Browsing by Author "SALAS, SP"

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    CONTROL OF PLASMA-VOLUME EXPANSION IN THE PREGNANT FOOD RESTRICTED RAT
    (PERGAMON-ELSEVIER SCIENCE LTD, 1990) SALAS, SP; GODOY, R; ROSSO, P
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    DIURETIC EFFECT OF BREMAZOCINE, A KAPPA-OPIOID WITH CENTRAL AND PERIPHERAL SITES OF ACTION
    (1989) SALAS, SP; ROBLERO, J; URETA, H; HUIDOBROTORO, JP
    Intracerebroventricular or i.p. injections of bremazocine produced a dose-dependent diuretic response and increased glomerular filtration rate in hydrated as well as in nonhydrated rats. The potency and magnitude of the bremazocine-induced diuresis were more pronounced in the nonhydrated group of rats. That bremazocine has a central component of action is deduced from the fact that 0.1 .mu.g of the opioid administered centrally caused a significant increase in urine output; proportionally, larger doses of bremazocine were required to produce the same diuretic effect when the drug was administered parenterally. Bremazocine did not change the total amount of urinary Na+ and K+ as compared to the saline controls; it increased significantly the free water clearance. The bremazocine-induced diuresis was antagonized in a competitive fashion by 10 mg/kg of naloxone giving further support to the notion that the mechanism of action of bremazocine involves activation of kappa-opioid receptors. Bremazocine injected i.v. to nonanesthetized rats increased mean systemic blood pressure in a dose-dependent manner; the pressor action of the opiate was blocked and prevented by 1 mg/kg of naloxone. In contrast, i.c.v. administration of bremazocine did not change mean systemic blood pressure but produced a dose-related increase in urine output. To determine whether in addition to a central site bremazocine also activates a renal mechanism, experiments were performed in the isolated perfused rat kidney. Bremazocine (0.15-2.5 .mu.M) caused a dose-dependent diurectic response and a significant rise in the perfusion pressure as well as in glomerular filtration rate. In contrast to the whole animal studies, in vitro administration of bremazocine resulted in a marked natriuresis and kaliuresis proportional to the dose. The renal effects were antagonized by naloxone, suggesting the existence of a local opiate renal mechanism. In conclusion, the present results demonstrate that in addition to a central site of action, bremazocine activates renal mechanisms to regulate water and electrolytes metabolism. The complexity of the pharmacology of opiates in the regulation of urine output may be related to this dual mechanism.
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    HEMODYNAMIC-CHANGES IN UNDERWEIGHT PREGNANT-WOMEN
    (ELSEVIER SCIENCE INC, 1992) ROSSO, P; DONOSO, E; BRAUN, S; ESPINOZA, R; SALAS, SP
    Twelve normal-weight and 12 underweight women were compared to test whether fetal growth retardation in underweight gravidas is related to inadequate maternal hemodynamic adjustments. Plasma volume (+/- standard error) was 3227 +/- 103 mL in normal-weight and 2731 +/- 84 mL in underweight women (P < .002). Cardiac output was 6340 +/- 167 mL/minute in controls and 5689 +/- 213 mL/minute in underweight women (P < .03). Total peripheral vascular resistance was lower in controls than in underweight subjects (1025 +/- 31 versus 1198 +/- 58 dyne/second/cm5). Mean birth weight was 2837 +/- 125 g in underweight women and 3362 +/- 106 g in controls (P < .005). Similarly, placental weight was reduced in the underweight group. All infants delivered by control mothers had a normal birth weight, whereas six infants from underweight gravidas were growth-retarded. In all cases combined, maternal plasma volume correlated significantly with both birth weight (r = 0.6, P < .002) and placental weight (r = 0.56, P < .01); total peripheral vascular resistance also correlated significantly and inversely with newborn weight and placental weight. Cardiac output correlated only with placental weight (r = 0.54, P < .02). These results are consistent with the hypothesis that underweight mothers are at higher risk of fetal growth retardation because of a smaller plasma volume and lower cardiac output.
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    MATERNAL HEMODYNAMIC ADJUSTMENTS IN IDIOPATHIC FETAL GROWTH-RETARDATION
    (KARGER, 1993) ROSSO, P; DONOSO, E; BRAUN, S; ESPINOZA, R; FERNANDEZ, C; SALAS, SP
    The hemodynamic characteristics of 11 normotensive gravidas with idiopathic fetal growth retardation (FGR), were compared with 11 controls of similar age, parity and body size. At weeks 36-38 of gestation, plasma volume was 3,161 +/- 121 ml in controls and 2,624 +/- 95 ml in the FGR group (p < 0.003); cardiac output (CO) was 6,191 +/- 132 ml/min in controls and 5,483 +/- 186 ml/min in the FGR group (p < 0.01). Total peripheral vascular resistance (TPVR) was lower in controls than in FGR (1,031 +/- 33 vs. 1,306 +/- 62 dyn/s/cm5; p < 0.001). Birth weight was correlated with both plasma volume (r = 0.61; p < 0.01) and CO (r = 0.53; p < 0.02) and inversely correlated with TPVR (r = -0.69; p < 0.001). These results are in line with the hypothesis that a reduced plasma volume leads to a lower CO and, secondarily, to reduced uterine blood flow and FGR.
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    MATERNAL PLASMA-VOLUME EXPANSION AND HORMONAL CHANGES IN WOMEN WITH IDIOPATHIC FETAL GROWTH-RETARDATION
    (LIPPINCOTT WILLIAMS & WILKINS, 1993) SALAS, SP; ROSSO, P; ESPINOZA, R; ROBERT, JA; VALDES, G; DONOSO, E
    Objective: To explore the mechanisms underlying the reduced maternal plasma volume associated with idiopathic fetal growth retardation (FGR).
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    [N-METHYL-TYR1, N-METHYL-ARG7-D-LEU8]-DYNORPHIN-A-(1-8) ETHYLAMIDE, A STABLE DYNORPHIN ANALOG, PRODUCES DIURESIS BY KAPPA-OPIATE RECEPTOR ACTIVATION IN THE RAT
    (1992) SALAS, SP; ROBLERO, JS; LOPEZ, LF; TACHIBANA, S; HUIDOBROTORO, JP
    The i.v. administration of E-2078 {[N-methyl-Tyr1-N-methyl-Arg7-D-Leu8]-dynorphin-A-(1-8) ethylamide} to conscious animals in doses of 15, 50 or 200-mu-g/rat caused a dose-related diuretic response associated with a significant in crease in glomerular filtration rate (GFR) and in blood pressure. The overall excretion of Na+ was not modified by the opioid, whereas it reduced K+ output and its fractional excretion. Time course studies demonstrated that the increase in GFR and in blood pressure were transient and did not parallel the changes in urine outflow. Pretreatment of the animal with 1 mg/kg of naltrexone or of naloxone reduced the pressor response but did not reduce the renal action of E-2078. Doses of naltrexone 10 times larger (10 mg/kg) were required to attenuate the diuretic effect and abolish completely the changes in K+ excretion; however, the increase in GFR was not antagonized by 10 mg/kg of naltrexone. Consonant with the studies in conscious rats, perfusion of isolated rat kidneys with 0.2 to 1.8-mu-M E-2078 increased urine flow in a dose-dependent manner, and this effect was prevented by the simultaneous perfusion of 2-mu-M naltrexone with the peptide. In pentobarbital-anesthetized animals, E-2078 elicited a diuretic response that was not parallelled by changes in GFR or electrolyte excretion. In addition, E-2078 caused a long-lasting decrease in blood pressure which was blocked completely by pretreatment of the animal with 1 mg/kg of naltrexone. The diuretic effect of E-2078 was not modified by pretreatment of the animals with beta-funaltrexamine. Rats anesthetized with ether or halothane also showed a decrease in blood pressure after E-2078. Anesthesia with ether or halothane attenuated or anulled the pressor action of bremazocine or U-50,488, whereas barbiturate anesthesia resulted in a precipitous and prolonged hypotension. These results suggest that the stable dynorphin analog, E-2078, produces its effects on urinary excretion primarily via a kappa receptor mediated mechanism.
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    THE NEUROGENIC RESPONSE TO 55-DEGREE HEAD-UP TILT IN NORMAL PREGNANT-WOMEN
    (1986) VALDES, G; SALAS, SP; FORADORI, AC; GORMAZ, G; CROXATTO, HR
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    URINARY KALLIKREIN ACTIVITY DURING RAT PREGNANCY
    (1987) SALAS, SP; ROBLERO, JS; CROXATTO, HR; VALDES, G
    Changes in urinary kallikrein activity and its possible correlation with changes in blood pressure and renal excretory function during pregnancy were studied in the rat. To establish a possible physiological role of kallikrein in this condition aprotinin, which inhibits kallikrein as well as other serine protease was administered to pregnant rats. Urinary kallikrein activity was markedly increased during pregnancy and correlated positively with urine volume and electrolytes excretion, but not with blood pressure. Aprotinin administration almost completely inhibited kallikrein activity, however, blood pressure levels, urine volume and electrolytes were not changed after one day of aprotinin treatment. In conclusion, although renal kallikrein is highly enhanced during pregnancy, its physiologic role in this condition remains elusive.
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    URINARY KALLIKREIN EXCRETION IN PREGNANT ADRENALECTOMIZED RATS
    (1986) CROXATTO, HR; SALAS, SP; ROSAS, RB; JARPA, S
    The mechanisms responsible for the increase of the urinary kallikrein activity (UKA) during pregnancy is still unknown. Since aldosterone has been described as one of the stimulatory factor of UKA, and this hormone is considerably elevated in normal pregnancy it is feasible to postulate that it might be involved in the process. A preliminary approach to solve the role of the mineralocorticoid was to investigate the effect of the adrenalectomy upon UKA, of pregnant rats. UKA activity and blood pressure (BP) were measured at weekly intervals in four groups of rats: pregnant-adrenalectomized (P-ADX); pregnant-sham operated (P-C); non pregnant-adrenalectomized (NP-ADX) and non pregnant-sham operated (NP-C). In addition serum aldosterone levels in pregnant rats were determined. All the groups were maintained in similar conditions drinking 1% NaCl solution. The increase in UKA was not detected in P-C, as observed in normal pregnant rats drinking tap water, indicating that a high NaCl intake prevents the rise in UKA during gestation. However, P-C rats had higher UKA than P-ADX on day 14 of pregnancy (p < 0.05). The lowest level of UKA was found in NP-ADX. In NP-C and NP-ADX BP rose progressively throughout the experiment. BP in P-ADX rats during pregnancy and on day 7 of post partum was significantly lower than in P-C rats (p < 0.01-0.02) but in both pregnant groups it decreased significantly before parturition (p < 0.02) increasing at post-partum. Serum aldosterone levels on days 14 and 21 of gestation, showed higher values in P-C than in P-ADX (p < 0.01-0.005). The results provide support to the assumption that adrenal gland has a regulatory action on UKA during pregnancy and that aldosterone can be one of the main factors involved.