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Biomedical subjects

G B Picotti

Publications and source records attributed to G B Picotti.

At least 73 records · Page 4Linked to original sources
PubMed1979

A renal abnormality as a possible cause of "essential" hypertension.

The renal abnormality which causes hypertension in the Milan hypertensive strain of rats disappears as hypertension develops. Because of the many analogies between the condition in these rats and "essential" hypertension in man, the same pattern of change may occur if a renal abnormality is the cause of essential hypertension in man. This hypothesis was tested in two groups of young normotensive subjects matched for age, sex, and body-surface area; in the first group both parents were hypertensive, and in the second group both parents were normotensive. Renal plasma-flow, glomerular filtration-rate, plasma-volume, plasma-renin activity, plasma-concentrations of Na+, K+, and catecholamines, 24 h urinary excretion of Na+, K+, and aldosterone, and the cardiac index were measured so that renal function and the role of factors affecting blood-pressure regulation could be assessed. Renal plasma-flow was significantly higher (p less than 0.01) in the first group, whereas results of tests for all the other factors were almost the same in both groups. The hypothesis that a primary kidney abnormality causes hypertension in a proportion of patients with essential hypertension is proposed.

Adult↗
PubMed1979

Plasma catecholamines and blood pressure responses to the carotid baroreceptor reflex in essential hypertension.

1. Slight decreases and increases in carotid baroreceptor activity were induced in subjects with essential hypertension by slight alterations in carotid transmural pressure (variable pressure neck-chamber technique) in order to obtain limited increases and reductions in sympathetic adrenergic activity. 2. When sympathetic activity was reflexly increased there was a rise in arterial pressure but no significant increase in plasma catecholamines. Likewise when sympathetic activity was reflexly reduced there was a fall in arterial pressure but no significant reduction in plasma catecholamines. 3. Plasma noradrenaline and adrenaline significantly and markedly increased in the same subjects when sympathetic activity was increased by activation of both arterial and low pressure baroreceptor reflexes with tilting. 4. It is suggested that measurements of catecholamines in systemic plasma may reveal marked degrees of sympathetic activation but may not be a sensitive index of more moderate changes in sympathetic tone.

Adult↗
PubMed1979

Storage pool disease: comparative fluorescence microscopical, cytochemical and biochemical studies on amine-storing organelles of human blood platelets.

The platelet content of ATP, ADP, serotonin (5-HT), dopamine, noradrenaline and adrenaline as well as the net uptake of radiolabelled 5-HT and mepacrine were subnormal in six patients with Storage Pool Disease (SPD). Fewer amine-storing organelles were found by fluorescence microscopy with the fluorescent probe mepacrine and by electron microscopy with a cytochemical (uranaffin) reaction specific for 5'-phosphonucleotides. Both methods showed that SPD platelets have atypical organelles with a reduced capacity to store amines, 5'-phosphonucleotides and mepacrine. The changes were most marked in platelets of the two patients who also had oculocutaneous albinism.

Adenosine Diphosphate↗
PubMed1979

Content and subcellular localization of catecholamines and 5-hydroxytryptamine in human and animal blood platelets: monoamine distribution between platelets and plasma.

1 The content of adrenaline (Ad), noradrenaline (NA) and dopamine was measured in human, guinea-pig, cat, rabbit and rat blood platelets by a highly sensitive and specific radioenzymatic method.2 In all platelet specimens analyzed, the content of the three catecholamines (CA) was several thousand times lower than that of 5-hydroxytryptamine (5-HT).3 In basal conditions, the NA concentration in platelets and plasma always exceeded that of Ad and dopamine.4 In rat and rabbit platelets, Ad, NA and dopamine were present only in the free (unconjugated) form.5 Platelets of rats with storage pool deficiency (Fawn-hooded) contained much less 5-HT and CA than normal rat platelets.6 Following restraint stress, platelets of Fawn-hooded rats, in contrast to normal rat platelets, did not accumulate CA in spite of a dramatic rise in plasma CA.7 Reserpine, a monoamine depletor, released CA as well as 5-HT from rabbit platelets in vivo.8 Subcellular fractionation experiments with rabbit platelets indicate that both CA and 5-HT are most concentrated in the fraction consisting of pure 5-HT organelles.9 Both in humans and rabbits the concentration gradient between platelets and plasma was much lower for CA than for 5-HT, indicating that a high affinity transport mechanism operates in vivo for 5-HT but not for CA.10 In conclusion, the present data show that both human and animal platelets contain Ad, NA and dopamine. The bulk of the CA seems to be stored as unconjugated amines together with 5-HT, histamine and p-octopamine in a multitransmitter storage site, namely the 5-HT organelle.

Adult↗
PubMed1978

Plasma adrenaline, noradrenaline and dopamine in man and different animal species.

1. The catecholamines adrenaline (A), noradrenaline (NA) and dopamine (DA) were determined in plasma samples of man and various animal species using a highly sensitive radioenzymatic method.2. Basal values were determined under conditions producing virtually no physical or psychic stress in blood obtained through acutely inserted venous catheters in human volunteers, rabbits and cows, through chronic indwelling catheters in cats and rats, and by cubital venipuncture in trained dogs.3. Basal values (pg/ml.) for A, NA, and DA were respectively 64, 203 and 98 in man, 73, 609 and 276 in cats, 166, 392 and 216 in rabbits, 56, 152 and 91 in cows, 204, 376 and 173 in dogs, and 175, 509, and 84 in SPF rats. The NA concentrations were always higher than those of A and DA.4. Gentle handling of rats for 30 sec greatly increased the levels of all catecholamines, especially of A. Even more marked rises were observed during and up to 5 min after restraint stress.5. Blood from the trunk of decapitated rats contained about 20 times more A and 3-4 times more DA and NA than venous blood from catheters in the absence of handling.6. Basal values of plasma catecholamines in small animals can only be obtained through indwelling catheters and in the absence of handling. Most of the previously reported values are too high and are experimental artifacts.

Adolescent↗
PubMed1978

Parathyroid hormone responses to catecholamines and to changes of extracellular calcium in cows.

Modifications of the plasma level of immunoreactive parathyroid hormone (PTH) in cattle were induced by changes of the plasma concentrations of epinephrine, isoproterenol, or calcium. During abrupt hypocalcemia, PTH, obtained by infusions with ethylene glycol-bis (beta-aminoethylether) N, N'-tetraacetate (EGTA), increased during the first 4-8 min. After a transient decline, the hormone levels rose again and remained elevated. Infusions of calcium suppressed the hypocalcemia-induced augmentation of PTH levels within a few minutes. Prolonged epinephrine (and isoproterenol) infusions also rapidly increased PTH levels, however, in this case, they returned to basal concentrations after 50-60 min. Additional epinephrine infusions could not further raise PTH values. Moreover, three short-lasting infusions of epinephrine (7 min each), given at 30-min intervals, increased PTH levels to the same extent, whereas additional infusions were much less effective. The PTH response to epinephrine was completely restored, when the interval after a prolonged epinephrine infusion had been prolonged to > 100 min. During moderate hypocalcemia, occurring at the end of EGTA infusions and lasting for 90 min, the PTH response to a short-lasting epinephrine infusion (7 min) was more pronounced than in normocalcemic animals. During severe hypocalcemia, in which superimposed short-lasting infusions of EGTA (7 min) led to an additional abrupt fall of plasma calcium concentrations but not to a corresponding additional rise of the PTH levels, epinephrine rapidly and further increased PTH concentrations. On the other hand, at the end of prolonged infusions of epinephrine, when additional infusions of epinephrine were ineffective in raising PTH levels, EGTA-induced hypocalcemia consistently increased PTH concentrations. The EGTA-induced augmentation of PTH levels was enhanced by epinephrine and isoproterenol but not by propranolol. The present findings indicate, that variations of the extracellular calcium concentrations and beta-adrenergic agonists modify PTH levels by two different and independent mechanisms. On the other hand, it appears that the magnitude of change of the PTH levels to either stimulus is partially modulated by exposure to the other.

Animals↗
PubMed1978

Carbidopa inhibits the growth hormone- and prolactin-suppressive effect of L-dopa in acromegalic patients.

The plasma GH, PRL, TSH, and dopamine (DA) responses to an infusion of L-dopa were examined in six acromegalic patients before and after pretreatment with carbidopa, a drug which inhibits the peripheral conversion of L-dopa to DA. Carbidopa neither modified baseline DA nor induced changes in baseline GH, PRL, or TSH levels. The drug instead markedly reduced the L-dopa-induced DA rise, an effect which was concomitant to a striking reduction of the suppressive effect of L-dopa on plasma GH and a partial inhibition of the suppressive effect of L-dopa on plasma PRL. TSH levels did not change either after L-dopa alone or L-dopa plus carbidopa. These data demonstrate that in "responder" acromegalics, L-dopa inhibits GH secretion through its peripheral conversion to DA and not via activation of central DA neurotransmission. For the effect of L-dopa on PRL secretion, in addition to a peripheral dopaminergic component, a central component cannot be disregarded.

Acromegaly↗
PubMed1977

Effects of mazindol and d-fenfluramine of 5-hydroxytryptamine uptake, storage and metabolism in blood platelets.

Mazindol induced a dose-related inhibition of the uptake of labelled 5-hydroxytryptamine (5-HT) by guinea pig blood platelets. It was more potent than d-fenfluramine. Mazindol and d-fenfluramine decreased 5-hydroxy-indoleacetic acid formation in intact platelets but not in sonicated ones. The inhibitory effects of both drugs appeared to the competitive in nature and were markedly reduced in platelets suspended in plasma instead of in Tyrode solution. Mazindol neither decreased the stored endogenous 5-HT nor caused efflux of the labelled amine from preloaded platelets, whereas d-fenfluramine induced a significant release of the amine. It is concluded that mazindol, like d-fenfluramine, competes with 5-HT for the same transport mechanisms at the cytoplasmic membrane level but this effect is not accompanied, as is the case with d-fenfluramine, by a concomitant release of the amine.

Animals↗
PubMed1977

Effects of mazindol, fenfluramine and chlorimipramine on the 5-hydroxytryptamine uptake and storage mechanisms in rat brain: similarities and differences.

Mazindol and fenfluramine inhibited in vitro the uptake of 5-HT into rat forebrain synaptosomes, whether the synpatosomes were incubated in vitro with the drugs or obtained from animals pretreated in vitro. Chlorimipramine was also effective in this latter preparation. Dose-response relationships and time course of this effect for the various drugs were determined. Fenfluramine also caused release of 5-HT from preloaded synaptosomes in in vitro incubations. Mazindol did not. Brain 5-HT levels were measured after acute and chronic administration of mazindol, fenfluramine and chlorimipramine. Mazindol had no effect, fenfluramine was active in reducing brain 5-HT concentrations acutely and chlorimipramine only after chronic administration. Therefore, it seems that even a long lasting inhibition of the uptake, such as that induced by mazindol, is not sufficient, per se, to cause depletion of brain 5-HT.

Animals↗
PubMed1977

Mazindol and amphetamine as inhibitors of the uptake and releasers of 3H-dopamine by rat striatal synaptosomes.

The effects of mazindol, amphetamine and fenfluramine on uptake and release of 3H-DA by synaptosomes were studied in different systems. In in vitro incubations of 3H-DA with synaptosomes isolated from the caudate nucleus of the rat, mazindol inhibited the uptake of the radioactivity more potently than did amphetamine. When the synaptosomes were isolated from the caudate nuclei of rats treated in vivo with either mazindol or amphetamine, the uptake of 3H-DA during in vitro incuation was lower with synaptosomes of amphetamine-treated rats than with those of mazindol-treated rats. When synaptosomes of untreated rats were prelabelled with 3H-DA and incubated in the presence of amphetamine or of mazindol, amphetamine caused a greater release of radioactivity than did mazindol. Fenfluramine was without activity in all these systems. In spite of the quantitative differences, both amphetamine and mazindol appear to have similar effects on uptake and release of dopamine, and this may account for their analogous pharmacological profile.

Animals↗
PubMed1976

Uptake and liberation of mepacrine in blood platelets.

1. Isolated platelets of guinea pigs incubated in Tyrode showed a rapid accumulation of 14C-mepacrine which was less dependent on temperature than that of 14C-5-hydroxytryptamine (5HT). 2. The uptake of mepacrine was not inhibited by imipramine, cocaine, ouabain, KCN, NaF, and reserpine. 3. Various 5HT-liberating drugs, e.g. Ro 4-1284 (benzoquinolizine derivative with reserpine-like action), amphetamine, tyramine and imipramine did not markedly affect the 14C-mepacrine content of platelets previously loaded with this compound. 4. Thrombin and chlorpromazine caused a liberation of 14C-mepacrine from the platelts which was however, less pronounced than that of 14C-5HT. 5. From these and previous findings it is concluded that 14C-mepacrine accumulates in the 5HT storage organelles by a reserpine-insensitive mechanism not dependent on an active transport at the cytoplasmatic membrane level.

2H-Benzo(a)quinolizin-2-ol, 2-Ethyl-1,3,4,6,7,11b-↗