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Biomedical subjects

C Missale

Publications and source records attributed to C Missale.

94 records · Page 6Linked to original sources
PubMedDate not supplied

Insulin-mediated effects of glucose on dopamine metabolism.

Administration of various doses of glucose to rats produced a significant decrease of dopamine turnover in both striatum and olfactory tubercle. From the dose-response curve, a close connection between 3.4-dihydroxyphenylacetic acid (DOPAC) variation and insulin plasma level was demonstrated. However, glucose did not affect dopamine metabolism in starved or streptozotocin-treated rats. This indicates that the effect of glucose on the central dopaminergic system is mediated by pancreatic insulin, even in the presence of endogenous brain insulin. Therefore, insulin may influence synaptic transmission in the central nervous system.

3,4-Dihydroxyphenylacetic Acid↗
PubMedDate not supplied

Neuropeptidergic inhibitory regulation of Met-enkephalin immunoreactive material release from rat spinal cord in vitro.

The release of Met-enkephalin immunoreactive material (ME-IR) from rat spinal slices was measured in vitro. This release increased about 4 fold in response to the addition of K+ ions. K+-evoked release of ME-IR was Ca++ dependent. Veratridine, a depolarizing agent, also stimulated the release of ME-IR. Veratridine-induced ME-IR release was completely prevented by tetrodotoxin (TTX), a Na+ channel blocker. Somatostatin (SRIF) inhibited both basal and K+-evoked release of ME-IR at 10(-7) M. Substance P had a similar effect although higher concentrations were needed. gamma-Aminobutyric acid (GABA) and neurotensin (NT) did not affect the basal release but slightly decreased K+-evoked release at 10(-5) M. Serotonin (5-HT) and noradrenaline (NA), did not affect ME-IR release. These results suggest that some of the neuropeptides present in the spinal cord, especially SP and SRIF, may be potent modulators of ME-IR release at the spinal level.

Animals↗
PubMedDate not supplied

Enalapril decreases plasma prolactin levels in hypertensive patients.

Angiotensin II stimulates prolactin release both in vivo in the rat and in vitro in anterior pituitary cell cultures. Moreover, angiotensin II binding sites have been identified in pituitary lactotrophs and it has been shown that angiotensin converting enzyme (ACE) is present in rat anterior pituitary. We studied the effect of enalapril, a potent converting enzyme inhibitor, on baseline prolactin levels in nine hypertensive postmenopausal women. The results indicate that 15-day inhibition of ACE by enalapril reduced prolactinaemia, suggesting that angiotensin II plays a role in the control of prolactin secretion in hypertensives.

Aged↗