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Biomedical subjects

M Marin-Grez

Publications and source records attributed to M Marin-Grez.

At least 37 records · Page 2Linked to original sources
PubMed1989

Effect of atrial natriuretic peptide on the release of rat renal kallikrein.

The effect of atrial natriuretic peptide (ANP) on renal kallikrein release was investigated in barbiturate anesthetized rats. ANP injections in a pharmacological dose (1 microgram i.v.) increased kallikrein excretion for about 15 min. The effect of ANP on kallikrein excretion was abolished when amiloride (2.5 mg i.v.) was administered prior to the injection of the peptide. Intravenous infusion of ANP (1 or 5 micrograms/h) or of isotonic saline (2 or 4 ml/h) did not alter urinary kallikrein output. When the ANP infusion was discontinued, the excretory rate of the enzyme tended to decrease. This decrease was prevented by the administration of 0.1 mg/h desoxycorticosterone-glucoside. A transient increase in kallikrein excretion, coincident with the appearance of diuresis, was observed during ANP infusion in the mineralocorticoid-treated animals. The rate of kallikrein release into the incubation medium by rat kidney slices was not affected by the presence of ANP (10(-9)M). These results can be interpreted as effects following an increased distal sodium delivery rather than a direct effect of ANP on connecting tubule cells (CNT cells).

Amiloride↗
PubMed1989

[Oleothorax 40 years later].

Between 1930 and 1950 the induction of an oleothorax was widely accepted as treatment of patients with progressive tuberculosis. Now, the late complications of this therapeutic approach can occasionally be observed. A patient with an oleothorax induced forty years ago and extensive x-ray exposure through frequent fluoroscopie follow-up is presented. In addition, he has a carcinoma of the lung infiltrating the chest wall. The late complications of oleothorax and the possibility of a radiation-induced malignancy are discussed.

Carcinoma, Bronchogenic↗
PubMed1989

[Stereotactically targeted radiotherapy of cerebral arteriovenous malformations].

A report is given about radiotherapy in 41 patients suffering from cerebral vessel anomalies. A modified linear accelerator was used in a moving field technique with multiple pendulum planes to apply single doses between 8 and 28 Gy by means of stereotaxis into the angiographically determined target volume. The medium follow-up is 23 months. The latency of radiogenic effects is between one and two years. Radiological controls with an interval of more than 18 months after therapy are available in 17 out of 41 patients. Angiographic investigation showed complete obliterations of pathological vessels in six out of these patients and partial obliterations in six patients; five patients remained unchanged. There were no acute complications. Seven patients presented neurological deficiencies with a latency of 6 to 12 months, however, in all cases but one they regressed completely. Even taking into consideration the small number of patients and the short time of observation, a comparison with the results of other radiotherapeutical proceedings allows to draw the conclusion that the presented technique of stereotaxic convergent-beam irradiation represents a relatively simple, reliable and, in case of precise indication, efficient method for the therapy of cerebral arteriovenous malformations.

Adult↗
PubMed1989

Combined neutron-photon-therapy of locally recurrent rectosigmoidal tumors.

21 patients with unresectable recurrent adenocarcinoma of the rectum were treated with combined photon-neutron radiation therapy. 40 Gy photon were given to the whole pelvis followed by a boost field of 6.6 or 10 Gy utilizing 14 MeV monoenergetic neutrons. The latter was given with an arc therapy technique whereby the dose output fluctuations normally encountered during gantry rotation were compensated for by a computer guided system. All patients had severe pain symptoms before therapy. Twelve patients had a full remission of the symptoms and nine reported considerable relief of pain during follow-up examination. In three patients, further pain symptoms developed after six, seven, and nine months due to renewed tumor progression. In spite of the relative high neutron doses applied, side effects with the arc-technique remained minimal and did not exceed those encountered with photon therapy alone. Although the total follow-up time is relatively short at a maximum of 20 months, with a mean time of 8.5 months, the preliminary results so far are extremely optimistic leading us to further pursue the study.

Adenocarcinoma↗
PubMed1988

Effect of dopamine antagonists on the urine flow of rats infused with hypotonic saline.

1. The probable involvement of dopamine in the regulation of water excretion was investigated by administering dopamine antagonists intravenously to barbiturate--anaesthetized rats undergoing a water diuresis induced by the infusion of 0.83% glucose with 0.3% NaCl at the rate of 9 ml h-1. 2. Administration of 100 micrograms of the D1-/D2-dopamine antagonist, haloperidol, reduced the enhanced urine flow of rats infused with the hypotonic solution by 69% (from 75.4 +/- 13.0 to 23.6 +/- 6.0 microliter min-1, P less than 0.01). Similarly, the D1-receptor antagonist, SCH 23390, reduced urine flow by 58% (from 77.5 +/- 9.2 to 32.7 +/- 7.2 microliters min-1, P less than 0.01) and the D2-receptor antagonist, sulpiride, by 47% (from 66.2 +/- 8.6 to 35.1 +/- 6.8 microliter min-1, P less than 0.05). 3. The injection of SCH 23390 increased the urine osmolality from 189.6 +/- 27.5 to 479.8 +/- 45.8 mosm kg-1 (P less than 0.05). There was no significant change in sodium and potassium excretion in any of the experiments. Blood pressure (BP) decreased after haloperidol and SCH 23390 injection from control values of 121.7 +/- 1.7 and 116.5 +/- 7.4 to 113.3 +/- 3.3 and 106.0 +/- 8.8 mmHg respectively (P less than 0.05). 4. To study whether the influence of dopamine antagonists on urine flow during water diuresis depends on antidiuretic hormone (ADH), we administered 0.6 micrograms d(CH2)5-D-Phe-Ile-AVP (an ADH antagonist) shortly after the injection of 100 micrograms SCH 23390. The preferential V2 ADH-antagonist abolished the antidiuretic effect of SCH 23390 but did not affect its blood pressure reducing effect (from 118.6 +/- 5.6 to 103.2 +/- 4.6 mmHg, P <0.01). 5. These results suggest that dopamine antagonists blunted the hypotonic saline-induced diuresis by favouring ADH release through an interference with an inhibitory dopaminergic pathway.

Animals↗
PubMed1987

Amiloride inhibits the rise of urinary kallikrein excretion induced by frusemide administration in the rat.

The effect of amiloride administration on the urinary kallikrein response to the injection or continuous infusion of frusemide in normal Sprague-Dawley rats was investigated. Injections of frusemide induced repeatedly an increase in urinary kallikrein excretion. This effect was suppressed by amiloride. Amiloride also blocked the response to mannitol injection. A continuous infusion of frusemide lasting 100 min also induced an increase in urinary kallikrein excretion which persisted throughout the experiment. This response was completely blocked by the injection of amiloride. Urinary kallikrein excretion was directly and positively related to urine volume and urinary sodium excretion before and after amiloride injection. The regression lines had markedly decreased slopes after amiloride administration. The urinary kallikrein excretion was also positively related to the urine volume and urinary sodium excretion when frusemide was continuously infused. However, these relationships were abolished after amiloride injection. In both the injection and the infusion experiments, there was a direct relationship of urinary kallikrein excretion to urinary potassium excretion. Although this relationship persisted after amiloride injection, the regression line was shifted to the left. The suppression of the kallikrein stimulating effect of frusemide by the sodium channel blocker amiloride indicates that distal tubule sodium reabsorption is the triggering factor in urinary kallikrein excretion. The study suggests that the mechanism involved in the release of kallikrein by the distal tubular cells is linked to the renal mechanism affected by amiloride.

Amiloride↗
PubMed1987

Evidence for an involvement of dopamine receptors in the natriuretic response to atrial natriuretic peptide.

Intravenous injection of atrial natriuretic peptides (ANP) induces a preferential vasodilatation of the renal resistance vessels. A similar effect is exerted by dopamine. Exogenous administration of this catecholamine induces, like the atrial peptides, diuresis and natriuresis, an effect prevented by dopamine receptor antagonists. In view of these parallels, the influence of dopamine antagonists on the diuretic response of anaesthetized rats to ANP was tested. The unselective dopamine antagonists haloperidol (50 micrograms, i.v.) and chlorpromazine (50 micrograms, i.v.) prevented the diuretic and natriuretic effect of a partially purified atrial extract, and significantly blunted that of alpha-hANP (1 microgram). Dopamine receptors are classified as DA-1 and DA-2. The DA-2 receptor antagonists metoclopramide (50 micrograms, i.v.) and sulpiride (50 micrograms, i.v.) did not affect ANP induced natriuresis. The DA-1 receptor antagonists SCH 23390 and SK&F 83566 dose-dependently counteracted the renal response to the intravenous administration of ANP. The administration of haloperidol (25, 50 and 100 micrograms, i.v.) to rats undergoing a putative ANP dependent natriuresis (isotonic saline loading) dose-dependently reduced both urine volume and sodium excretion. Atriopeptin II (10(-9)-10(-10) M) displaced tritiated spiperone, a dopamine antagonist, from specific binding sites in homogenates of renal medulla, papilla and cortex. These results suggest that dopamine receptors, most probably of the DA-1 subclass, are involved in the natriuretic response to ANP. The present experiments do not allow the conclusion as to whether ANP directly interacts with the dopamine receptors or whether it affects these receptors by releasing dopamine.

Animals↗
PubMed1986

Kinins in cerebrospinal fluid: reduced concentration in spontaneously hypertensive rats.

Rat cerebrospinal fluid contains peptides which displace radiolabeled bradykinin from its specific antibodies. Two peptides which showed the same retention time as kallidin and bradykinin in a reverse phase high pressure liquid chromatography system were detected in cerebrospinal fluid of rats. The concentration of radioimmunologically detected kinins in the cerebrospinal fluid of spontaneously hypertensive rats of the Okamoto strain was lower than that of the Wistar Kyoto control rats.

Animals↗
PubMed1986

Filtration pressure response to infusion of atrial natriuretic peptides.

The present experiments were undertaken to assess the effect of an atrial extract (ANF) and of the synthetic atriopeptin II (APII) on filtration pressure of rat kidneys. Continuous recordings of stop flow pressure (SFP) were made to obtain an index of the change of glomerular capillary pressure produced by atrial peptides and its time course. Short-term infusion of ANF or APII increased SFP from 40.6 +/- 0.99 to 50.7 +/- 1.42 mm Hg (p less than 0.001) and from 44.0 +/- 1.28 to 52.7 +/- 1.75 mm Hg (p less than 0.001) respectively. The maximum response was achieved promptly. Return of SFP to control was slow: 20 minutes after termination of the infusion SFP was still elevated by 4.9 +/- 1.27 mm Hg (p less than 0.01). Tubule and stellate vessel pressures increased less than 2mm Hg, changes that were not significant. Arterial pressure fell 6 mm Hg (p less than 0.05). When arterial pressure was reduced by an aortic clamp to 85-90 mmHg prior to administration of APII the response of SFP was markedly blunted (from a mean increase of 9.0 +/- 1.07 mm Hg to 4.5 +/- 0.53 mm Hg). The increase of SFP probably reflects an increase of glomerular capillary pressure. The finding suggests that atrial peptides increase glomerular filtration rate at least in part by increasing filtration pressure.

Animals↗
PubMed1986

Urinary kallikrein response to repeated frusemide injections in rats: effect of adrenalectomy and deoxycorticosterone acetate treatment.

The effect of repeated intravenous injections of frusemide (0.17 mg/kg) on the urinary kallikrein excretion of normal, adrenalectomized and deoxycorticosterone acetate (DOCA)-treated adrenalectomized rats was studied. Adrenalectomy decreased baseline urinary kallikrein excretion, while DOCA treatment restored it to normal. Frusemide injections repeatedly increased urinary kallikrein excretion in the three groups of rats studied. Compared with control and DOCA-treated animals, adrenalectomized rats were less responsive. The excretion of urinary kallikrein was positively correlated with urine volume and with the excretion of sodium and potassium in all groups. The regression lines were shifted to the left in DOCA-treated adrenalectomized rats showing that mineralocorticoids enhance the effect of frusemide on urinary kallikrein excretion. The regression lines between urinary kallikrein excretion and the measured variables in adrenalectomized rats did not differ from those of control animals. We conclude that the response of urinary kallikrein to frusemide is influenced by the level of mineralocorticoid activity. The effect of frusemide on urinary kallikrein excretion does not appear to be a 'wash-out' of the enzyme since its influence did not subside after repeated injections.

Adrenalectomy↗
PubMed1986

[Size determination of abdominal and retroperitoneal organs by means of ultrasound].

Measurements of the liver, spleen and kidneys have shown that the measured size depends on the respiratory phase and on the position of organs in the abdomen or retroperitoneum, respectively. Hence, statements of the size of these organs or organ parts must be accompanied by data on the respiratory phase and positioning of the patient.

Abdomen↗
PubMed1985

The influence of tetracosactide and adrenal steroids on renal kallikrein activity and urinary kallikrein excretion in rats.

The effect of adrenal steroids (mineralo- and glucocorticoids) as well as that of the adrenocorticotrophic peptide tetracosactide (beta 1-24 corticotropin) on the renal kallikrein activity and on the urinary kallikrein excretion of rats was investigated. After the animals had been adapted to metabolic cages, they were injected with deoxycorticosterone acetate (15 mg/kg day), corticosterone (40 mg/kg day), both steroids combined or the vehicle (sesame oil). Additional groups of rats received tetracosactide (0.05, 0.1 or 0.2 mg/day) or the vehicle (100 microliter of 38 X 10(-3) M ZnCl2). After four days of treatment the urinary kallikrein excretion was higher in deoxycorticosterone-treated rats than in their controls. This increase was prevented when corticosterone was administered simultaneously. The renal kallikrein activity of corticosterone as well as that of deoxycorticosterone plus corticosterone-treated rats was subnormal. A dose-related reduction of both the renal kallikrein activity and the urinary kallikrein excretion was observed 2 days after starting the tetracosactide administration. It may be concluded that a stimulation of the endogenous release of glucocorticoids in the rat reduces the renal kallikrein activity and that glucocorticoids can prevent the stimulating effect of mineralocorticoids.

Adrenal Cortex Hormones↗
PubMed1985

Dopamine receptor antagonists inhibit the natriuretic response to atrial natriuretic factor (ANF).

The diuretic and natriuretic response of anesthetized rats to low doses of semi-purified atrial extracts or synthetic alpha-hANP was completely blocked by intravenous injection of 50 micrograms of haloperidol or chlorpromazine. Sulpiride or metoclopramide at the same doses did not show this effect. We conclude from these results that dopamine receptors, probably of the D1-type, are involved in the natriuretic effect of the atrial peptides.

Adenylyl Cyclases↗
PubMed1984

The influence of isotonic saline administration on the urinary excretion of kallikrein in rats.

Acute saline loading is known to increase kallikrein excretion. To clarify whether this is a specific stimulatory effect or rather a non-specific wash-out, pentobarbital anesthetized rats were loaded thrice (5 min infusions) at 40 min intervals with a volume of 150 mM NaCl equal to 5% of their body wt. The effect of such a load on the central venous pressure was studied in a separate group of rats. Control animals did not receive the infusions. Kallikrein excretion (amidolytic assay) increased with the first, but decreased with the subsequent saline administrations. The rise observed after the first load lost significance when kallikrein excretion was related to that of creatinine. The reduction observed after the second and third infusions remained significant even when expressed per mg of creatinine. Thus, saline load induced kallikrein "stimulation" is due to a non-specific wash-out. Similar transient enhancements of central venous pressure were observed after each of the three loads. This, together with the unchanged creatinine excretion (except for the rise seen after the first load) indicate that the lack of kallikrein stimulation after the second and third loads was not due to the appearance of heart failure. Saline loaded rats had a renal kallikrein activity at the end of the experiment which did not differ from that of controls. Plasma aldosterone concentration was reduced in saline infused rats, and it correlated with the kallikrein excretion when both, NaCl loaded and control rats, were taken into account.

Animals↗
PubMed1984

Inactivation of atrial natriuretic substance by kallikrein.

To further characterize the properties of the potent natriuretic and diuretic substance that can be extracted from atrial tissue, we investigated its susceptibility to inactivation by kallikrein and other proteolytic enzymes. Extracts of rat atrial tissue (tissue wet wt 100 mg/ml) were incubated with enzymes under standard conditions and tested by injection into nondiuretic anesthetized rats. One hour of incubation at 37 degrees C with pure porcine pancreatic kallikrein at concentrations of 250 micrograms/ml or greater significantly reduced the activity of atrial natriuretic substance. The reduction in activity was dependent on both enzyme concentration and time of incubation. The kallikrein-catalyzed degradation was completely blocked by aprotinin but was only partially retarded by soybean trypsin inhibitor. Trypsin reduced natriuretic and diuretic activity of extracts at concentrations of 400 micrograms/ml or greater, with nearly complete inactivation at a concentration of 1,000 micrograms/ml. Carboxypeptidase B also caused a concentration-dependent inactivation of the natriuretic material. Last, alpha-chymotrypsin (1,000 micrograms/ml) and elastase (1,000 micrograms/ml) were found to destroy the natriuretic activity. In a separate set of experiments natriuretic activity was observed to be retained by a 1,000 mol wt cutoff membrane. Inactivation of the natriuretic peptide by renal kallikrein is a possible mechanism for in vivo regulation of natriuretic activity.

Animals↗
PubMed1984

Opposing effects of captopril and aprotinin on tubuloglomerular feedback responses.

We investigated the effect of two protease inhibitors, captopril and aprotinin, on tubuloglomerular feedback. In anesthetized rats, 15 or 25 mg/kg captopril significantly reduced the change of early proximal flow rate achieved by raising loop of Henle perfusion rate from 0 to 40 nl/min. Consistent with this reduction of maximum responses, there was a rise of single nephron glomerular filtration rate from 30.7 +/- 1.15 to 35.0 +/- 0.93 nl/min (P less than 0.01) following 25 mg/kg captopril. Infusion of aprotinin at 40,000 KIU/h produced an increase in maximum feedback responses from 38.2 +/- 1.66 to 56.8 +/- 2.35% (P less than 0.05). Infusion of aprotinin in two different doses (20,000 or 40,000 KIU/h) diminished or prevented the effect of 25 mg/kg captopril on maximum feedback responses. Since the main action of aprotinin is believed to be kallikrein inhibition, our data suggest that the magnitude of feedback responses may be affected by the kallikrein-kinin system and that the action of captopril may be in part mediated by its interference with kinin metabolism.

Absorption↗
PubMed1984

Steroid induced changes of the renal kallikrein-kinin system in rats.

In male Sprague-Dawley rats the influence of salt loading (1% NaCl), deoxycorticosterone acetate (2 X 15 mg/kg/day resp. 250 mg/kg sc), corticosterone (2 X 20 mg/kg/day sc) and adrenocorticosterone (0.5 mg/kg/day tetracosactid sc) on the activity of renal kallikrein and renal renin activity was investigated. Salt loading lowered renal kallikrein activity, deoxycorticosterone stimulated its activity and in combination they had no effect on renal kallikrein activity. The time course of kallikrein stimulation by deoxycorticosterone showed no relationship to the escape phenomenon of the kidney from the sodium retaining effect of the mineralocorticoid hormone. Reduction of endogenous mineralocorticoid hormones by adrenalectomy caused a marked reduction of urinary and renal kallikrein activity. Corticosterone suppressed the activity of the renal kallikrein-kinin system at the same time as the reduction in urinary aldosterone excretion. Adrenocorticotrophin caused the same decrease in the activity of renal kallikrein as corticosterone. Urinary aldosterone excretion, however, was significantly stimulated. Thus, the known positive correlation between kallikrein and aldosterone was missing. In all experiments the urinary excretion of kallikrein correlated highly with the kallikrein activity measured in renal cortical tissue. However, no correlation was found between kallikrein and urine volume or urinary excretion of sodium and potassium. In our experiments no relationship between the activity of the renin-angiotensin system and that of the renal kallikrein-kinin system was observed. Furthermore, no clear relationship was found between systemic blood pressure and the activity of the renal kallikrein-kinin system.

Adrenalectomy↗