SD group, as well as in a subgroup, with normal sodium and potassium balance, previously studied (N3, n = 6). In the SD vs. N group, significantly higher values of PRA and urinary aldosterone excretion were found. The renal antinatriuretic mechanism was activated and the diuretic response to water load depressed. During polyuria, the urinary 6-keto-PGF1 alpha and TxB2 excretions were significantly higher, probably reflecting an increase in the renal synthesis of their precursors. During the late LVP infusion, the urinary PGE2 excretion was also significantly increased, in absence of significant differences in urinary flow rate. In both SD and N3 groups, enalapril decreased the mean arterial pressure (MAP). Despite the decrease in MAP, not significantly different in SD vs. N3 group, the drug did not significantly affect the creatinine clearance. Also, the urinary prostanoid excretions were not significantly affected by enalapril. However, in the SD group, but not in the N3 group, the drug was effective in significantly decreasing the absolute and fractional excretions of sodium and chloride. Moreover, the plasma potassium concentration significantly decreased, despite the concurrent decrease in urinary potassium excretion. The data suggest that: (1) in salt depletion, the prostanoid release from the renal cortical structures was stimulated; (2) the renal prostanoid synthesis, either activated (sodium depletion) or not (normal sodium and potassium balance), was not affected by the RAS pharmacological blockade in the short-term; (3) in salt depletion, the RAS blockade recruited a homeostatic mechanism responsible for the improved renal salt conservation, as well as for the redistribution of potassium between the extra- and intra-cellular compartments.

Adult↗
PubMed1994

Interactions between the renin-angiotensin system and prostanoids in modulating renal function in potassium-depleted healthy women.

Plasma renin activity (PRA) and urinary aldosterone excretion were determined in healthy women with normal potassium balance (N, n = 20) or experimental potassium depletion (KD). KD was induced by natriuretic treatment--associated with replacement of net NaCl and water losses--and low dietary potassium intake (< or = 10 mmol/d). By using different depletion patterns, three groups were obtained with cumulative potassium deficits (mean +/- SEM) of 160 +/- 43 (KD1, n = 8), 198 +/- 22 (KD2, n = 6) and 215 +/- 54 mmol (KD3, n = 6). The renal function by the clearance (cl.) method and urinary concentrations of prostaglandin E2 (PGE2), 6-keto-PGF1 alpha (6KPGF), and thromboxane B2 (TXB2) by the RIA method were estimated during hypotonic polyuria (oral water load) and subsequent moderate antidiuresis induced by low-dose infusion of lysine-8-vasopressin (LVP). 1. In all KD groups the depletion treatment significantly reduced both potassium plasma concentration (PK) and urinary potassium excretion while it increased basal PRA; the basal urinary aldosterone excretion was not significantly different from normokalemic controls. In the KD3 vs KD1 group the P kappa value was significantly lower. 2. In both KD2 and KD3 groups as compared to the N group, several hypokalemic-like renal dysfunctions--absent in the KD1 group--occurred. Particularly, in the KD2 + KD3 vs N group the renal ability in both urine diluting (water load) and concentrating (LVP infusion) was significantly impaired.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗
PubMed1994

Effects of angiotensin-converting enzyme inhibition on renal dysfunction induced by moderate potassium depletion in healthy women.

The role of the renin-angiotensin system in renal hypokalaemic dysfunction has been investigated by evaluating the effects of the angiotensin (AT)-converting enzyme inhibition by enalapril. Healthy women were studied either in normal potassium balance (N3, n = 6) or moderate potassium depletion (KD3, n = 6). Potassium depletion (KD) was induced by low potassium dietary intake (greater than or equal to 10 mmol per day) and natriuretic treatment associated with replacement of net NaCl and water losses; the cumulative potassium deficit achieved was 214 +/- 54 mmol. The renal function and the urinary excretions of some prostanoids (PGE2, 6-keto-PGF1 alpha, TxB2) were evaluated during hypotonic polyuria (oral water load) and subsequent moderate antidiuresis (lysine-8-vasopressin (LVP) low-dose infusion). Paired studies were performed in absence (control) and presence of enalapril. Basal plasma renin activity (PRA) and urinary aldosterone excretion were determined before the water load of control studies. Renal dysfunction typical of chronic KD occurred in the KD3 group, i.e. increase in PRA, decrease in creatinine clearance, depression of the diuretic response to water load, inhibition of distal fractional chloride reabsorption, and blunted efficacy of LVP in increasing the urinary solute concentration. The urinary prostanoid excretions were reduced. Basal urinary aldosterone excretion was not changed significantly. In KD3 group enalapril decreased mean arterial pressure (MAP), increased the plasma potassium concentration, improved the diuretic response to water load and corrected the impairment of the distal fractional chloride reabsorption. Despite the decrease in MAP enalapril did not affect significantly the creatinine clearance. Neither urinary prostanoid excretions nor the renal response to LVP were affected by the drug. The data suggest that in KD the increased activity of the renin-angiotensin system affected the renal function both through direct effects and through effects dependent on the angiotensin-supported secretions of aldosterone and probably of vasopressin. Finally, by comparing the effects of enalapril and indomethacin in experimental groups with an equivalent degree of KD, evidence is provided in favour of the interaction between renin-angiotensin and prostanoid systems in controlling the glomerular filtration rate and the salt and water handling by renal tubules.

Adult↗
PubMed1993

Studies on renal function in healthy women with different degrees of induced potassium depletion. 2). Patterns of hypokalemic renal dysfunction.

In order to investigate the renal functional effects of potassium depletion (KD) we have submitted 20 healthy women to different potassium depletive treatments by dietary and pharmacological means. By changing these treatments we have obtained three KD groups with cumulative potassium deficit of 160 +/- 43 (KD1, n = 8), 198 +/- 22 (KD2, n = 6) and 214 +/- 54 mmol (KD3, n = 6). Another 20 subjects were also studied as controls in normal potassium balance (N group). In all subjects the renal function has been evaluated by clearance (cl.) technique both during induced hypotonic polyuria and subsequent moderate antidiuresis induced by low dose infusion of lysine-8-vasopressin (LVP). A renal dysfunction occurred in differences between these two groups, they have been pooled in a single KD2 + KD3 group. In this group as compared to N the following renal dysfunctions were observed during hypotonic polyuria: a) reduction in creatinine cl. (in absence of significant differences in mean arterial pressure); b) inhibition of the fractional reabsorption of chloride by diluting segments; c) depression of the diuretic response to water load. Moreover in KD the LVP was less effective in reducing the creatinine cl. while it became effective in reducing the fractional excretions of NaCl. These findings indicate that the degree of KD reached in the KD2 + KD3 group was adequate to induce a renal dysfunction similar to that occurring in conditions of chronic hypokalemia. It is probable that hypokalemia by itself along with changes of both prostaglandin and angiotensin renal systems are involved in this renal dysfunction.

Blood Pressure↗
PubMed1993

Studies on renal function in healthy women with different degrees of induced potassium depletion. 3) Effective roles of prostanoids and angiotensin II in hypokalemic renal dysfunction.

By using two similar dietary and pharmacological patterns of potassium depletive treatment, two experimental groups--KD2 (n = 6) and KD3 (n = 6)--with cumulative potassium deficit not significantly different, were obtained. The basal values of plasma potassium concentration and PRA, as well as the expression of renal hypokalemic dysfunction were not significantly different. Paired studies in the absence and presence of indomethacin (KD2 group) or enalapril (KD3 group) were performed. The aim of the research was evaluation of the effective roles of prostanoid and angiotensin (AT) II systems in renal hypokalemic dysfunction. The results show that: 1) AT II and cortical vasodilating prostanoids exerted opposite effects on the preglomerular arteriolar tone; 2) medullary prostanoids antagonized the vasopressin effects. Therefore, in potassium depletion the decreased synthesis of cortical and medullary prostanoids, in the face of the increased generation of AT II, contributed to reducing the glomerular filtration rate and facilitate the expression of vasopressin action. These components of the renal hypokalemic dysfunction probably exert a protective role with regard to the urinary chloride and potassium losses.

Angiotensin II↗
PubMed1992

Urinary prostanoid excretion in healthy women with different degrees of induced potassium depletion.

Plasma renin activity (PRA), urinary excretions of PGE2, 6-keto-PGF1 alpha (6KPGF), TXB2 and renal function were determined in healthy women both in normal potassium balance (N, n = 14) and in experimental potassium depletion (KD). KD was induced by natriuretic treatment--associated to replacement of net NaCl and water losses--in the presence of either normal (congruent to 50 mmol/d) or low (less than or equal to 10 mmol/d) dietary potassium intake. By using different depletive patterns, three groups with estimated cumulative potassium deficit (mean +/- SEM) of 124 +/- 38 (KD0, n = 8), 160 +/- 43 (KD1, n = 8) and 198 +/- 22 mmol (KD2, n = 6), respectively, were obtained. Renal function by the clearance (cl.) method and urinary prostanoid concentrations by the RIA method were estimated during hypotonic polyuria (oral water load) and subsequent moderate antidiuresis induced by a low-dose infusion of lysine-8-vasopressin. 1. In KD0 group the potassium depletive treatment was inefficacious in significantly reducing either the plasma potassium concentration (PK) or the urinary potassium excretion (UKV). The reductions of PK and UKV as well as the enhancement of PRA became significant in KD1 and KD2 groups. 2. The urinary prostanoid excretions were not significantly changed in the KD0 and KD1 groups while in the KD2 group they were reduced, mainly concerning the urinary 6KPGF excretion. 3. Furthermore in the KD2 group, with larger potassium depletion, some of the typical hypokalemic renal dysfunctions appeared. The data suggest that a pathophysiologically critical degree of potassium depletion is associated with an inhibited renal prostanoid synthesis as well as an increased renin secretion.

6-Ketoprostaglandin F1 alpha↗
PubMed1992

Effects of experimental potassium depletion on renal function and urinary prostanoid excretion in normal women during moderate anti-diuresis.

The hypothesis that potassium depletion (KD) might play a role in stimulating the renal synthesis of prostanoids, and that these materials can contribute to hypokalaemic renal dysfunction, has been tested. Healthy women were studied either in normal potassium balance (N,n = 14), or in experimental KD. KD was induced by low dietary potassium intake (less than or equal to 10 mmol day-1) and natriuretic treatment, associated with replacement of net NaCl and water loss. By using different depletive patterns, two groups with estimated cumulative potassium deficits of 160 +/- 43 mmol (KD1, n = 8) and 198 +/- 22 mmol (KD2, n = 6), respectively, were obtained. Renal function by the clearance (cl.) method and urinary PGE2, 6-keto-PGF1 alpha, TxB2 concentrations by the RIA method were measured during hypotonic polyuria (oral water load) and subsequent moderate antidiuresis induced by the infusion of low-dose lysine-8-vasopressin (LVP). Compared to the N group, only in the KD2 group do glomerular and tubular dysfunctions typical of hypokalaemia and reduced prostanoid excretions (significant for 6-keto-PGF1 alpha and TxB2 but not for PGE2) appear during polyuria besides the significant reductions of plasma potassium concentration, urinary potassium excretion and the significant increase in plasma renin activity. During LVP infusion the urinary prostanoid excretions were all significantly lower in absence of significant differences in urinary flow rate. Concerning its renal effects, LVP lost its ability to reduce the creatinine cl., while expressing a trend towards reduction in fractional chloride excretion. Indomethacin pretreatment restored the LVP effect on creatinine cl. and increased the antichloruretic LVP effect (although not significantly). To the extent that urinary prostanoid excretions reflect their intrarenal synthesis, our data demonstrate that KD inhibits this biosynthesis. A depressed production of prostanoids endowed with vasodilating and chloruretic activity probably played a role in attenuating the renal vascular hyporeactivity and the urinary chloride dispersion induced by KD.

Adult↗
PubMed1990

Effects of experimental potassium depletion on renal function and urinary prostanoid excretion in normal women during hypotonic polyuria.

During hypotonic polyuria renal function studies by the clearance (cl.) method, and urinary PGE2, 6-keto-PGF1 alpha and TxB2 determinations were performed on 14 healthy women in normal potassium balance (N) and 14 healthy women in sustained potassium depletion (KD) induced by low dietary potassium intake (less than or equal to 10 mmol day-1) and natriuretic treatment. By using different depletive patterns, two groups with estimated cumulative potassium deficits of 160 +/- 43 mmol (KD1, n = 8) and 198 +/- 22 mmol (KD2, n = 6), respectively, were obtained. (1) In both the KD1 and KD2 groups as compared to normal potassium balance (N), plasma potassium concentration and urinary potassium excretion were significantly lower; plasma renin activity was significantly higher. (2) Only in KD2 did significant changes appear in renal function and urinary prostanoid excretions. Besides a decrease in creatinine cl. and the urinary flow rate, an increase in fractional chloride excretion and a reduction in distal fractional chloride reabsorption were manifest. The plasma chloride concentration was reduced too. Urinary prostanoid excretions were significantly (6-keto-PGF1 alpha, TxB2) or tendentially (PGE2) lower. (3) Indomethacin treatment resulted in changes in mean arterial pressure (increase) and creatinine cl. (decrease) which were not significantly different in normal potassium balance and KD groups. Only in KD2 did the drug significantly reduce the fractional salt and water excretions and the fractional sodium and chloride deliveries to the diluting segments. However, indomethacin was unable to correct the inhibition of distal fractional chloride reabsorption. Therefore, the potassium depletion attained in the KD2 group was efficacious in depressing renal prostanoid synthesis. This fact, in the presence of high levels of angiotensin II, induced a reduction of the glomerular filtration rate thus contributing to renal ability to retain chloride and potassium.

Adult↗
PubMed1990

[Selective inhibitory effects of experimental potassium depletion on urinary excretion of prostanoids and their possible functional significance].

The urinary concentrations of prostaglandins(PG) E2, 6-keto-PGF1 alpha (6KPGF) and thromboxane (Tx) B2 were measured by RIA method during both hypotonic polyuria (oral water load) and subsequent antidiuresis (low-dose infusion of lysine-8-vasopressin). The study was performed on healthy women either in normal potassium balance (N, n = 14) or sustained potassium depletion (D3, n = 6). Potassium depletion (KD) was induced by low potassium dietary intake (less than or equal to 10 mmol/d) and natriuretic treatment over a period of 8 days; the net losses of NaCl and H2O were replaced; the cumulative potassium deficit was 198 +/- 22 mmol. Further studies were performed after indomethacin treatment in both experimental conditions. 1) As compared to normal potassium balance in KD group the urinary prostanoid excretions were reduced even in absence of significant differences in urinary flow rate. The urinary excretion of 6KPGF was more impaired than that of TxB2 in both polyuria and antidiuresis. 2) Indomethacin inhibited the urinary prostanoid excretions in normal potassium balance and KD groups. The urinary excretion of PGE2 was more impaired than that of both 6KPGF and TxB2.

Adult↗
PubMed1989

Antagonistic effects of sulpiride--racemic and enantiomers--on renal response to low-dose dopamine infusion in normal women.

In healthy women during moderate hydrosaline retention we have evaluated the antagonistic effects of sulpiride--enantiomers and racemic--on the renal action of a low-dose dopamine (DA) infusion (0.1 microgram/kg/min). The studies were performed, in hypotonic polyuria, by the clearance (C1) method in (1) hydrosaline retention (n = 23), (2) retention + dl-sulpiride (n = 8), (3) retention + d-sulpiride and (4) retention + l-sulpiride (in the latter two cases n = 7 subjects submitted to paired studies). Hydrosaline retention was induced by deoxycorticosterone acetate treatment. A common pattern of sulpiride treatment was applied. The DA renal hyperemia is abolished by l-sulpiride while it is transitorily attenuated by d-sulpiride. In both conditions 3 and 4 the increase in glomerular filtration rate, the inhibition of fractional isosmotic sodium reabsorption and the increase in urinary sodium excretion--induced by DA in condition 1--are suppressed. On the contrary, DA inhibition of fractional anisosmotic sodium reabsorption is not affected by sulpiride. The data indicate that DA renal hyperemia results from the action of DA on DA2 receptors; the DA inhibition of sodium transport by the diluting segments does not appear to be mediated by typical DA receptors.

Adult↗
PubMed1989

[Renal function in experimental potassium depletion. I. Effects of lysine-8-vasopressin in hypotonic polyuria].

Renal function has been studied by the clearance (cl.) method during hypotonic polyuria--four 15-min cl. periods--and successive antidiuresis--two 60-min cl. periods (A1, A2)--induced by lysine-8-vasopressin (LVP), 5 mU in bolus followed by infusion at a rate of 0.04 mU/min. The endogenous creatinine cl. (Cc) and the osmotic cls. (Cosm, CH2O) were determined by the usual methods as well as the absolute and fractional urinary excretions of water, sodium, chloride and potassium. The urinary concentrations of PGE2, 6-keto-PGF1 alpha and TxB2 were determined by the RIA method. This study protocol has been applied to 28 healthy women either in normal potassium balance (N, n = 14) or after potassium depletion (KD) induced by low potassium dietary intake (less than or equal to 10 meq/d) plus natriuretic treatment according to two different time patterns: two KD groups were obtained with potassium cumulative deficit of 160 +/- 43 (D2, n = 8) and 198 +/- 22 meq (D3, n = 6). The early % effects of LVP, i.e. (A1-P)% of P (mean polyuria), were significantly different only in D3 as compared to N. Precisely, the LVP-effect to reduce Cc was blunted; moreover a LVP-effect to reduce renal sodium and chloride fractional excretions and a tendentiously enhanced LVP-effect to reduce water fractional excretion were observed. These tubular effects are likely related to the inhibited renal synthesis of prostanoids in the D3 group.

6-Ketoprostaglandin F1 alpha↗