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Biomedical subjects

M Palermo

Publications and source records attributed to M Palermo.

At least 19 recordsLinked to original sources
PubMed1991

Adrenergic stimulation of the human pituitary-adrenal axis is attenuated by an analog of met-enkephalin.

It has previously been suggested that endogenous opioid peptides may suppress the pituitary-adrenal axis in man by inhibiting an excitatory alpha 1-adrenoceptor input to neural mechanisms liberating corticotrophin-releasing factor or factors (CRFs). This hypothesis has been tested here by investigating the effect of the met-enkephalin analog, DAMME (FK-33,824), on the elevation in serum cortisol induced by the catecholamine-releasing agent d-amphetamine (10 and 25 mg p.o.) and the direct alpha 1-adrenoceptor agonist methoxamine (6 micrograms/kg/min i.v.) in two groups of 6 normal male subjects. In both studies, the rise in serum cortisol was significantly attenuated by the analog of met-enkephalin. These data suggest that exogenous opioids act as a site downstream to the alpha 1-adrenoceptor input to CRF release; it appears that opioids modulate adrenocorticotrophic hormone release in man at a minimum of two distinct and separate sites.

Adrenal Glands↗
PubMed1990

Interaction of glucose and pyridostigmine on the secretion of growth hormone (GH) induced by GH-releasing hormone (GHRH).

In order to investigate the mechanisms by which hyperglycaemia induces an inhibition of GHRH-induced GH release, we gave the following treatments to seven normal men: a) GHRH 100 micrograms iv; b) pyridostigmine (PD) 120 mg po 60 min before GHRH; c) glucose 250 mg/kg iv as a bolus (10 min before GHRH) plus 10 mg/kg/min until the end of the test; d) glucose pyridostigmine and GHRH as above. Glucose significantly reduced GHRH-stimulated GH levels, whereas PD significantly enhanced them. When PD and glucose were given together, the effect on GHRH-stimulated GH secretion was not different from the algebraic sum of the single effects of the two substances. Thus glucose seems to be able to exert its inhibition, at least partially, also when pyridostigmine is coadministered.

Adolescent↗
PubMed1989

Opioids stimulate growth hormone (GH) release in man independently of GH-releasing hormone.

The Met-enkephalin analog DAMME [D-Ala2,MePhe4-Met-enkephalin-(o)-o1, FK 33-824] can stimulate GH secretion in man. In this study we investigated the effects of the guanyl derivative of DAMME (G-DAMME) on the serum GH response to an analog of GHRH in normal men. GHRH-(1-29)NH2 and G-DAMME each induced a rise in serum GH, and the increase was greater when both were given together. Since the GHRH-(1-29)NH2 dose (100 micrograms) used was a maximally stimulatory one, these results suggest that the enhancing effect of G-DAMME on GHRH-induced GH release may be mediated through inhibition of somatostatin release.

Adult↗
PubMed1988

Opposite effects of amines on lymphocyte- and monocyte-mediated ADCC.

The effect of different amines on antibody-dependent cellular cytotoxicity (ADCC) activity of human mononuclear cells was tested. Whereas monocyte cytotoxic capacity was significantly stimulated in the presence of methylamine (MA), dansylcadaverine (DC) and glycine ethylester (GEE), lymphocyte ADCC was markedly suppressed by these agents. The pharmacological actions of these compounds in our system are not related to their ability to inhibit transglutaminase (TGase) enzymes, since tertiary amines such as sarcosine ethylester (SEE) and chloroquine (CQ) elicited identical responses to MA, DC and GEE. The calmodulin (CAM) inhibitors trifluoperazine (TFP) and the more specific N-(6-aminohexyl)-5-chloro-1-naphtalene sulfonamide (W-7) [Hidaka, Sasaki, Tanaka, Endo, Ohno, Fujii & Nagata (1981) Proc. natn. Acad. Sci. U.S.A., 78, 4353-4357] mimicked the effects of amines on ADCC, suggesting the possibility that a CAM-regulated process might be involved in the functional changes provoked by amines on ADCC. Finally, binding of 125I-immune complexes to the effector cells in the presence of amines showed lack of correlation between alterations in ADCC capacity and Fc gamma R expression.

Amines↗
PubMed1987

Dopaminergic and cholinergic influences on the growth hormone response to growth hormone-releasing hormone in man.

It is well established that compounds that modify dopaminergic and cholinergic activity in man may induce changes in circulating growth hormone (GH). We have, therefore, investigated the effect of a dopamine agonist, bromocriptine, and a dopamine antagonist, domperidone, as well as a muscarinic cholinergic antagonist, pirenzepine, on the GH response to an analogue of GH-releasing hormone (GHRH) in normal male subjects. GHRH(1-29)NH2 induced a rise in serum GH that was augmented by bromocriptine, antagonized by pirenzepine, but was unaltered by domperidone. As this dose of GHRH(1-29) NH2 has been shown to be maximally stimulatory to GH release, it is suggested that there are dopamine stimulatory and cholinergic inhibitory receptors to GH release independent of GHRH in man.

Adrenergic Fibers↗
PubMed1983

Cholinergic receptor control mechanisms for L-dopa, apomorphine, and clonidine-induced growth hormone secretion in man.

The effect of pirenzepine, an anticholinergic agent, on GH release induced by L-dopa (500 mg po), apomorphine (0.75 mg sc), and clonidine (0.150 mg iv) administration was studied in a group of normal men. Pirenzepine, a cholinergic muscarinic antagonist, completely blocked the GH rise induced by dopamine- and adreno-receptor stimulation. In contrast, the PRL-inhibiting action of L-dopa was not modified by the cholinergic antagonist. The data suggest that acetylcholine and its receptors are important regulators of the neurosecretory mechanisms that control GH secretion in man.

Adult↗
PubMed1982

Active and inactive renin after a single dose of captopril in hypertensive patients.

In 25 hypertensive patients (15 with renal artery stenosis and 10 with essential hypertension), captopril, in a single 12.5 mg dose, caused a prompt decrease in arterial pressure without changing the heart rate. Plasma active and trypsin-activated renin significantly increases, whereas inactive renin and plasma aldosterone decreased. The plasma active/inactive renin ratio was also increased, suggesting that captopril, together with a release of active renin, may induce an in vivo activation of inactive renin. No correlations were found between blood pressure changes and both pretreatment and captopril-induced variations of active, inactive and trypsin-activated renin or the active/inactive ratio. However, the percent decrease in mean arterial pressure was significantly related to the increase in the active/inactive renin ratio in a group of patients whose blood pressure was brought to normal (r = -0.78; p less than 0.001). This finding suggests the possibility that vasodilating substances, in addition to inhibiting angiotensin II formation, might play some role both in exerting a full effect of captopril on blood pressure and in triggering the in vivo mechanisms of inactive renin activation.

Blood Pressure↗
PubMed1982

Active and inactive renin during acute reduction of renal perfusion pressure in essential hypertensives.

Arterial and renal venous active and inactive renin were studied in 5 patients with long established moderate hypertension following unilateral acute reductions of renal perfusion pressure (15% and 70% of control) by inflating a balloon catheter introduced into the right renal artery. This procedure failed to induce the expected release of active renin; total and inactive renin levels were also unchanged. On the contrary in a single normotensive patient smaller reductions of the renal perfusion pressure (-15% and -30%) were able to acutely increase the release of active renin with a concurrent conversion of inactive renin but without inducing blood pressure changes. These findings show that the renin pattern typical of unilateral renovascular hypertension, including the intrarenal activation of inactive renin, could be reproduced acutely in a normotensive subject. Moreover, a complete reversal of the above mentioned active and inactive renin pattern was observed in a recent onset renovascular hypertensive patient within 30 min from successful percutaneous transluminal dilation. The negative results observed in our hypertensive patients suggest that structural changes induced by the long duration of hypertension might have reduced the sensitivity of the baroceptors involved in renin release.

Adult↗
PubMed1981

Trypsin activation of inactive renin in human plasma. An assessment of some methodological aspects.

The following methodological aspects of the use of trypsin as activator of inactive renin in human plasma have been studied: a) the effect of SBTI on renin activity and angiotensin; b) the reaction velocity of trypsin on inactive renin; c) the optimum trypsin concentration; d) the ability of human plasma to neutralize exogenous trypsin. Our results show that: 1) Some commercially available SBTI may exert an angiotensinase-like effect which can be abolished by PMSF. 2) At 4 degrees C activation of inactive renin reached a maximum within the first two minutes then no further activation could be demonstrated. 3) Trypsin 2 mg/ml yielded more inactive renin than trypsin 1 or 0.5 mg/ml. A higher concentration (3 mg/ml) gave substantially equivalent activation as (with) trypsin 2 mg/ml whereas when using a still higher concentration (4 mg/ml) a degradation of the renin system components could be noted. 4) Endogenous trypsin inhibitors can eventually inactivate exogenous trypsin up to 3 mg/ml. About 20% of renin is destroyed by trypsin 4 mg/ml within 2 min at 4 degrees C while an additional 40% is lost during the incubation at 37 degrees C if no SBTI is added.

Enzyme Activation↗
PubMed1979

[Radiologic diagnosis of the retroperitoneal masses (author's transl)].

A series of 75 patients with retroperitoneal masses (60 malignant and 15 benign tumours) have been studied. Urography and angiography were employed. The results of the two methods are correlated. The following criteria are taken into consideration: a) site; b) nature; c) extension of the mass. The importance of a precise definition of the extension of the tumour is stressed. In fact this can greatly influence the choice of the therapy.

Angiography↗