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J E Pinto

Publications and source records attributed to J E Pinto.

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

[The mitral valve apparatus: an anatomo-echocardiographic approach].

The shape of the mitral valve ring, the position of its chordae and of its leaflets were studied in 34 normal hearts fixed through intra-ventricular injection of tamponate formalin. As the authors have assumed that the post-rigor left ventricle has an architecture very similar to that seen at to the end of ventricular systole, comparisons were made between the anatomical and the echocardiographic features usually seen at the end of the phase of the cardiac cycle. The mitral ring has the shape of a hyperbolic paraboloid, and this peculiar geometry explains why the "apical-four chambers" view, which explores the most superficial ring segments, is the more appropriate view for detecting mitral valve prolapses. In that incidence the valvar diameter is longer (2.43 +/- 0.45 cm) that in the "parasternal view" (1.99 +/- 0.45 cm) and the angle made by the leaflets is comparatively less acute ("four chambers" = 127.41 +/- 16.45 degrees; "parasternal" = 102.05 +/- 0.17 degrees). In the "four chamber" view the point of coaptation (which represents the vertex of the referred angle) is 0.45 +/- 0.17 cm far from the echographic line usually taken as the valvar plane (EVPL-echocardiographic valvar plane line) whereas in the other view, it is more distant from this line (0.59 +/- 0.16 cm). These two last factors make both leaflets closer to the left atrium and explains why mitral valve prolapse, when present, is more easily seen in that incidence.(ABSTRACT TRUNCATED AT 250 WORDS)

Echocardiography↗
PubMed1988

Angiotensin II binding sites in the superior cervical ganglia of spontaneously hypertensive and Wistar-Kyoto rats after preganglionic denervation.

Angiotensin II binding was higher in superior cervical ganglia of adult spontaneously hypertensive rats (SHR) when compared to ganglia of Wistar-Kyoto (WKY) rats (571 +/- 29 and 375 +/- 9 fmol/mg protein, SHR and WKY, respectively, P less than 0.05). Unilateral preganglionic denervation reduced binding site density in ganglia of WKY (-39%, P less than 0.05 vs sham operated ganglia in WKY), and the decrease of binding sites was larger in SHR (-59%, P less than 0.01, operated vs sham operated ganglia in SHR). Part of the binding sites in the superior cervical ganglia may be present in or be associated to preganglionic nerves, and the number of these sites is higher in SHR.

Animals↗
PubMed1988

Glyphosate Induces 3-Deoxy-d-arabino-Heptulosonate 7-Phosphate Synthase in Potato (Solanum tuberosum L.) Cells Grown in Suspension Culture.

The activity of the first enzyme of the shikimate pathway, 3-deoxy-d-arabino-heptulosonate 7-phosphate synthase, varies during the growth cycle of Solanum tuberosum L. cv superior cells in suspension culture. Maximum specific enzyme activity was observed midway through the linear phase of growth. When mid-log phase cells are exposed to glyphosate, the specific activity of the enzyme increases severalfold within 24 hours. The glyphosate-induced increase in enzyme activity is due to an increase in the amount of enzyme as determined by immunoblotting. Glyphosate (up to 2 millimolar) has no effect on the enzyme activity in vitro. Dehydroquinate synthase, the second enzyme of the shikimate pathway, is not induced by glyphosate.

Journal Article↗
PubMed1987

Effects of doxorubicin on the release of catecholamines from the bovine adrenal medulla.

We have studied the effects of the anthracycline doxorubicin on the release of catecholamines from the perfused bovine adrenal gland. Doxorubicin produced different concentration-dependent effects on adrenomedullary catecholamine secretion. At a 3 x 10(-6) M concentration, doxorubicin facilitated the secretory response induced by acetylcholine and 56 mM K+ but did not affect the spontaneous catecholamine output or that evoked by NaCl deprivation. Conversely, a higher concentration of doxorubicin (10(-4) M) resulted in a significant and irreversible inhibition of the spontaneous secretion of catecholamines, as well as of that caused by acetylcholine or high K+. Doxorubicin at this high concentration did not modify the catecholamine release induced by NaCl deprivation. These results suggest that doxorubicin effects could be mediated at the plasma membrane of the chromaffin cells. The present study is compatible with the idea that increased adrenomedullary catecholamine release is involved in the cardiotoxic action of relatively low doses of doxorubicin.

Acetylcholine↗
PubMed1986

3-Deoxy-d-arabino-Heptulosonate 7-Phosphate Synthase from Potato Tuber (Solanum tuberosum L.).

3-Deoxy-d-arabino-heptulosonate 7-phosphate synthase, the first enzyme of the shikimate pathway, was purified to electrophoretic homogeneity from tubers of Solanum tuberosum L. cv Superior. The enzyme is a dimer with a native molecular weight of 110,000. The enzyme appears to be hysteretic. The enzyme activity is stimulated by Mn(2+) and l-tryptophan. Chromatofocusing resolved two forms of the enzyme with isoelectric points of 7.8 and 8.4, respectively. The enzyme closely resembles an analogous activity previously isolated from roots of Daucus carota (JA Suzich, JFD Dean, KM Herrmann 1985 Plant Physiol 79: 765-770).

Journal Article↗
PubMed1985

Inhibitory effect of hyperosmolality on catecholamine secretion from the bovine adrenal medulla.

We examined the effect of hyperosmolality on exocytotic catecholamine secretion in isolated-perfused bovine adrenals, in both the absence and presence of Ca2+ in the extracellular medium. Exposure of adrenal glands to hyperosmotic media (600 mOsm/Kg H2O) for 20 minutes significantly decreased spontaneous catecholamine output, and was independent of extracellular Ca2+ concentration. Adrenal glands were exposed to a hyperosmotic Locke solution (600 mOsm/Kg H2O) for 10 minutes and then stimulated with acetylcholine. Hyperosmolality produced a significant, reversible inhibition of acetylcholine-evoked catecholamine secretion. As the osmotic strength of the perfusion fluid was increased, either by addition of sucrose or NaCl, there was a progressive reduction in the acetylcholine response. Hyperosmolality also decreased catecholamine release induced by 56 mM K+ and by removal of NaCl from the perfusion medium. Similar results were seen in glands exposed to a NaCl-free solution in the absence of extracellular Ca2+. These results suggest that inhibitory effects of hyperosmolality on stimulus-secretion coupling in the adrenal medulla are exerted after Ca2+ enters the chromaffin cells, and support one of the primary criteria of the chemiosmotic hypothesis.

Acetylcholine↗
PubMed1984

Different inhibitory sites of action for magnesium and verapamil in the bovine adrenal medulla.

The effects of verapamil and Mg2+ on catecholamine release induced by the substitution of NaCl by sucrose in the extracellular medium were studied in the perfused bovine adrenal medulla. Verapamil (3 X 10(-4) M) totally blocked the acetylcholine-evoked release of amines, but failed to antagonize the secretory response promoted by NaCl-omission. Perfusing glands with a Locke solution containing 10 mM Mg2+, produced a 61.4 and 62.8% inhibition of catecholamine release induced by acetylcholine and by NaCl-deprivation respectively. A similar inhibitory effect of Mg2+ (10-20 mM) was obtained in glands exposed to a NaCl-free solution in the absence of extracellular Ca2+. In adrenal glands previously perfused with verapamil (3 X 10(-4) M) and then exposed to a Locke solution containing verapamil (3 X 10(-4) M) and Mg2+ (10 or 20 mM) the inhibition of the secretory responses promoted by NaCl-omission was of the same magnitude as that obtained when the glands were perfused with Mg2+ (10 or 20 mM) in the absence of verapamil. A similar lacking effect of verapamil on the blocking action of Mg2+ on catecholamine release evoked by NaCl-deprivation was observed in the absence of extracellular Ca2+. These results are compatible with the idea that in the bovine adrenal medulla verapamil and Mg2+ could have different inhibitory sites of action. Verapamil would exert its blocking effect at an extracellular site, while the inhibitory action of Mg2+ may be mediated by an intracellular site. An additional extracellular locus of action for Mg2+ at the external surface of the chromaffin cell cannot be discarded. These results also suggest that calcium channels may not be involved in the inward transport mechanism of Mg2+ to its intracellular locus of action.

Acetylcholine↗
PubMed1983

Contrasting effect of verapamil on catecholamine release induced by acetylcholine and by NaCl-omission from the bovine adrenal medulla.

Verapamil (3 X 10(-4) M) produced a 92.2% inhibition on the release of catecholamines induced by acetylcholine in perfused bovine adrenal glands. This blocking effect was slowly reversible. On the other hand, verapamil (3 X 10(-4) M) failed to antagonize the secretory response evoked by the substitution of NaCl by sucrose in the perfusion fluid. A similar lack of inhibitory effect of verapamil on catecholamine output produced by NaCl-omission was observed in the absence of extra-cellular Ca2+. These results suggest that Ca2+ influx might not be involved in adreno-medullary secretion induced by the substitution of NaCl by sucrose in the perfusion medium.

Acetylcholine↗
PubMed1979

The blocking effect of magnesium on the secretion of adrenal catecholamines induced by the omission of sodium from the extracellular medium.

The blocking action of Mg++ on catecholamine release induced by the substitution of extracellular Na+ by an osmotic equivalent amount of sucrose was studied in isolated, perfused bovine adrenal glands. Perfusing glands with 10 mM Mg++ produced at 51.1% inhibition on catecholamine release evoked by Na+ omission. Increasing the concentration of Mg++ to 20 mM this inhibitory effect was enhanced to 90.3%. D-600 (0.3 mM) promoted a marked blockade of acetylcholine-induced release of catechol hormones that was partially and significantly reverted increasing the concentration of Ca++ in the perfusion medium. D-600 (0.3 mM) failed to inhibit the catecholamine-releasing effect of Na+ deprivation. In adrenal glands previously perfused with D-600 (0.3 mM) and then exposed to a Locke solution containing D-600 (0.3 mM) + Mg++ (10 or 20 mM) the inhibition of the secretory responses evoked by the omission of Na+ was of the same magnitude as that obtained when the glands were perfused with Mg++ (10 or 20 mM) in the absence of D-600. These results are compatible with the view that the blocking effect of Mg++ may involve an intracellular site of action and that the access of Mg++ into the chromaffin cell may not be mediated through the Ca++ channels.

Acetylcholine↗
PubMed1979

Effects of methoxyverapamil on the stimulation by Ca2+, Sr2+ and Ba2+ and on the inhibition by Mg2+ of catecholamine release from the adrenal medulla.

1 Bovine adrenal glands were perfused with Ca2+-free Locke solution and catecholamine release was induced either by the introduction of Ca2+, Sr2+ or Ba2+ into the perfusion fluid or by the substitution of Na+ by an osmotically equivalent amount of sucrose. 2 Methoxyverapamil (D600) at a concentration of 3 X 10(-4) M blocked the release of catecholamines in response to Ca2+, Sr2+ or Ba2+ stimulation but failed to block the release evoked by the omission of Na+. 3 Mg2+ (10 to 20 mM) blocked the release induced by Na+-deprivation; however, this inhibitory effect of Mg2+ was not modified by D600. 4 D600 blocked the increase in the efflux of 45Ca from the perfused gland induced by the introduction of Ca2+ into the perfusion fluid and blocked the uptake of 45Ca into adrenal medullary slices induced by K+ depolarization. 5 The results suggest that Ca2+, Sr2+ and Ba2+ may enter the chromaffin cell through the same channel and that this channel is blocked by D600. Mg2+ may enter the cell through the same Ca2+ channel but with a high rate of permeation or it may enter through a channel which is resistant to D600. Alternatively, Mg2+ may exert this inhibitory effect at an extracellular site.

Adrenal Medulla↗
PubMed1977

Calcium movements during the release of catecholamines from the adrenal medulla: effects of methoxyverapamil and external cations.

1. Cortex-free adrenal glands previously labelled with the isotope (45)Ca have been perfused with Locke or modified Locke solution to assess Ca(2+) movements under different conditions.2. Substitution of Na(+) by either sucrose or choline during perfusion with Ca(2+)-free Locke solution induced a significant and sustained decrease in the (45)Ca efflux. Concomitant with this effect there was an increase in the output of catecholamines from the perfused gland.3. In the presence of Ca(2+) (2.2 mM) in the perfusion fluid, Na(+) omission induced an increase in the (45)Ca efflux. This increase was significantly reduced if 3 x 10(-4)M methoxyverapamil (D-600) was present in the perfusion fluid. However, the increased catecholamine output in response to Na(+) deprivation remained unchanged.4. Excess of Mg(2+) (20 mM) in the extracellular medium blocked the increase in catecholamine output in response to Na(+) omission. However, the decrease in the (45)Ca efflux produced by Na(+) deprivation in the presence of this high concentration of Mg(2+) was similar to that observed in the presence of 1.2 mM-Mg(2+).5. In the absence of Mg(2+) in the extracellular medium, substitution of Na(+) by either sucrose or choline induced a sharp and transient increase in the (45)Ca efflux rate coefficient. This increased (45)Ca efflux, which has similar time course as the enhanced catecholamine output, was not affected by the presence of 3 x 10(-4)M methoxyverapamil.6. In the absence of Mg(2+), the graded substitution of Na(+) in the perfusion medium by sucrose enhanced the efflux of (45)Ca. This increase in the (45)Ca outward movement was linearly related to the logarithm of the extracellular Na(+) concentration.7. After perfusion of glands with Ca(2+)-free Locke solution, the reintroduction of Ca(2+) (2.2 mM) into the perfusion fluid produced an increase in the (45)Ca efflux. This was accompanied by a discharge of catecholamines.8. Although Mg(2+) (20 mM) was effective in blocking catecholamine release, this divalent cation did not modify the increase in the (45)Ca efflux produced by Ca(2+) reintroduction.9. In contrast to these later observations, methoxyverapamil (3 x 10(-4)M) was effective in inhibiting both increases in catecholamine output and (45)Ca efflux in response to Ca(2+) reintroduction.10. It is concluded from these experiments that (a) Ca(2+) movements in the adrenal medulla may involve both Na(+)-Ca(2+) and Ca(2+)-Ca(2+) exchange mechanisms; (b) the omission of Na(+) from the extracellular environment produces not only an increase in the output of catecholamines but it may increase the intracellular levels of Ca(2+) and that this may result in an increased Ca(2+) efflux when Mg(2+) is omitted from the perfusion fluids, and that (c) the competition between Ca(2+) and Mg(2+) during the secretory process may involve an intracellular site.

Adrenal Medulla↗
PubMed1977

Action of a beta-bungarotoxin on autonomic ganglia and adrenergic neurotransmission.

A beta-bungarotoxin was isolated from the venom of Bungarus multicinctus by column chromatography on Sephadex G-50 and SP-Sephadex. The toxin produced presynaptic effects on neuromuscular transmission with characteristics similar to those described by others. In a sympathetic ganglion, the toxin increased spontaneous acetylcholine (ACh) release and decreased ACh release evoked by preganglionic nerve stimulation. The toxin did not block the response of isolated ileum to cholinergic nerve stimulation, did not block the release of noradrenaline from the adrenergic nerve terminals of a nictitating membrane preparation, and did not alter the responses of smooth and cardiac muscle preparations to noradrenaline. It is suggested that the specificity of beta-bungarotoxin for certain nerve terminals is related either to selective binding of the toxin or to the selective presence of a necessary substrate for its action. An attempt to show selective binding of 125I-toxin to cholinergic nerve terminals in skeletal muscle was not successful.

Acetylcholine↗
PubMed1976

The different effects of D-600 (methoxyverapamil) on the release of adrenal catecholamines induced by acetylcholine, high potassium or sodium deprivation.

1 Bovine adrenal glands were perfused with Locke solution and catecholamine release was induced by acetylcholine, by a depolarizing concentration of potassium, or by omission of sodium from the perfusion fluid. 2 D-600 (methoxyverapamil) at the concentration of 30 muM produced a 23% inhibition of catecholamine release evoked by acetylcholine (0.1 mM) in the presence of physostigmine (10 muM). 3 A concentration of D-600 of 0.3 mM produced 86% and 85% inhibition in the output of catecholamines in response to acetylcholine and high potassium respectively. 4 D-600 (0.3 mM) failed to block the release of catecholamines evoked by sodium deprivation. 5 The results suggest the involvement of intracellular calcium in the exocytotic release of catecholamines induced by sodium omission.

Acetylcholine↗
PubMed1976

Possible involvement of a transmitter different from norepinephrine in the residual responses to nerve stimulation of the cat nictitating membrane after pretreatment with reserpine.

Pretreatment with reserpine (0.3 or 3 mg/kg, 24 hours before the experiment) reduced the norepinephrine (NE) levels in the medial muscle of the cat nictitating membrane to approximately 2% of the control values. Under these experimental conditions, the responses to postganglionic nerve stimulation were not abolished, reaching up to 50% of the maximum development of tension to exogenous sympathomimetic amines both in vivo and in vitro. In contrast to the responses to nerve stimulation obtained in normal nictitating membranes, the residual responses to nerve stimulation obtained after pretreatment with reserpine were not blocked by phentolamine (3.1 and 31 muM) or by 0.29 muM phenoxybenzamine. The effectiveness of phentolamine and phenoxybenzamine in blocking responses to exogenous NE was the same when the normal nictitating membrane was compared to the smooth muscle obtained from cats pretreated with reserpine. The residual responses to nerve stimulation were reduced when the calcium concentration in the medium was decreased to 0.65 mM. These residual responses were abolished in the presence of tetrodotoxin. Scopolamine, 0.078 muM, did not reduce the residual responses to nerve stimulation while it antagonized the responses to exogenous acetylcholine, indicating that a cholinergic mechanism is not involved in this phenomenon. Adenosine triphosphate (ATP) and adenosine diphosphosphate (ADP) behaved as agonists on the smooth muscle of the normal and of the reserpine-pretreated nictitating membrane and the responses to ATP were not blocked by phentolamine. It is concluded that the residual responses to nerve stimulation obtained after pretreatment with reserpine could be due to the release of a transmitter different from NE. The possibility that ATP or ADP might be involved in these residual responses to nerve stimulation is discussed.

Adenosine Triphosphate↗