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Biomedical subjects

N Frisina

Publications and source records attributed to N Frisina.

At least 73 records · Page 4Linked to original sources
PubMed1993

Effects of intravenous administration of recombinant human erythropoietin in rats subject to hemorrhagic shock.

The effects of recombinant human erythropoietin (rHuEPO) on survival and blood pressure in hypovolemic hemorrhagic shock in rats have been studied by intravenous administration. The hormone caused an increase in the time of survival compared to the group of rats without treatment (102 +/- 4.5 vs. 25 +/- 4.5 min, p < 0.01, vehicle; 102 +/- 4.5 vs. 25 +/- 2 min, p < 0.01, saline solution) and an increase in the percentage of the surviving animals (5/7 after 120 min vs. 0/7, p < 0.05). The animals treated showed an increase in mean arterial pressure that was not present in the control group. Through their data, the authors suggest the vasopressor effect of erythropoietin. Furthermore, from other studies done before, they hypothesize that the vasoactive ability of the hormone is endothelin mediated.

Animals↗
PubMed1991

Influence of therapy with recombinant erythropoietin on serum levels of neopterin in hemodialyzed subjects.

The authors wished to investigate some aspects of the cell-mediated immunity in hemodialyzed subjects undergoing a treatment with recombinant erythropoietin (rHuEPO). The study was carried out through the dosage of the serum levels of neopterin, a substance produced by the macrophages and usable as a marker of their state of activation. The results show a significant reduction of the serum levels of pteridine already at the second month of treatment with rHuEPO (61 +/- 9 vs. 95 +/- 12 nmol/l), thus proving a probable inhibitory action carried out by erythropoietin on certain cells of the immune system.

Anemia↗
PubMed1990

Effects of intracerebroventricular administration of magnesium sulphate on blood pressure and heart rate in anesthetized normotensive and hypertensive rats.

Intracerebroventricular (i.c.v.) injection of magnesium sulphate (MgSO4:2.5, 5 and 10 mumol in 5 microliters) decreased blood pressure and heart rate in both anesthetized normotensive (WKY) and hypertensive rats (SHR). The effects were greater in WKY than in SHR. Moreover, a pretreatment with hexamethonium (2 mg/kg, i.v.) significantly blunted the hypotensive and bradycardic effects induced by i.c.v. injection of 10 mumol of MgSO4 in both WKY and SHR. Our data suggest that MgSO4 produces hypotensive and bradycardic effects when injected i.c.v. in both WKY and SHR.

Anesthesia↗
PubMed1989

A comparison of synthetic human and rat ANP administered intracerebroventricularly in freely moving normotensive and hypertensive rats.

The effects of intracerebroventricular (i.c.v.) injection of alpha-human atrial natriuretic peptide (alpha-hANP) and alpha-rat atrial natriuretic peptide (alpha-rANP) were studied in normotensive [Wistar-Kyoto (WKY)] and spontaneously hypertensive rats (SHR). Intracerebroventricular injection of alpha-hANP (200, 400, and 800 ng in 5 microliters) did not modify mean arterial pressure (MAP), heart rate (HR), and water intake in both WKY rats and SHR. On the contrary, alpha-rANP (200, 400, and 800 ng in 5 microliters) caused strong dipsogenic, pressor, and bradycardic effects that were greater in hypertensive than in normotensive rats. Saralasin (9 microns in 5 microliters), injected 2 min prior to alpha-rANP, abated these effects, thus indicating an involvement of brain angiotensin. Our results suggest that, at least as far as the cerebral effects of ANP are concerned, some difference exists between alpha-rANP and human atrial natriuretic peptide.

Animals↗
PubMed1989

Effects of calmodulin and calcium channel blockers on the Ca2+ induced outflow of K+ in intact red blood cells of patients with essential hypertension.

The correlation between the alterations of free intracellular calcium concentrations and the essential arterial hypertension has been largely investigated. Calmodulin, a cytoplasmic protein with low molecular weight, is one of the factors known to be able to affect the activity of calcium-dependent enzymes. The authors have investigated the effect of calcium and calmodulin on the plasmatic membrane of intact erythrocytes in a group of patients with essential arterial hypertension. To this purpose, the ionophor A23187, propranolol at low concentrations and a few calcium channel blocking drugs, alone or associated with calmodulin have been used. The results demonstrate that calmodulin, capable of blocking calcium outside the cell, can exert its effect only when propranolol is also present in the erythrocytes of normotensive but not in the hypertensive patients. The authors discuss some pathogenetic hypotheses.

Adult↗
PubMed1989

[Effect of angiotensin converting enzyme inhibitors on lipid, purine and glucose metabolism].

Recent intervention trials failed to show a significant decrease in mortality of ischemic heart disease in hypertensive patients given pharmacological treatment. These results led to a reassessment of cardiovascular risks of antihypertensive drugs per se and particularly diuretics. Captopril and Enalapril, antihypertensive drugs acting as converting enzyme inhibitors, might have some theoretical advantage over other antihypertensive drugs. The chronic ACE inhibitors therapy does not compromise glucose, lipid and urate and it seems not to be persistent in long-term administration.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1989

[Erythropoietin: current aspects and prospects].

Authors have reviewed recent literature on erythropoietin. They report new information regarding synthesis, modulation, changes during several diseases and the possibility for a clinical use of erythropoietin for the correction of many anaemias. Finally the Authors report some personal observations about the physiopathology of erythropoietin. They have studied the circadian rhythm, action of aging and the prostaglandin system, and plasma levels of E. in patients with anaemia of active rheumatoid arthritis.

Adult↗
PubMed1987

Human alpha atrial natriuretic peptide inhibits angiotensin stimulated aldosterone biosynthesis in bovine adrenal glands.

The behaviour of aldosterone output was evaluated in isolated and superfused bovine adrenal glands during superfusion with human alpha atrial natriuretic peptide on its own or with angiotensin II or a antagonist dopaminergic drug: metoclopramide. H alpha-ANP even in high concentrations did not reduce the basal amount of aldosterone released from bovine adrenal glands, nor did it modify aldosterone response to metoclopramide, but it partially inhibited aldosterone stimulation by angiotensin II. These data suggest that atrial natriuretic factor may affect sodium secretion through the modulation of aldosterone secretion.

Adrenal Glands↗
PubMed1987

Central dipsogenic effect of synthetic rat atrial natriuretic polypeptide in normotensive rats.

The effect of intracerebroventricular (i.c.v.) injection of synthetic rat atrial natriuretic polypeptide (alpha-rANP) on drinking behavior was studied in normotensive rats, alpha-rANP (0.2, 0.4 or 0.8 micrograms in 5 microliter) caused a dose-dependent dipsogenic effect which was abated by i.c.v. pretreatment with saralasine (9 micrograms in 5 microliter). These results suggest that alpha-rANP possesses dipsogenic effects in water repleted rats and that brain angiotensin is involved. In addition, our data indicate that, at least as far as the effect of cerebral ANP is concerned, there are some differences between alpha-rANP and human atrial natriuretic polypeptide.

Animals↗
PubMed1985

Role of brain cholinergic system in the antihypertensive effect of clonidine in different models of rat hypertension.

Acetylcholine in the central nervous system appears to be involved in some aspects of hypertension. Clonidine and methyldopa may inhibit acetylcholine (Ach) release in several brain areas. The present study was therefore designed to determine whether a depletion of brain Ach could modify the antihypertensive effect of clonidine in freely moving spontaneously hypertensive (SHR), Grollman hypertensive (GHR) and DOCA-salt hypertensive (DHR) rats. Intravenous injection of clonidine (15, 30 and 75 micrograms/kg) reduced mean arterial pressure (MAP) and heart rate (HR) in all hypertensive animals. The hypotensive effect was more marked in SHR than in DHR and GHR. The effect was also reproducible when the drug dose was repeated 3 h later in rats pretreated with saline (5 microliters) in the lateral cerebral ventricle (i.c.v.). When clonidine administration was repeated in hypertensive animals 3 h after i.c.v. hemicholinium-3 (20 micrograms/5 microliters), the decrease in MAP and HR was significantly reduced compared with that observed in the same animals after the first injection. The data suggest that the antihypertensive effect of clonidine depends partially upon the integrity of central cholinergic neurons.

Acetylcholine↗
PubMed1984

On the role of dopamine receptors in aldosterone secretion.

We studied the effects of infusion of dopamine (4 microgram/kg/min for 120 min) alone or with domperidone infusion (235 microgram/min for 120 min) on aldosterone secretion before and after stimulation by ACTH (0,5 mg i.v.) in normal subjects. We also studied the effects, of pimozide (12 mg p.o.), of domperidone infusion (235 microgram/min for 120 min) before and after stimulation with ACTH (0,5 mg i.v.) on aldosterone secretion in two other sets of normal subjects. The infusion of dopamine does not modify the basal secretion of aldosterone whereas in other trials it caused reduction (P less than 0,05) of blood aldosterone response to ACTH versus controls. Domperidone and pimozide, D2 antagonist, do not modify the aldosterone secretion before and after ACTH stimulation. Furthermore domperidone does not remove inhibition of dopamine on aldosterone response to ACTH. We can exclude an action of central or peripheral D2 dopaminergic receptors in aldosterone secretion in man. Dopamine, which does not cross the blood brain barrier, reduced the blood aldosterone response to ACTH; for those reasons we can hypothesize that receptors D1, stimulated by dopamine modulate aldosterone secretion.

Adrenocorticotropic Hormone↗