RESUMEN

Based on geometric morphometrics and discriminant analysis, the percentage of silverside Odontesthes hatcheri and Odontesthes bonariensis individuals identified by a taxonomic key and misclassified by discriminant analysis was obtained and a negative correlation between the percentage of misclassified individuals of O. hatcheri and the distance to the nearest hatchery stocking silversides was found, suggesting a genetic introgression. Morphological analyses between species, between populations and within populations pointed to the same anatomical structures, suggesting a nested variation related to environmental cues such as availability of littoral shelter. The dependence between the cephalic morphology of O. hatcheri and body size would be in agreement with the trophic niche shifts of the species. Introgression adds a new threat to the already observed decline of populations of O. hatcheri and suggests that this species deserves particular consideration in terms of conservation guidelines.

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RESUMEN

The fast and slow components of the response to noradrenaline in rat aorta were studied to assess their relative contribution to the total mechanical response. The fast component, the magnitude of which varied with the concentration of noradrenaline in a dose-dependent manner, was shown to be dependent on release of calcium from intracellular stores. In calcium-free medium with ethylene glycol bis-(beta-aminoethylether) N,N,N',N-tetra-acetic acid (EGTA) a noradrenaline challenge (1 microM) produced a transient increase in force which faded in about 10 mins. Addition of calcium at this point produces a slow component of similar amplitude to the total response to noradrenaline. Recycling of calcium through the intracellular store does not appear to play an important role under these experimental conditions, since the presence of noradrenaline in the bath prevented its refilling. It is concluded that extracellular calcium by itself (ie, the slow component) can account for the total contractile response to noradrenaline in rat aorta.

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The calcium channels blocker, nifedipine (NIF) inhibited in a partial non competitive manner the changes in perfusion pressure (delta P) caused by noradrenaline (NA) in the rat hindquarters, being the maximum inhibition of 31.0 +/- 8.3% (n = 5) for NIF 1.10(-5) M. The vasoconstrictor response of K+ 80 mM - phentolamine 3.10(-6)M was inhibited with lower concentrations of NIF than the one produced by phenylephrine (F) 1.10(-4)M. When the hindquarters were perfused with Krebs OCa-EGTA 2 mM NA developed contractile response. The administration of Ca 2.5 mM after the intracellular calcium store had been depleted, generated vasoconstriction in the presence of F 1.10(-4)M and K+ 80 mM - phentolamine 3.10(-6)M which were blocked in a 60.4 +/- 5.7 (n = 12) and 91.1 +/- 2.3% (n = 10) respectively by NIF 1.10(-5)M. The results suggest that the activation of the adrenergic receptor by NA in the perfused rat hindquarters, probably releases calcium from intracellular stores and promotes calcium influx through pathway scarcely sensitive to NIF. Both mechanisms would be responsible for the partial blockade found in our results.

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RESUMEN

The calcium channels blocker, nifedipine (NIF) inhibited in a partial non competitive manner the changes in perfusion pressure (delta P) caused by noradrenaline (NA) in the rat hindquarters, being the maximum inhibition of 31.0 +/- 8.3

(n = 5) for NIF 1.10(-5) M. The vasoconstrictor response of K+ 80 mM - phentolamine 3.10(-6)M was inhibited with lower concentrations of NIF than the one produced by phenylephrine (F) 1.10(-4)M. When the hindquarters were perfused with Krebs OCa-EGTA 2 mM NA developed contractile response. The administration of Ca 2.5 mM after the intracellular calcium store had been depleted, generated vasoconstriction in the presence of F 1.10(-4)M and K+ 80 mM - phentolamine 3.10(-6)M which were blocked in a 60.4 +/- 5.7 (n = 12) and 91.1 +/- 2.3

(n = 10) respectively by NIF 1.10(-5)M. The results suggest that the activation of the adrenergic receptor by NA in the perfused rat hindquarters, probably releases calcium from intracellular stores and promotes calcium influx through pathway scarcely sensitive to NIF. Both mechanisms would be responsible for the partial blockade found in our results.

RESUMEN

The contractile response to norepinephrine (NE) in rat aorta has an initial fast (F) component attributable to Ca release, followed by a slow (S) component due to Ca influx. The relaxant action of the Ca entry blocker Diltiazem (DT) 10 microns was measured in three different responses to NE: a) a NE contraction in Ca = 1.35 mM (in which both the F and S components participate) was relaxed by 36 +/- 4%; b) previous incubation with Prazosin 0.01 microM eliminated the F component. Only the S component appeared (with a force equal to that of the previous total response) and it was relaxed by DT by 47 +/- 3%; c) the intracellular Ca pool was depleted by exposure to NE in Ca-free solution + EGTA. Further exposure to Ca = 1.35 mM produced only an S component, which was relaxed by DT by 61 +/- 4%. Since the preceding experiments suggested that the relaxant effect of DT increased as the participation of the Ca pool in the NE response decreased, an intermediate situation was looked for. The Ca pool was depleted as in (c) and then it was partially refilled by brief exposure to Ca = 1.35 mM. DT relaxation decreased to 51 +/- 3% (20 sec of refilling) and to 41 +/- 3% (60 sec of refilling). Similar results were obtained with DT 0.1, 1 and 100 microM. It is concluded that the relaxant action of DT on a NE contraction in rat aorta is inversely related to the amount of NE-releasable intracellular Ca that contributed to that contraction.

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RESUMEN

The contractile response to norepinephrine (NE) in rat aorta has an initial fast (F) component attributable to Ca release, followed by a slow (S) component due to Ca influx. The relaxant action of the Ca entry blocker Diltiazem (DT) 10 microns was measured in three different responses to NE: a) a NE contraction in Ca = 1.35 mM (in which both the F and S components participate) was relaxed by 36 +/- 4

; b) previous incubation with Prazosin 0.01 microM eliminated the F component. Only the S component appeared (with a force equal to that of the previous total response) and it was relaxed by DT by 47 +/- 3

; c) the intracellular Ca pool was depleted by exposure to NE in Ca-free solution + EGTA. Further exposure to Ca = 1.35 mM produced only an S component, which was relaxed by DT by 61 +/- 4

. Since the preceding experiments suggested that the relaxant effect of DT increased as the participation of the Ca pool in the NE response decreased, an intermediate situation was looked for. The Ca pool was depleted as in (c) and then it was partially refilled by brief exposure to Ca = 1.35 mM. DT relaxation decreased to 51 +/- 3

(20 sec of refilling) and to 41 +/- 3

(60 sec of refilling). Similar results were obtained with DT 0.1, 1 and 100 microM. It is concluded that the relaxant action of DT on a NE contraction in rat aorta is inversely related to the amount of NE-releasable intracellular Ca that contributed to that contraction.

RESUMEN

Experiments were performed in isolated aortic rings from rats anesthetized with sodium pentobarbital ("P") or sacrificed by cervical traumatism ("T"). The response of both aortic rings ("P" and "T") was compared after K depolarizing solution (35, 50 and 100 mM) and after noradrenaline (10(-6)M. Neither the response to the different concentrations of K nor to the alpha agonist effect of NOR was significantly different in rats "P" or "T". The effect of NOR in rats "P" or "T" was not different either in the rapid or slow phase of contraction. The pentobarbital added to the bath, however, depressed the contractile response to either K+ or NOR. This depression, however, was reversible after the rinse of the preparation. We conclude that in spite of the depression produced by the sodium pentobarbital to the contractile response of aorta rings, this depression is reversible and disappeared after the usual period of stabilization. The effect then cannot explain differences in results in reports in which the animals were previously anesthetized or not.

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RESUMEN

Experiments were performed in isolated aortic rings from rats anesthetized with sodium pentobarbital ([quot ]P[quot ]) or sacrificed by cervical traumatism ([quot ]T[quot ]). The response of both aortic rings ([quot ]P[quot ] and [quot ]T[quot ]) was compared after K depolarizing solution (35, 50 and 100 mM) and after noradrenaline (10(-6)M. Neither the response to the different concentrations of K nor to the alpha agonist effect of NOR was significantly different in rats [quot ]P[quot ] or [quot ]T[quot ]. The effect of NOR in rats [quot ]P[quot ] or [quot ]T[quot ] was not different either in the rapid or slow phase of contraction. The pentobarbital added to the bath, however, depressed the contractile response to either K+ or NOR. This depression, however, was reversible after the rinse of the preparation. We conclude that in spite of the depression produced by the sodium pentobarbital to the contractile response of aorta rings, this depression is reversible and disappeared after the usual period of stabilization. The effect then cannot explain differences in results in reports in which the animals were previously anesthetized or not.