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Biomedical subjects

V Corti

Publications and source records attributed to V Corti.

11 recordsLinked to original sources
PubMed1989

Indirect evidence for a role of prostaglandins as second messengers of the prejunctional effect of opioids in guinea-pig ventricular preparations.

The cardiac response to adrenergic nerve stimulation was dose dependently reduced in a statistically significant manner by 1-10 microM dynorphin-(1-13) in isolated atria, and by 0.1-1 microM dynorphin-(1-13) in guinea-pig ventricular preparations. The inhibitory effect of dynorphin was maintained in atria that had been pretreated with two cyclooxygenase inhibitors at concentrations that induce an 80% inhibition of the enzyme, namely indomethacin 3 microM and acetylsalicylic acid 200 microM. The inhibitory effect of dynorphin disappeared in similarly pretreated ventricular preparations. These results suggest that, whilst the mediation of the effect of dynorphin is carried out mainly by specific opioid receptors in the atrial section, in the ventricular tissue it occurs through the endogenous prostanoid system.

Animals↗
PubMed1988

Influence of lithium on the positive inotropic effect of phenylephrine and isoprenaline in guinea-pig heart.

The influence of lithium on the positive inotropic effects mediated by alpha- and beta-adrenoceptor stimulation was studied in isolated guinea-pig ventricular preparations stimulated at 1 Hz. Lithium chloride (10(-3)-2 X 10(-2) M) shifted the concentration-response curve for the inotropic effect of phenylephrine to the right in a dose-dependent manner. [3H]Prazosin binding was not inhibited by 10(-2) M lithium. The antagonistic effect of lithium was almost completely prevented by the presence of 10(-2) M myoinositol, and was potentiated by 10(-4) M 2-2'-anhydro-2-C-(hydroxymethyl)-myo-inositol, an antagonist of myo-inositol. The positive inotropic effect of isoprenaline was completely unaffected by either 10(-2) M lithium, 10(-2) M myo-inositol, or 10(-4) M 2-2'-anhydro-2-C-(hydroxymethyl)-myo-inositol. Since it is known that lithium interferes with inositol phosphate metabolism, our results produce further indirect evidence of an involvement of inositol phosphates in the myocardial response to alpha-adrenoceptor, but not to beta-adrenoceptor, stimulation. Our findings also suggest that chronic lithium treatment could interfere with the adrenergic modulation of myocardial contractility in those physio-pathological conditions in which the role of myocardial alpha-adrenoceptors becomes predominant.

Animals↗
PubMed1988

Indirect evidence for a role of phosphatidylinositol turnover in the cardiac response to H1-receptor stimulation.

The influence of lithium on the positive inotropic effect of the H1-agonist 2-pyridyl-ethylamine (PEA) and of the H2-receptor agonist 4-methylhistamine was studied in isolated guinea-pig ventricular strips electrically stimulated at 1 Hz. Lithium (1-10 mM) was devoid of any effect on cardiac contraction; the positive inotropic effect of 4-methylhistamine was unaffected in the presence of 10 mM lithium. On the other hand, lithium (1-10 mM) dose-dependently shifted the dose-inotropic effect curve for PEA to the right; an antagonistic effect, qualitatively similar to that of lithium, was induced by the myoinositol antagonist 2-2'-anhydro-2-C-hydroxymethyl-myoinositol, at a concentration of 100 microM. Moreover the antagonistic effect of the higher lithium concentration (10 mM) was almost completely prevented in preparations superfused with 10 mM myoinositol. Since it is known that lithium is able to reduce the cellular availability of myoinositol by an interference with the phosphatidylinositol (PI) cycle, these results suggest that the H1-receptor-mediated increase in contractility may be linked to an increased turnover of PI, while the H2-receptor-mediated one is not.

Animals↗
PubMed1987

On the presence of opioid receptors in guinea-pig ventricular tissue.

The cardiac response to sympathetic nerve stimulation, induced by trains of field pulses, was studied in isolated guinea-pig ventricular strips. Dynorphin-(1-13) and [D-Ala2, D-Leu5]enkephalinamide, but not morphine, reduced, in a dose-dependent manner, the cardiac sympathetic response. The effect of the two opioid peptides was antagonized by naloxone. The opioid agonists did not affect the response to exogenous noradrenaline. Neither naloxone nor a mixture of peptidase inhibitors modified the cardiac response to sympathetic nerve stimulation.

Animals↗
PubMed1987

Development of tolerance to effects of morphine on cardiac sympathetic response.

1. In isolated guinea-pig atria, morphine potentiated the response to sympathetic stimulation in a naloxone-insensitive, but calcium-sensitive way. The potentiating effect of morphine disappeared in the presence of desmethylimipramine; moreover morphine enhanced the dose-effect curve for exogenous noradrenaline. 2. Morphine was ineffective in guinea-pig atria obtained from animals implanted with morphine pellets for 4 days; on the other hand DADLE and dynorphin-(1-13) maintained their usual inhibitory effect on cardiac sympathetic response in the same kind of preparation. 3. In atria obtained from morphine-tolerant animals and maintained in vitro in the presence of morphine, removal of morphine from the bathing solution caused a new potentiating effect.

Animals↗
PubMed1986

Effects of dl-methadone on the response to physiological transmitters and on several functional parameters of the isolated guinea-pig heart.

The effects of high concentrations of dl-methadone (1-10 microM) on several parameters of cardiac function were studied in isolated guinea-pig heart preparations. The opioid agonist dose-dependently potentiated the inotropic cardiac response to sympathetic nerve stimulation; this effect was naloxone-insensitive and was antagonized by an increase in extracellular calcium concentration. Moreover, methadone enhanced the dose-inotropic response curve of exogenous noradrenaline. The cardiac response to parasympathetic stimulation was antagonized by the drug through a postsynaptic effect; the responses to histamine and isoprenaline were also antagonized in a noncompetitive way. The spontaneous rate and contractility of atrial preparations were depressed by methadone concentrations above 1 microM; the functional refractory period was increased and the maximal driving rate was reduced at the same range of concentrations. All the above mentioned effects were naloxone-insensitive. In isolated sheep Purkinje fibers methadone, at concentrations of 10 microM and higher, significantly affected the transmembrane action potential parameters, by chiefly decreasing the maximum rate of depolarization and increasing the action potential duration. It was concluded that high concentrations of dl-methadone are able to affect several parameters of cardiac function through an unspecific mechanism different from the stimulation of opiate receptors.

Action Potentials↗
PubMed1985

Sensitivity to dynorphin-(1-13) of the presynaptic inhibitory opiate receptors of the guinea-pig heart.

Dynorphin-(1-13) at the concentrations of 1-10 microM, produced a dose-dependent inhibition of the cardiac response to field stimulation of the adrenergic nerve terminals in guinea-pig atria pretreated with peptidase inhibitors. This inhibitory effect was competitively antagonized in a dose-dependent manner by 5 and 10 microM naloxone. Since dynorphin-(1-13) did not modify the dose-inotropic effect curve of exogenous noradrenaline, it was concluded that the depressant effect of the opioid agonist was due to the stimulation of the presynaptic inhibitory opiate receptors belonging to the kappa subtype.

Animals↗
PubMed1985

Cardiodepressant effects of ethanol on guinea-pig atria: presynaptic and postsynaptic components.

Ethanol, at concentrations ranging from 0.5 to 1.5%, depressed myocardial contractility of electrically-stimulated guinea-pig atria. This effect was evident in preparations bathed with a low calcium concentration, but was progressively reduced by increasing the extracellular calcium. The same concentrations of ethanol produced a dose-dependent inhibition of the cardiac response to field stimulation of the adrenergic nerve terminals. This effect was again calcium-dependent. These results support the hypothesis that the pre- and postsynaptic components of the cardiodepressant effects of ethanol are due to a reduction in calcium availability both at the nerve endings and in the contractile cells.

Animals↗