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Biomedical subjects

S Spampinato

Publications and source records attributed to S Spampinato.

At least 91 records · Page 5Linked to original sources

Antinociceptive activity of salmon calcitonin injected intrathecally in the rat.

Salmon calcitonin injected intrathecally in unanesthetized rats produced long-lasting, dose-dependent elevations of nociceptive threshold as measured in the hot plate test. This antinociceptive action was nonopiate in nature as it was uninfluenced by the narcotic antagonists naloxone and MR 1452; moreover, the peptide was still able to raise the nociceptive threshold in morphine-tolerant rats. It is suggested that the spinal cord may represent one of the sites of action for calcitonin-induced antinociception.

Animals↗

Effects of hypothalamic lesions on the content of dynorphin immunoreactivity in pituitary.

Radiofrequency lesion of medial basal hypothalamus (MBH) caused a approximately 50% depletion of immunoreactive dynorphin (ir-dyn) both in the anterior and neurointermediate lobe of the pituitary, whereas radiofrequency lesions of both supraoptic and paraventricular nuclei (SON, PVN) resulted in an approximately 30% reduction in neurointermediate lobe only. MBH cells and/or fibers contribute, therefore, to adenohypophysis pool of ir-dyn. Moreover, since the loss of ir-dyn in neurohypophysis ascertained after MBH lesion is significantly higher than that obtained with SON and PVN destruction, it may be assumed that MBH also participate to ir-dyn pool in neurohypophysis.

Animals↗

Immunoreactive dynorphin in rat tissues and plasma.

Distribution of immunoreactive dynorphin (ir-dyn) has been determined in rat tissues using a highly specific antiserum. Concentrations are highest in the pituitary, brain and spinal cord, as previously reported. In peripheral tissues highest levels occur in the stomach and upper intestine, but ir-dyn has also been detected in several other tissues, including heart and skeletal muscle. Unilateral vagotomy did not affect the amount of ir-dyn in heart or stomach, and denervation did not affect the amount in skeletal muscle. Gel permeation chromatography of the ir-dyn in gastrointestinal tract, heart, and skeletal muscle revealed a larger apparent molecular weight than that of the 17-residue dynorphin. Using octadecylsilyl-silica cartridges, it was possible to extract and concentrate ir-dyn from rat plasma. By gel permeation chromatography plasma immunoreactivity was found in two peaks, both of higher apparent molecular weight than dynorphin. This immunoreactivity was unaltered by hypophysectomy or adrenalectomy.

Animals↗

ACTH1-24 counteracts the prolactin-releasing effect of an opioid.

The administration of the synthetic and stable opioid peptide[D-Ala2,MePhe4,Met(O)5o1]enkephalin (FK 33-824) at the dose of 0.2 mg/kg i.v. induced a rise in plasma levels of prolactin in the rat, an effect which was prevented by 1 mg/kg i.v. of the opiate antagonist naloxone. A simultaneous i.v. injection of 20 microgram/kg i.v. of ACTH1-24 significantly reduced the prolactin releasing effect of FK 33-824, therefore giving further evidence of an in vivo interaction between ACTH-related peptides and opioid peptides.

Adrenocorticotropic Hormone↗

Prostaglandins in the brain of rats given, acutely, and chronically, a hyperthermic dose of met-enkephalin.

An enhanced prostaglandinlike activity is shown in homogenates of brain from rats treated intracerebroventricularly with 100 microgram of metenkephalin. The increase is significantly reduced by naloxone pretreatment. A relationship is proposed between generation of prostaglandins in the brain following met-enkephalin administration and hyperthermic effect of the opiatelike factor in the rat. Normalization of prostaglandinlike activity following chronic administration of met-enkephalin in the rat may also account for the development of tolerance to its thermic effect.

Animals↗

Prostaglandins in rat placenta following acute and chronic administration of morphine.

The objective of the present study was to obtain information on prostaglandin (PG) biosynthesis in placenta following narcotic administration. PG biosynthetic capacity was determined in whole rat placenta homogenates in the presence of Na arachidonate, by evaluating net production of PGs assayed against PGE1 on rat stomach strips. An enhanced prostaglandin-like activity is shown in homogenates of placenta from rats treated subcutaneously with 10 mg/kg of morphine. This increase was prevented by naloxone pre-treatment. Continual morphine administration during gestation, results in a normalization of placental biosynthetic capacity thus suggesting the development of a tolerance to the narcotic effect.

Animals↗

Prolactin and growth hormone releasing activity of [D-Met2, Pro5]-enkephalinamide in the rat after systemic administration.

The growth hormone (GH) and prolactin releasing (PRL) activity of [D-Met2, Pro5]-enkephalinamide (EKNH2). an opioid peptide analog with higher opiate agonist activity that morphine, was compared in the unanesthetized male rat to those of equimolar doses of morphine upon systemic injection. EKNH2 proved to be a higher PRL, but not GH, releaser than the opiate alkaloid.

Animals↗

Effects of naloxone on the mechanical activity of isolated rat hearts perfused with morphine or opioid peptides.

In isolated rat hearts, the infusion for 10 min of 10(-10), 10(-8) or 10(-6) M (-)naloxone affected the cardiac function by markedly increasing the coronary pressure and by reducing both the heart rate and the developed tension. A lower dose of (-)naloxone (10(-11) M) or a dose of 10(-6) M (+)naloxone, did not modify the cardiac function. Morphine (10(-6) or 10(-5) M) and 10(-10), 10(-8) or 10(-6) M methionine-enkephalin or leucine-enkephalin, both significantly reduced the coronary pressure of the isolated rat hearts, during the first 4-6 min of perfusion, but the coronary pressure progressively increased above the control value in the last 4 min of perfusion. Each opioid also influenced the mechanical activity of the isolated rat heart, by significantly lowering both the heart rate and the developed tension. (-)Naloxone, at all the doses tested, was only able to antagonise the hypotensive effect induced by the opioids on the coronary pressure and was ineffective in counteracting the negative inotropic and chronotropic effects produced by each opioid. The perfusion in the presence of (+)naloxone (even at a dose of 10(-6) M) did not affect the opioid-induced changes on both the coronary pressure and the mechanical performance of the isolated heart.

Animals↗

Inhibitory action of opioid peptides on ouabain-sensitive Na+-K+ and Ca2+-dependent ATPase activities in bovine cardiac sarcolemma.

The present study demonstrates that morphine (10(-6) and 10(-5) M), methionine-enkephalin or leucine-enkephalin (10(-10), 10(-8), and 10(-6) M) were able to inhibit significantly, in a dose-dependent manner, both the sarcolemmal Ca2+-dependent ATPase and the ouabain-sensitive Na+-K+ ATPase activities. The inhibitory action of these opioids on the two ATPases was not antagonized by preincubation with naloxone (10(-6) M). Naloxone alone (10(-8), 10(-6) and 10(-5) M) did not affect both the sarcolemmal Ca2+-dependent ATPase and the ouabain-sensitive Na+-K+ ATPase activities. Heat-denatured methionine-enkephalin (10(-6) M) or leucine-enkephalin (10(-6) M) also unaffected both the ATPases. The possibility is also discussed that opioid peptides may regulate myocardial contractility by modulating the movement of ions across the heart sarcolemma.

Animals↗

Transfer and expression of DNA constructs into cells by using retrovirus vectors: a new tool for pharmacological research.

Recombinant retroviruses are useful vectors for introducing DNA sequences into eukaryotic chromosomes and obtain their expression. The principles and techniques for producing these vectors and their applications are discussed in view of their use in pharmacological research. Particularly, retroviral vectors seem to be attractive for expressing into mammalian cells antisense RNA, that is RNA complementary to target mRNA and capable of preventing the synthesis of the gene product.

Animals↗