PubMed Health⌕ Search

Biomedical subjects

A Giachetti

Publications and source records attributed to A Giachetti.

At least 127 records · Page 7Linked to original sources
PubMed1983

Properties of cytosolic proteins that confer vasoactive intestinal polypeptide-sensitivity to rat brain adenylate cyclase.

Rat brain cortex, caudate nucleus and cerebellum contain one or more factors that confer Vasoactive Intestinal Polypeptide (VIP)-, dopamine (DA)- and norepinephrine (NE)-sensitivity to adenylate cyclase in the absence of added GTP. These factors also stimulate the basal activity of the enzyme. The activity is found in a 100 000 X g supernatant; has an apparent molecular weight greater than 450 000 daltons; is inactivated by pronase, alkaline phosphatase and ammonium sulphate, and partially degraded by trypsin; and is stable to heat and acidic treatment. The effect of the factors is additive with that of guanosine-5'-triphosphate (GTP), and is not abolished by guanosine 5'-0-(2-thiodiphosphate) (GDP-beta-S). These results suggest that stimulation of adenylate cyclase by VIP, and most likely by DA and NE, can be modulated by soluble proteins.

Adenylyl Cyclases↗
PubMed1980

Atropine inhibits thromboxane A2 generation in isolated lungs of the guinea-pig.

1 Histamine (0.5 to 5 micrograms) and slow reacting substance of anaphylaxis (SRS-A, 0.05 to 0.3 u), injected in the isolated, perfused lungs of normal and ovalbumin-sensitized guinea-pigs, promote formation and release of thromboxane A2(TXA2) and other arachidonate metabolites, the effect being more pronounced in sensitized lungs. 2 Carbachol injected (1 to 10 micrograms) or perfused (1 micrograms ml-1 min-1) through normal or sensitized lungs does not elicit formation of TXA2 and prostaglandins. Furthermore the increased generation of arachidonate metabolites due to histamine is not altered by carbachol. 3 Atropine and ipratropium bromide (1 microgram ml-1 min-1) reduce significantly the increased rate of production of TXA2 caused by histamine and SRS-A both in normal and sensitized lungs, whereas hexamethonium (10 to 25 micrograms ml-1 min-1) is ineffective. 4 The mechanism of action of atropine in inhibiting the increased generation of TXA2 is clearly not related to its antimuscarinic or antihistaminic properties. The drug might act at the early events, involved in the activation of arachidonic acid metabolism. The results suggest new sites of action for atropine which, besides the control of the vagal bronchomotor tone, interferes directly with the primary mediators of anaphylaxis.

Animals↗
PubMed1980

Lack of evidence that the central serotoninergic system plays a role in the activation of prolactin secretion following inhibition of dopamine synthesis or blockade of dopamine receptors in the male rat.

Administration of alpha MT to inhibit catecholamine synthesis or dopamine (DA) receptor blockade with spiroperidol had no effect on the hypothalamic concentration of 5HT or 5HIAA. Fluoxetine to block serotonin uptake had no influence on the elevation of serum prolactin levels induced by alpha MT or DA receptor blockers and conversely alpha MT did not influence the prolactin-releasing action of 5HTP alone or in combination with fluoxetine. Depletion of brain serotonin stores with p-chlorophenylalanine did not affect the prolactin-releasing action of alpha MT or DA receptor blockers. In contrast, the serotonin blocker methysergide, but not cyproheptadine, inhibited the prolactin-releasing effect of alpha MT or alpha-flupentixol, a DA receptor blocker, but not of spiroperidol, another DA receptor blocker. The intensity of the inhibition induced by methysergide paralleled the intensity of inhibition induced by apomorphine. Methysergide conspicuously lowered serum prolactin in animals with electrolytic destruction of the median eminence, whereas cyproheptadine had only a slight effect. The prolactin-inhibiting effect of methysergide could be prevented by pretreatment of the lesioned rats with spiroperidol. It is concluded (1) that elimination of the influence of the DA system does not activate the central serotoninergic system; (2) that activity of the serotoninergic system has no role in the activation of prolactin secretion induced by suppression of the inhibitory dopaminergic influence, and (3) that the inhibiting action of methysergide on the prolactin-releasing effect of alpha MT or alpha-flupentixol is due to its dopamine receptor agonist activity rather than to blockade of serotonin receptors.

5-Hydroxytryptophan↗
PubMed1979

Axonal transport of vasoactive intestinal peptide in sciatic nerve.

Dense plexuses of neurones containing immunoreactive vasoactive intestinal peptide (VIP) have been found in discrete areas of the central nervous system and in peripheral organs, including the gastrointestinal tract, pancreas and urogenital system. In many of these locations VIP is concentrated in nerve endings, where it can be released by high K+ concentrations in a Ca2+-dependent manner. VIP release may also be provoked by electrical stimulation of nerves, for example the vagus. VIP thus shows some of the features of neurotransmitter or neuromodulator substances. The presence of immunoreactive VIP in the fine terminal varicosities as well as in the cell bodies of neurones suggests that it might be transported from the perikaryon, where it is presumably formed, to the nerve endings, through the axonal transport system. Such transport would be in keeping with a role for the peptide as a neurohumor or neurohormone. We report here that VIP accumulates in constricted rat sciatic nerves in a manner suggesting fast, anterograde axonal flow.

Animals↗
PubMed1979

Axoplasmic transport of noradrenaline in the sciatic nerves of spontaneously diabetic mice.

The intraaxonal transport of noradrenaline and tyrosine hydroxylase was studied in the sciatic nerves of diabetic, obese and appropriate control mice. Noradrenaline and tyrosine hydroxylase accumulated proximal to a constriction applied to the nerves. Noradrenaline concentration in the non-constricted sciatic nerves did not differ significantly in nondiabetic and diabetic mice (0.67 +/- 0.04 and 0.58 +/- 0.01 ng/cm respectively); in obese mice and lean littermates the noradrenaline concentration was 0.47 +/- 0.05 ng/cm and 0.46 +/- 0.01 ng/cm. After nine hours of constriction the concentration of noradrenaline increased in the axons of nondiabetic (1.15 +/- 0.06 ng/cm), in obese (0.90 +/- 0.08 ng/cm) and lean mice (1.10 +/- 0.07 ng/cm) but remained low (0.68 +/- 0.07 ng/cm) in diabetic mice.--Administration of insulin (10 U/kg/day) to diabetic mutants completely reversed the decrease in NA accumulation. NA accumulated only in the nerve segment proximal (1 cm) to a constriction and was transported distally at an apparent velocity of 0.75 mm/hr in control axons. The difference of NA accumulation between diabetic and nondiabetic control indicate a reduced rate of axoplasmic flow in the noradrenergic axons of diabetic animals.

Animals↗
PubMed1978

Binding of (3H)dihydroalprenolol to beta adrenoceptors of cells isolated from adult rat heart.

Myocardial cells isolated from adult rat heart bind (3H)dihydroalprenolol. Sixty-one percent of this binding appeared to be at the beta adrenoceptors since it was inhibited by saturating quantities of the beta antagonist propranolol or by the beta agonist isoprenaline. The binding is stereoselective as the l-isomer of isoprenaline caused greater inhibition than the d-isomer. The binding of (3H)dihydroalprenolol to beta adrenoceptors was saturable; half maximum binding occurred at about 8 nM and full saturation at 30--40nM.

Alprenolol↗
PubMed1978

The functional state of sympathetic nerves in spontaneously diabetic mice.

I investigated biochemical parameters of sympathetic nerve function in spontaneously diabetic mice(C57 BL/KsJdb/db) and in their lean littermates. The concentration of norepinephrine (NE) in organs innervated by sympathetic nerves was significantly reduced in the heart, kidney, and salivary glands of mice (24 weeks old) with severe diabetic-like symptoms (blood glucose is greater than 300 mg./100ml.). In the spleen, vas deferens, and adrenal glands of the same animals the NE levels were not changed in relation to control. Other measurements of NE in young (six weeks old) diabetic mice revealed no differences between diabetic and nondiabetic controls. The turnover of NE, a measure of the functional state of sympathetic nerves, decreased significantly in the heart and salivary glands of 24-week-old mice but remained unchanged in the kidney and spleen. In young, diabetic mice the rates of NE turnover in several organs were similar to those found in age-matched controls. The hearts of 24-week-old diabetic mice contained significantly less dopamine-beta-hydroxylase (DBH), an intraneuronal enzyme active in the terminal step of NE biosynthesis. The kidney of the same animals was hypertrophic and showed a massive elevation of monoamine oxidase (MAO), an enzyme that degrades NE to inactive products. Other experiments showed that the regeneration of sympathetic neurons that follows the reversible chemical denervation with 6-hydroxydopamine was comparable in diabetic and nondiabetic animals. It appears that mice with spontaneous diabetes show changes of sympathetic nerve function similar to those noted in diabetic patients with autonomic neuropathy.

Animals↗