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L Vittone

Publications and source records attributed to L Vittone.

5 recordsLinked to original sources

Phosphorylation of phospholamban in the intact heart. A study on the physiological role of the Ca(2+)-calmodulin-dependent protein kinase system.

The aim of the present study was to further elucidate the physiological role of the calcium-calmodulin (Ca(2+)-Cm)-dependent protein kinase system on phospholamban phosphorylation in the intact functioning heart. The effect of increasing extracellular calcium concentration [Ca]o on phospholamban phosphorylation (PHPL) was studied under different experimental conditions: (a) regular twitches and ryanodine induced-tetani both in the presence and in the absence of 3 x 10(-8) M isoproterenol and (b) Post-stimulation potentiation (PSP), i.e. the potentiation of contractility that follows a period of rapid repetitive stimulation. In the regular twitch, the increase in [Ca]o enhanced contractility both, in the absence and in the presence of beta-stimulation without changing basal or isoproterenol stimulated cAMP levels respectively. This increase in contractility was accompanied by a significant enhancement of PHPL-from 90.6 +/- 16.4 to 216 +/- 35.2 pmols 32Pi/mg protein at 0.25 and 3.85 mM [Ca]o respectively-only when isoproterenol was present. The calmodulin antagonist W-7 significantly decreased the isoproterenol-induced phosphorylation of phospholamban at [Ca]o 1.35 mM. Similar results were obtained under tetanic conditions. When myocardial contractility was enhanced by PSP up to ten-times with respect to the regular twitch, no detectable effect in PHPL was observed. Indirect evidence obtained from skinned rat cardiac trabeculae suggested that the failure of the cAMP-independent mechanisms to phosphorylate phospholamban is not related to a deficient increase in intracellular calcium. The results support the notion that the increase in intracellular calcium induces an increase in PHPL only at high intracellular cAMP levels.

Animals

Positive lusitropic effect and diminished myofibrillar sensitivity to calcium produced by cAMP on toad (Bufo arenarum Hensel) ventricle.

In intact ventricular strips from toad heart, we studied the relaxant or positive lusitropic effect of different interventions known to increase intracellular cAMP levels. Isoproterenol increased developed tension (DT), maximal rate of contraction (+T), and maximal velocity of relaxation (-T). From 10(-8) to 10(-4)M isoproterenol, -T increased proportionally more than +T being the ratio +T/-T significantly decreased. A single dose of isoproterenol (3 x 10(-8)M) increased cAMP levels from 0.174 +/- 0.022 to 0.329 +/- 0.039 pmoles/mg ww (P < 0.05), increased contractility by 69 +/- 13% and decreased +T/-T by 18.5 +/- 4.55%. Administration of 10(-3)M of dibutyryl cyclic AMP (dcAMP) significantly increased DT and +T and decreased the ratio +T/-T. Similar effects were obtained with milrinone, a specific cAMP phosphodiesterase inhibitor. Papaverine, a non selective phosphodiesterase inhibitor, failed to increase +T but significantly increased -T. In chemically skinned ventricular trabeculae, calcium sensitivity of the myofibrils was significantly increased by 10(-5)M of the phosphodiesterase inhibitor 3-isobutyl-1-methyl-xanthine (IBMX). 10(-3)M dcAMP failed to affect calcium sensitivity of chemically skinned ventricular trabeculae when given alone, but produced a decrease in calcium sensitivity of the myofibrils in the presence of 10(-5)M of either IBMX or papaverine. The results would indicate that the relaxant effect of isoproterenol is mediated in toad ventricle by an increase in intracellular cAMP levels. They furthermore suggest that a decrease in myofilament sensitivity to calcium may be a mechanism by which cAMP produces its relaxant effect.

Animals

[Tattoos].

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Dermabrasion

[A case of Ehlers-Danlos syndrome].

A case of Ehlers-Danlos syndrome, personally observed, is described. Stress is laid on the rarity of this syndrome (less than 200 cases in the world literature) and on its peculiar symptoms. The familial character of this syndrome was not proved in the case observed.

Capillary Fragility

Characteristics of ryanodine-induced tetani in the perfused rat heart. Tetanic tension is not the highest force that cardiac muscle can generate.

The aim of the present study was to elucidate the conditions required to obtain tetanic contractions in rat intact heart and to investigate whether tetanic tension was actually the maximal tension that isolated rat heart is able to generate. Experiments were performed on isolated rat hearts (Langendorff technique) perfused at constant coronary flow (8-9 ml/min). Rapid repetitive stimulation (400 to 3000 pulses/min) failed to elicit a fused tetanus. The first twitch that occurred at the end of the rapid stimulation period was a potentiated beat (PSP) of significantly greater magnitude than that of the regular twitch. This potentiation declined in successive beats. When rapid electrical stimulation (600 to 3000 pulses/min) was applied to hearts treated with 5 x 10(-6) M ryanodine, the result was a fused and steady tetanic tension. Ryanodine suppressed PSP. Tetanic tension could be graded by stepwise increase of [Ca2+]o from 0.25 to 5 mM. Maximal tetanic tension occurred at a [Ca2+]o between 3.85 and 5 mM. At any of the [Ca2+]o, tetanic tension was significantly greater than the tension of the twitch obtained at approximately the natural frequency of rat heart in the intact animal (250 beats/min) but it did not differ significantly from the twitch obtained at 100 beats/min. Moreover, the tension of PSP at 0.25 and 1.35 mM [Ca2+]o was significantly greater than the maximal tetanic tension that could be obtained. Similar results to that obtained with ryanodine, were obtained in additional experiments in which caffeine was used to evoke tetanic contraction.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals