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A M Moura

Publications and source records attributed to A M Moura.

At least 19 recordsLinked to original sources
PubMed1988

Interaction between aldosterone and vasopressin on vascular smooth muscle permeability to sodium.

The s.c. injection of aldosterone (10 micrograms/kg) induces a release of vasopressin. The peak of plasma vasopressin level occurs at the same time as the late in vivo effect of aldosterone on passive 22Na efflux from arterial smooth muscle. These results indicate that vasopressin mediates the delayed in vivo effects of aldosterone on ouabain-insensitive 22Na efflux, since on the other hand, it has been possible to show that the action of the peptide is accelerated by a previous exposure to the mineralocorticoid. Indeed, after a 120-min pretreatment with 10(-8) M aldosterone, vasopressin induces an effect on 22Na efflux in 30 min, as opposed to the 120 min needed in the absence of the steroid.

Adrenalectomy↗
PubMed1988

[Ex vivo and in vitro effects of trandolapril on the efflux of 22Na from the caudal artery of the SHR rat. Inhibition of vascular angiotensin II production].

The inhibition of converting enzyme (CE) activity in target tissues other than blood and lung vascular endothelium may be important for the antihypertensive action of CE inhibitors (ICE) (Unger et al 1983). In order to determine if ICE may have an effect on the transmembrane Na movements implicated in the regulation of vascular tone, we have studied the effects of trandolapril and enalapril on 22Na effluxes from the tail artery of 20 weeks old SHR. In vivo, the chronic oral treatment (14 days) with trandolapril (1.3 mg/kg/day) decreased the ouabain-sensitive 22Na efflux (controls: 0.050 +/- 0.004 min-1 (n = 8); trandolapril (1 mg/kg): 0.030 +/- 0.03 min-1 (n = 10) p less than 0.01), and the ouabain-insensitive 22Na efflux (controls: 0.088 +/- 0.0030 min-1; trandolapril (1 mg/kg): 0.080 +/- 0.003 min-1 (n = 10) p less than 0.05). Enalapril had no effect at the dose of 10 mg/kg/day (14 days). In vitro, trandolapril diacid (RU 44403) decreased the ouabain-sensitive 22Na efflux (controls: 0.045 +/- 0.002 min-1 (n = 6); RU 44403 (10(-9) M): 0.031 +/- 0.002 min-1 (n = 6) p less than 0.01), and the ouabain-insensitive efflux (controls: 0.096 +/- 0.004 min-1 (n = 6); RU 44403 (10(-9) M): 0.084 +/- 0.006 min-1 (n = 6) p less than 0.05). The effects were dose-dependent. Enalapril diacid (MK 422) also dose-dependently decreased 22Na effluxes but it was approximately 10 fold less active.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1987

Prevention by calcitonin of the pathological modifications of the rabbit arterial wall induced by immunization with elastin peptides: effect on vascular smooth muscle permeability to ions.

Immunization of rabbits with elastin peptides prepared from purified bovine ligamentum nuchae elastin produces calcified arteriosclerotic lesions and fragmentation of elastic lamellae. Simultaneous administration of porcine calcitonin largely prevents the development of lesions. Experiments were carried out to clarify the mechanisms involved in the development of lesions as well as those involved in the preventive effect of calcitonin. Control experiments were carried out using bovine serum albumin (BSA) as antigen. Circulating antibodies and soluble immune complexes increased steadily in the sera of animals immunized with elastin peptides or BSA. The cellular immune reaction was weak as assessed by [3H]thymidine incorporation into lymphocytes in the presence of antigen or phytohemagglutinin. Arterial lesions appeared only in the animals immunized with elastin peptides, not in those immunized with BSA. Ion flux measurements were also carried out on strips of aorta obtained from immunized and control animals. Immunization with elastin peptides significantly increased the ouabain-insensitive 22Na+ efflux, the 86Rb efflux (indicator of K+ efflux), and the 45Ca2+ influx. Simultaneous calcitonin administration prevented the increase in Ca2+ influx but did enhance passive permeability to Na+ and K+ as well as the sodium pump. When calcitonin was administered without immunization, it decreased arterial smooth muscle permeability to Na+ and K+ and also decreased the basal Ca2+ influx. It is concluded that the pathological modifications of the arterial wall triggered by immunization with elastin peptides is at least partly mediated by the effect of antielastin antibodies and immune complexes on the ion permeability of arterial smooth muscle. Prevention of the increased Ca2+ influx by calcitonin is probably a key effect in the prevention of the development of lesions. The fact that calcitonin alone can modify the ion permeability of arterial smooth muscle suggests that this hormone may play a role in the regulation of vascular homeostasis.

Animals↗
PubMed1987

Arterial effects of aldosterone and antimineralocorticoid compounds mechanism of action.

The aim of our work was to study the mechanism of action of aldosterone and antialdosterone compounds on Na+ and K+ fluxes in vascular smooth muscle. In the long term, regulation of salt metabolism depends on aldosterone effects on Na+, K+, H+ and H2O transport by the renal tubules. Furthermore, it has been shown that aldosterone modifies several epithelial transports, inducing a positive sodium balance. The chronic in vivo administration of aldosterone modifies transmembrane ionic fluxes in vascular smooth muscle. Garwitz and Jones suggested that aldosterone may enhance net Na+ transport through the stimulation of the sodium pump. The results obtained in our laboratory indicate that aldosterone has a direct stimulatory action on ouabain-dependent and on ouabain-independent Na efflux. Furthermore, the mineralocorticoid enhances passive K permeability, as well as the Na pump dependent K influx. Both effects are blocked by antimineralocorticoid compounds. Recent experiments have shown that vasopressin potentiates some of the in vivo effects of aldosterone.

Aldosterone↗
PubMed1987

[Involvement of vasopressin in the effects of aldosterone on the arterial wall].

We have previously shown that an humoral factor is involved in the delayed effect of aldosterone on the passive transmembrane movements of Na+ from arterial smooth muscle (Moura and Worcel, 1984). In absence of vasopressin, the effects of aldosterone on the same Na transports suggest that vasopressin may be this humoral factor (Moura, Angeli and Worcel, 1986) (Angeli, Moura and Worcel, 1986). We show here that the s.c. injection of aldosterone (10 micrograms/kg) to adrenalectomized Sprague Dawley rats induces a release of vasopressin. This peptide exerts a direct action on ouabain-sensitive and insensitive components of 22Na efflux from the rat tail artery, and potentiates the late effect of aldosterone on passive Na+ efflux. There is no additive effect of the two hormones on Na+ pump activity. In conclusion vasopressin is the humoral factor involved in the late effect of aldosterone on passive transmembrane movement of Na from vascular smooth muscle.

Adrenalectomy↗
PubMed1986

Arterial smooth muscle effects of aldosterone and vasopressin: action on ionic fluxes.

We have shown previously that aldosterone injected s.c. to adrenalectomized rats has a mineralocorticoid specific action on the transmembrane movements of sodium and potassium from the rat tail artery. These effects appeared to be partly due to an unknown humoral factor. Indeed, the late in vivo effects of aldosterone on 22Na and 86Rb effluxes are suppressed or reduced after in vitro exposure to the hormone. In rats perfused with a specific antagonist of the pressor effect of vasopressin, the in vitro administration of aldosterone induced a kinetic action similar to that observed after in vitro exposure to the mineralocorticoid. Vasopressin exerts a direct action on 22Na and 86Rb effluxes. These effects were correlated in the time with the late in vivo effects of aldosterone. Moreover, vasopressin appears to potentiate the in vitro effects of aldosterone on 22Na and 86Rb effluxes. It is not yet possible to ascertain if this effect is additive or permissive.

Aldosterone↗
PubMed1986

[Effects of aldosterone and vasopressin on transmembrane efflux of sodium from the arterial wall].

We have previously shown that, injected s.c. to adrenalectomized Sprague-Dawley rats (SD.ADx), aldosterone has a mineralocorticoid specific effect on transmembrane movements of 22Na from arterial smooth muscle. These effects appear to be partly due to the action of an humoral factor. Indeed, in vitro, the late increase in passive 22Na efflux is not observed (Moura and Worcel, 1984). In rats perfused with a specific antagonists of the pressor effect of vasopressin (Vp), the in vivo administration of aldosterone induced a kinetic action similar to that observed after in vitro exposure to the mineralocorticoid. These results suggested that Vp may be the humoral factor (Moura, Angeli and Worcel, 1985). In adrenalectomized homozygous Brattleboro rats (DI.ADx), aldosterone (10(-8)M) increases ouabain independent 22Na efflux (DI.AX: 0.073 +/- 0.002 min-1(n = 15); DI.ADx + Aldo: 0.096 +/- 0.002 min-1(n = 12)p less than 0.01) and ouabain-dependent 22Na efflux (DI.ADx: 0.031 +/- 0.001 min-1; DI.ADx + Aldo: 0.037 +/- 0.002 min-1 p less than 0.01). Vp also increases ouabain sensitive and insensitive 22Na effluxes and potentiates the effects of aldosterone on passive Na+ transferts (DI.ADx + Aldo + Vp: 0.015 +/- 0.003 min-1 (n = 16) p less than 0.01). In conclusion, these results suggest that Vp may be involved in the effects of aldosterone on 22Na effluxes. Furthermore Vp potentiates the effects of aldosterone on passive 22Na effluxes. But it is not yet possible to ascertain if Vp action is additive or permissive.

Adrenalectomy↗
PubMed1984

[Effect of an antiglucocorticoid steroid on the arterial hypertension induced by glucocorticoids in the rat].

Hypertension was induced in male rats by administration of a glucocorticoid agonist, RU 26988. Systolic blood pressure (SBP) increased by 35 mmHg. Administration of an antimineralocorticoid derivative, RU 28318, did not modify hypertension. In contrast administration of a steroid derivative with antiglucocorticoid properties, RU 38486, prevented glucocorticoid-induced hypertension in a large part. SBP augmented only by 10 mmHg. The glucocorticoid increased total and active, ouabain-sensitive, 22Na efflux, as measured from caudal arteries, whereas concomitant administration of the antiglucocorticoid derivative prevented these changes. It is suggested that glucocorticoid-induced hypertension may be related to vascular Na pump activation and to the subsequent ionic changes. These changes, as well as hypertension, are antagonized by steroid derivatives with antiglucocorticoid properties.

Androstanols↗
PubMed1982

Mode of action of cyclothiazide and triamterene. Ex vivo effect on 22Na and 86Rb efflux from arterial smooth muscle.

Acute oral cyclothiazide treatment of conscious rats increased ex vivo 86Rb efflux from tail artery smooth muscle. This effect was blocked by oral triamterene. Identical results were obtained in binephrectomized rats, suggesting that the two drugs had a direct effect on smooth muscle K+ (86Rb) permeability. Decreased ex vivo smooth muscle 22Na efflux induced by oral cyclothiazide and triamterene is probably secondary to their renal actions, since there was no effect in binephrectomized rats.

Animals↗
PubMed1979

Identification of different sodium compartments from smooth muscle cells, fibroblasts and endothelial cells, in arteries and tissue culture.

1. The (22)Na efflux curve from the rat tail artery, at 35 degrees C, can be analysed as the sum of three distinct components, from 0 to 90 min of washout. After an initial diffusional component the two late exponential components Be(-kBt) and Ce(-kCt) have the following values: B = 3.03 +/- 0.15 m-mole/kg wet wt. and C = 0.56 +/- 0.04; k(B) = 0.145 +/- 0.005 min(-1) and k(C) = 0.015 +/- 0.007.2. In order to identify the cellular origin of the different compartments we compared the (22)Na efflux curve from the rat tail artery with the curves obtained from whole rabbit aortal strips, rabbit aortal medial or adventitial strips; and primary cultures from rabbit aorta medial smooth muscle cells, cultures of a non-fusing muscle cell line (BC(3)H1), fibroblasts and endothelial cells.3. It is possible to identify under these experimental conditions the cellular compartments from which the different exponential components of the efflux from the whole arteries originate. Fibroblasts and endothelial cultures, as well as adventitial strips exchange (22)Na slowly with exponential constants resembling k(C). Their efflux rate constants are: fibroblast cultures 0.010 +/- 0.002 min(-1), endothelial cells 0.015 +/- 0.003 min(-1) and adventitia 0.019 +/- 0.007 min(-1). Smooth muscle cells are exclusively responsible for the intermediate component Be(-kBt), but they present also a slow component, indistinguishible from the slow exponential component from the other types of cells in the artery. The rate constants for muscle cells are: rabbit aortic media k(B) 0.25 +/- 0.09 min(-1) and k(C) = 0.013 +/- 0.004 min(-1); medial cultures k(B) = 0.202 +/- 0.005 min(-1) and k(C1) = 0.020 +/- 0.003 min(-1); and BC(3)H1 cell culture k(B) = 0.205 +/- 0.083 min(-1) and k(C) = 0.016 +/- 0.003 min(-1).4. The efflux from compartment B of smooth muscle cells is inhibited by ouabain and in the absence of extracellular K(+). The efflux from compartment C is inhibited only by ouabain but not by the suppression of extracellular K(+).5. We propose a distribution of Na(+) in smooth muscle cells in two intracellular compartments: (1) Na(+) freely dissolved in the sarcoplasm, exchanging with the kinetics of compartment B and (2) a second cellular compartment which could be contained in the sarcoplasmic reticulum exchanging with the kinetics of compartment C.6. On the basis of the previous model of Na(+) distribution, considering our values, and without any correction, the estimated sarcoplasmic concentration of Na(+) is 9.6 mM, compatible with the direct measurements obtained in skeletal and heart muscle. The Na(+) concentration in the sarcoplasmic reticulum would be 4-10 times higher than in the cytoplasm. In order to increase the accuracy of our calculations it would be necessary to account for the interdiffusion and back diffusion of Na(+) between compartments. It is not possible to attain this goal at the present time.

Animals↗
PubMed1978

Calcitonin diuretic effect in the rabbit.

In an attempt to study the renal effects of Calcitonin (porcine CT) in the rabbit, the excreted fractions of filtered water, osmolality, sodium, potassium and chloride, and the calcium and phosphorus urinary excretions were studied during isotonic (ISD) and hypertonic (HSD) saline diuresis. Four doses (0.1, 0.8, 4 and 20 IU MRC/kg were perfused during one hour in I.S.D.; 4 and 20 IU MRC/kg in HSD. During ISD, Calcitonin at doses of 4 and 20 IU MRC/kg/hr significantly increased the diuresis and the Na+, Cl-, K+, PO4 3-, Ca2+ excreted fractions. This effect was also observed, to a lesser extent, at a dose of 0.8 IU MRC/kg/hr, whereas 0.1 IU MRC/kg/hr produced no significant effect. During ISD, a log dose related effect of CT appeared to exist with all studied parameters. Moreover, a biphasic pattern of free-water clearance was observed during ISD: this parameter increased during the first half hour of CT perfusion, and then decreased dramatically. During HSD, CT perfusion induced a decrease of free-water reabsorption and urinary osmolality/plasma osmolality ratio. These results suggest that the diuretic effect and saliuretic effect of CT (in the rabbit) are mainly the consequence of the decrease of the proximal reabsorption of sodium. The possibility of a second site of action is discussed. The diuretic effects of CT are compared to data observed with the well-known diuretic drugs.

Animals↗
PubMed1978

Pharmacology of the adrenoceptors and cholinoceptors of the BC3H1 nonfusing muscle cell line.

1. We have studied the action of different transmitters on the transmembrane 42K or 86Rb efflux from tissue cultures of the BC3H1 muscle cell line. 2. The effect of catecholamines and carbachol (CCh) on the isotope efflux rate was measured by addition of the drugs at different times during the washout. 3. Noradrenaline (NA), phenylephrine (Phe), isoprenaline (Iso) and CCh increased 42K and 86Rb efflux rate in a dose-dependent manner. 4. The action of NA seems to be due exclusively to the stimulation of alpha-receptors, since its effect was blocked by phentolamine but not by propranolol. The effects of Iso on the 86Rb efflux were inhibited by propranolol. The beta-receptors in the BC3H1 cells seem to be the beta2-type since they are stimulated by Iso and insensitive to NA. 5. The effect of CCh was blocked (+)-tubocurarine but not by atropine. This result confirms the presence of nicotinic receptors in BC3H1 cells.

Carbachol↗
PubMed1976

The effects of hormones and prostaglandins on the calcium pools in cultured myocardial cells.

Determinations of the calcium pools in myocardial cells in vitro have shown the existence of at least three pools of exchangeable calcium. Epinephrine and glucagon were found to produce significant increases in the size of the two slower exchanging pools. Prostaglandins E1 and F1alpha also increased significantly calcium pool size whereas E2 and F2alpha did not; results which correlate well with the effects of the two former prostaglandins on intracellular cAMP levels. The results imply that these agents cause small, but significant, changes in the transmembrane exchange of calcium and large increases in the intracellular calcium pool. Effects which may involve the direct or indirect action of cAMP.

Animals↗