Browsing by Author "ROBLERO, J"

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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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    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 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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    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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    KALLIKREIN-LIKE ACTIVITY IN PERFUSATES AND URINE OF ISOLATED RAT KIDNEYS
    (1976) ROBLERO, J; CROXATTO, H; GARCIA, R; CORTHORN, J; DEVITO, E
    In the perfusate and the urine produced during perfusion of isolated rat kidneys a kallikrein-like enzyme similar to that found in the kidneys was detectable by bioassay 15-25 min after the beginning of the perfusion. The source of the kallikrein activity was the kidney itself, since before the perfusion was started the blood remaining in the kidneys was washed out, and the perfusion medium was free of kallikrein and its precursors and substrates. The kallikreinlike activity of the perfusate was characterized by an oxytocic effect on isolated rat uterus, a kininogenase activity on kininogen II, an esterase activity on N-benzoyl-L-arginine ethyl ester and a hypotensive effect on anesthetized rats. These properties were inhibited by diisopropyl fluorophosphate and aprotinin but not by pepstatin. Kallikreinlike activity in the perfused kidney was lower than that in the nonperfused organ, but the total amount of kallikrein activity released to the excreted urine and the perfusate was significantly greater than the corresponding activity that disappeared in the kidney. This result agrees with the concept that the renal tissue can synthesize kallikrein.
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    RELEASE OF ACTIVATABLE KALLIKREIN BY ISOLATED RAT KIDNEYS
    (1981) CORTHORN, J; ROBLERO, J
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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