Browsing by Author "CROXATTO, HR"

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    BLUNTING EFFECT OF PEPSANURIN INTRODUCED IN THE DUODENUM ON THE ATRIAL-NATRIURETIC-PEPTIDE DIURETIC ACTION IN RATS
    (1993) CROXATTO, HR; BORIC, MP; ROBLERO, JS; ALBERTINI, R
    Pepsanurin (PU) is a peptide(s) obtained by pepsin hydrolysis of human plasma or its globulin fraction. We have reported that the accelerated renal excretory rate induced by atrial natriuretic peptide (ANP) can be considerably blunted by PU either in the intact rat or in the isolated perfused rat kidney. We explored whether or not PU can be part of a signaling mechanism originated in the digestive tract, involved in the regulation of water and electrolyte homeostasis. PU obtained either from human (0.5 ml) or rat plasma (0.25-0.5 ml) administered into the duodenal lumen of rats, counteracted significantly the diuretic-saluretic action ot a 0.5- mug bolus of ANP, reproducing qualitatively the effect of its intraperitoneal administration. Human PU reduced the ANP-stimulated renal excretion by 67-90% for Na (P < 0.001) and by 35-54% for water (P < 0.02-P < 0.001); the inhibition induced by rat PU was 45-96% for Na (P < 0.05-P < 0.01) and 35-65% for water (P < 0.05-P < 0.01). Rat PU (0.5 ml) abolished the rise of glomerular filtration rate induced by ANP without affecting fractional Na excretion. All the samples tested decreased K excretion, but in some experiments, the difference did not reach statistical significance. Contrary to the effect of PU, the introduction in the duodenum of (i) isotonic glucose solution, (ii) hydrolysate of bovine serum albumin, or (iii) hydrolysate of casein prepared after the same procedure yielding PU from plasma failed to produce an inhibition of the ANP stimulation of renal excretory rate. In addition, human plasma incubated at 37-degrees-C for 24 to 48 hr, prior to pepsin digestion, did not yield PU, which indicates that PU is generated from a substrate sensitive to endogenous enzymes and/or that its stability is vulnerable to endogenous enzymes.
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    CHANGES IN RENAL KALLIKREIN ACTIVITY DURING PREGNANCY IN RATS
    (1982) CROXATTO, HR; NORAMBUENA, M
    Kallikrein activity in the kidney of rats was determined before insemination, on the 7th, 14th and 20th days of pregnancy and the 7th day after parturition. A significant decrease of renal kallikrein activity was found throughout pregnancy. After parturition it returns to the pre-gestation value. Expressed in ng of bradykinin equivalents the respective values of kallikrein activity were: before pregnancy, 609 .+-. 49; during pregnancy: 7th day, 415 .+-. 19; 14th day, 417 .+-. 45; 20th day, 386 .+-. 26; and 7th day after delivery, 630 .+-. 45. The significant increase in urinary kallikrein during gestation confirmed previous results. Renal kallikrein-kinin system evidently is involved in blood pressure regulation during pregnancy. [Implications for human hypertension during pregnancy are considered].
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    EFFECT OF AMILORIDE ON URINARY AND RENAL KALLIKREIN IN THE RAT
    (1986) CROXATTO, HR; CORTHORN, J; ROBLERO, J; VILLALON, P; PEREZ, F
    A single intraperitoneal injection of amiloride in the range of 2.7, 5.4, 10.9, and 21 .mu.mol/100 g body wt in female adult rats produced, in the two successive periods of 4 h following its administration, a significant decrease in the urinary excretory rate of kallikrein. Amiloride, 10.9 .mu.mol/100 g body wt, which significantly reduced active kallikrein, also decreased, but less significantly, the trypsin-activated kallikrein in the urine. The fall in the excretory rate of kallikrein cannot be explained by its enzymatic inhibition by amiloride, since the inhibition was only present at higher concentrations. In hyperhydrated rats amiloride did not change the kallikrein excretory rate in the urine collected within 4 h after the injection. Rats simultaneously injected with 7.6 .mu.mol/100 g body wt furosemide and 10.9 .mu.mol/100 g body wt amiloride excreted levels of kallikrein similar to those found in rats injected with furosemide alone. The kidneys of rats removed after 4 h of administration 10.9 .mu.mol/100 g body wt amiloride showed a significant lowering of the kallikrein activity compared with the respective controls. The decrease of renal kallikrein tended to be similarly pronounced in those rats that received amiloride and furosemide simultaneously. These results confirm the depressive effect of amiloride on kallikrein excretion, which may be explained by an inhibitory action on kallikrein release, activation, and synthesis by the renal cells.
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    EFFECTS OF NIFEDIPINE DURING LOW, NORMAL AND HIGH INTAKES OF SODIUM IN PATIENTS WITH ESSENTIAL-HYPERTENSION
    (1982) VALDES, G; SOTO, ME; CROXATTO, HR; BELLOLIO, T; CORBALAN, R; CASANEGRA, P
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    EFFECTS OF PROSTAGLANDIN-E2 AND PROSTAGLANDIN-F2ALPHA UPON URINARY KALLIKREIN EXCRETION IN RATS
    (1978) CROXATTO, HR; ARRIAGADA, R; ROJAS, M; ROBLERO, J; ROSAS, R
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    ESTERASE-ACTIVITY IN RENIN AND KALLIKREIN EXTRACTS OBTAINED FROM RAT KIDNEYS
    (1975) PORCELLI, G; MARINIBETTOLO, GB; CROXATTO, HR; CORTHORN, J; TEMPESTA, G
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    INHIBITION OF ATRIAL-NATRIURETIC-PEPTIDE INDUCED NATRIURESIS BY PLASMA HYDROLYSATES CONTAINING PEPSANURIN
    (1992) BORIC, MP; CROXATTO, HR; ALBERTINI, R; ROBLERO, JS
    The specificity of antidiuretic actions of pepsanurin, a peptidic fraction obtained by pepsin hydrolysis of plasma, was studied in anesthetized rats and in isolated perfused rat kidneys. Pepsanurin was obtained from fresh dialyzed human plasma digested with pepsin (2,400 units/ml, 18 hours at 37-degrees-C, pH 2.5), deproteinized (10 minutes at 80-degrees-C), and centrifuged. In the rat, intraperitoneal injections of pepsanurin (0.5 ml/100 g body wt) significantly inhibited the effects of an intravenous bolus of atrial natriuretic peptide (ANP) (0.5-mu-g) on water, sodium, and potassium excretion without altering systemic blood pressure. In addition, pepsanurin abolished the peak in glomerular filtration rate and reduced the ANP-induced rise in fractional sodium excretion. Pepsanurin also inhibited the natriuretic effects of amiloride (10-mu-g/100 g body wt i.v.) without changing glomerular filtration rate, but it did not inhibit the potassium-retaining effect of amiloride. In contrast, pepsanurin had no effect on basal urinary excretion, and it did not affect the diuretic response induced by furosemide (doses of 25, 50, or 100-mu-g i.v.). Control peptidic hydrolysates prepared from human plasma preincubated 48 hours at 37-degrees-C (PIPH), bovine albumin (BSAH), or human albumin did not inhibit ANP, amiloride, or furosemide. In perfused kidneys, pepsanurin significantly and reversibly reduced sodium and water excretion. Furthermore, pepsanurin, but not PIPH or BSAH, blocked the natriuretic and diuretic effects of ANP. These results support the existence of a specific plasma substrate able to release a peptide or peptides that counteract distal tubule diuresis and natriuresis by an intrarenal mechanism.
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    INHIBITORY EFFECT OF RENIN EXTRACTS UPON URINARY KALLIKREIN EXCRETION
    (1978) CROXATTO, HR; ROJAS, M; CORTHORN, J; ALBERTINI, R; ROBLERO, J
    I.p. injections of 1-5 IU of renin purified extracts, obtained either from hog or rat kidneys, in hyperhydrated rats receiving distilled water or 0.4% NaCl (5% body wt) produce not only a striking increase in the Na excretion rate but a very significant decrease in kallikrein excretion as well. In the urine excreted in the 1st h after renin administration kallikrein practically disappeared in the urine; with higher doses the inhibitory effect was very marked and lasted up to 120 min. In the same rats under a 2nd hyperhydration, not associated with renin injection, kallikrein tends to return to control levels.
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    ISOLATION AND CHARACTERIZATION OF RAT PLASMA GLANDULAR KALLIKREIN
    (1985) MASFERRER, J; ALBERTINI, R; CROXATTO, HR; GARCIA, P; PINTO, I
    A method was developed to purify glandular kallikrein present in rat plasma by using Sepharose-Aprotinin affinity chromatography and elution of the enzyme with p-aminobenzamidine. The isolated enzyme liberated kinins for kininogen II of low MW (sp. act. 14 ng kinins/min .times. mg) and p-nitroaniline (pNA) from the substrate S-2266 (sp. act. 1.23 nmol pNA/min .times. mg); it was inhibited by aprotinin, benzamidine and rat urinary antikallikrein antibody but not by ovomucoid. In polyacrylamide gel electrophoresis, the enzymatic activities of the preparation were associated with 2 light protein bands of MW equal to that of urinary kallikrein (35,000 daltons). Using this method, the recovery of [125I]kallikrein added to the plasma was 82-88%. The concentration of the enzyme in normal rat plasma was equivalent to 6.1 .+-. 2.1 ng kallikrein/ml. The mean value found in nephrectomized rats was 20.0 .+-. 6.3 ng kallikrein/ml. This increment was highly significant (P < 0.001). These results confirm the presence of glandular kallikrein in plasma which had been detected by other methods; they also demonstrate that the material purified from plasma is enzymatically active, suggesting that kallikrein may play a biological role in the control of blood circulation.
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    KALLIKREIN-KININ AND RENIN-ANGIOTENSIN SYSTEMS IN RENOVASCULAR HYPERTENSION IN RATS
    (1980) VIO, CP; ROBLERO, JS; CROXATTO, HR
    Plasma renin activity (PRA) and the levels of urinary kallikrein (UK) were studied simultaneously in Goldblatt 1- and 2-kidney hypertensive rats (1KG and 2KG) 5, 10 and 15 wk after clamping the left renal artery. Increase in PRA was statistically significant in 2KG rats (P < 0.0005 on the 5th and 10th wk, and P < 0.002 on the 15th wk). PRA was not significantly different to that of controls in 1KG rats. The urinary kallikrein levels were significantly lower in 1KG rats (P < 0.002) in relation to values found in normotensive rats. In 2KG rats, urinary kallikrein levels became significantly lower than those in controls only 15 wk after surgery.
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    PURIFICATION AND CHEMICAL STUDIES ON RAT URINARY KALLIKREIN
    (1975) PORCELLI, G; MARINIBETTOLO, GB; CROXATTO, HR; DIIORIO, M
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    PURIFICATION OF RENAL RAT KALLIKREIN AND CHEMICAL RELATIONS WITH URINARY RAT KALLIKREIN
    (1978) PORCELLI, G; MARINIBETTOLO, GB; CROXATTO, HR; DIIORIO, M; MICOTTI, G
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    RELEASE OF RENAL KALLIKREIN TO PERFUSATE BY ISOLATED RAT-KIDNEY
    (1976) ROBLERO, JS; CROXATTO, HR; ALBERTINI, RB
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    RENAL URINARY KALLIKREIN IN NORMOTENSIVE AND HYPERTENSIVE RATS DURING ENHANCED EXCRETION OF WATER AND ELECTROLYTES
    (1976) CROXATTO, HR; ALBERTINI, R; ARRIAGADA, R; ROBLERO, J; ROJAS, M; ROSAS, R
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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 AND PLASMA-RENIN ACTIVITY IN NORMAL HUMAN-PREGNANCY
    (1981) VALDES, G; ESPINOZA, P; MOORE, R; CROXATTO, HR
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    URINARY KALLIKREIN EXCRETION IN A SPONTANEOUSLY HYPERTENSIVE STRAIN OF RATS
    (1975) PORCELLI, G; BIANCHI, G; CROXATTO, HR