Biomedical subjects

M A Potenza

Publications and source records attributed to M A Potenza.

8 recordsLinked to original sources

PubMed1996

Hyporeactivity of mesenteric vascular bed in endotoxin-treated rats.

Vascular reactivity and activation of the nitric oxide (NO) pathway were investigated in perfused mesenteric vascular bed removed from rats 5 h after i.p. injection of bacterial lipopolysaccharide (E. coli lipopolysaccharide, 30 mg kg -1). Lipopolysaccharide treatment induced hyporesponsiveness to noradrenaline. Maximal noradrenaline-induced vasoconstriction was significantly reduced in lipopolysaccharide-treated vs. untreated preparations. Continuous infusion of L-arginine (L-Arg) (0.2 mM) enhanced noradrenaline hyporeactivity of lipopolysaccharide-treated rats. N omega-Nitro-L-arginine methyl ester (L-NAME) (0.2 mM), a non-selective inhibitor of NO synthase, failed to completely restore the noradrenaline hyporeactivity of lipopolysaccharide-treated + L-Arg-infused mesenteric vascular bed. After L-NAME treatment. Methylene blue (10 microM), a guanylate cyclase inhibitor, produced no additional increase of noradrenaline vasoconstriction in lipopolysaccharide-treated + L-Arg-infused mesenteric vascular bed, suggesting that an NO-independent activation of guanylate cyclase may be excluded. In lipopolysaccharide-treated preparations, L-Arg (0.2 mM) elicited a significant increase in nitrite production, which was antagonized by L-NAME. In conclusion, lipopolysaccharide-induced noradrenaline hyporesponsiveness of rat resistance vessels can only be partially explained by NO overproduction. Other mechanisms, probably related to vasoconstriction, may be involved.

Animals↗

PubMed1996

Prenatal exposure to carbon monoxide and vascular responsiveness of rat resistance vessels.

The aim of the present study was to investigate the influence of prenatal exposure to carbon monoxide (CO) on vascular reactivity of rat resistance vessels, in different stages of neurogenesis. Both prenatally CO-exposed and control male Wistar pups (5-7, 9-11, 14-16, 20-22 days) were tested vs respective 60 day adult rats. The results showed that: (i) at 5-7 days of age, TTX caused a more marked inhibition of perivascular nerve stimulation (PNS)-evoked vasoconstriction in CO-exposed animals with respect to controls; (ii) the NO-related relaxant effect by ACh in CO-exposed group appeared earlier (5-7 days) than in control group (9-11 days); (iii) the contractile response evoked by ACh on resting tone disappeared earlier (after 14-16 days) than in control group (after 20-22 days). These observations suggested that CO-exposure might induce changes in nerve electrophysiological properties and might cause a precocious maturation of the NO-related enzymatic mechanism implicated in ACh-relaxation.

Acetylcholine↗

PubMed1996

Postnatal developmental changes of receptor responsiveness in rat mesenteric vascular bed.

1. The response to perivascular nervous stimulation (PNS) and the responsiveness to receptor agonists, in different stages of neurogenesis, on rat mesenteric vascular bed (MVB), was investigated. Rats of different age groups (5-7, 9-11, 14-16, 20-22 days) were tested, using 60-day-old rats as controls. 2. In the 5-7 days age group, the response to PNS was resistant to TTX treatment (1 x 10(-6) M). The TTX inhibition increased with age and became almost complete in 60-day-old rats. 3. In the 1st week of postnatal life (pre-innervation period), noradrenaline (NA) and 5-hydroxytryptamine (5-HT) produced contraction, whereas isoprenaline (ISO) and dopamine (DA) caused relaxation. During the 1st and 2nd week, pD2 values of NA and ISO were significantly higher than in adult control rats. No significant difference in pD2 values of 5-HT and DA was observed during postnatal development. 4. At 5-7 days, the relaxation by acetylcholine (ACh), typical of adult age, was absent and ACh evoked only contractile responses. The relaxant effect by ACh appeared at 9-11 days, increased with age and, by the end of the 2nd week, did not differ from that of the adult group. 5. These results provide evidence that responsiveness of all tested receptors in the MVB is already present in the pre-innervation period (1st week). Adrenergic receptor responsiveness is higher at birth and decreases by the end of the 3rd week of postnatal life, when connections between the central nervous system and effector organs are established. Only muscular muscarinic receptors, responsible for ACh-induced contraction, are functional in the 1st week, while endothelial muscarinic receptors, responsible for ACh-induced relaxation, become gradually responsive later in postnatal life.

Acetylcholine↗

PubMed1996

Beta-adrenoceptor responsiveness of splenic macrophages in normotensive and hypertensive rats.

The aim of the present study was to investigate putative mechanisms implicated in the impaired phagocytic response of spontaneously hypertensive rats (SHR)1. The effect of in vitro treatment with isoproterenol (ISO), a beta-adrenergic drug, on phagocytosis and respiratory burst by splenic macrophages (SpMø) from normotensive Wistar-Kyoto rats (WKY) and SHR with established hypertension, respectively, was evaluated. Furthermore, the relaxant effect of ISO was determined in phenilephrine-precontracted thoracic aorta strips from SHR compared with age-matched WKY rats. Results indicate that exposure of rat SpMø to ISO generate a significant and dose-dependent reduction of phagocytosis and oxidative burst which was antagonized, almost completely, by the beta-adrenergic antagonist propranolol (PRO). Unlike normotensive, in hypertensive rats treatment with ISO fail to modulate phagocytosis and respiratory burst activity by SpMø. At vascular level, aortic relaxation by ISO was reduced in SHR when compared to WKY rats. These findings suggest that SHR exhibit changes not only in vascular, but also in macrophage beta-adrenoceptor-mediated responses. It is postulable that sympathetic overactivity could be responsible for impaired phagocytic functions and beta-receptor alterations observed in SHR.

Animals↗

PubMed1994

Decrease of phagocytic functions in hypertensive rats.

The present investigation was aimed to examine non-specific immunologic capabilities of spontaneously hypertensive rats (SHR) during the development of hypertension. In vitro phagocytosis and oxidative killing exerted by monocytes, polymorphonuclear cells (PMN) and splenic macrophages (SpM0) were evaluated in SHR at 5-, 8-, and 24-weeks of age. Age-matched normotensive Wistar-Kyoto (WKY) rats were used as controls. Results showed that in pre-hypertensive stage (5-wk) there was no difference between SHR and WKY rats with regard to non-specific immunologic functions. Statistically significant differences in both phagocytosis and oxidative killing arose in early hypertensive stage (8-wk) and became more marked in adult SHR with established hypertension (24-wk). In conclusion, our data provide evidence of novel immunologic abnormalities in SHR in terms of ingestion and bactericidal phagocytic capabilities. The mechanisms responsible for these impaired immunologic functions may depend on various suppressive factors which will be object of discussion.

Aging↗

PubMed1993

Supplementation of male inhibitory material to lipid A activated human mononuclear cell supernatants contributes to the suppression of polymorphonuclear cell phagocytosis.

Human normal peripheral blood mononuclear cells were stimulated with lipid A (LA), the biologically active moiety of bacterial lipopolysaccharides. LA-activated supernatants were able to suppress polymorphonuclear cell (PMN) phagocytosis of Candida albicans. This inhibitory activity was enhanced by the supplementation of male inhibitory material (MIM) to active supernatants. The addition of a recombinant human anti-interleukin-1 beta monoclonal antibody to activated supernatants in the absence or presence of MIM diminished or abrogated, respectively, the suppressive effect on PMN function. The mechanisms and the significance of MIM-mediated inhibition of phagocytosis under these circumstances are discussed.

Adult↗

PubMedDate not supplied

Vasodilatation induced by capsaicin in rat mesenteric vessels is probably independent of nitric oxide synthesis.

Vasal relaxation induced by capsaicin was investigated on perfused mesenteric vascular bed prepared from Wistar rats. Bolus infusion of capsaicin, from 3.5 to 16 nmol, elicited a dose-dependent vasal relaxation effect, which was antagonized by pretreatment with 3 x 10(-6) M calcitonin gene-related peptide (CGRP) (8-37), an antagonist of CGRP. In order to test whether NO-release is involved in vasorelaxant response to capsaicin, a preparation of mesenteric vascular bed was perfused and superfused for 1 h by N omega-nitro-L-arginine methyl ester (L-NAME) (3 x 10(-3) M), an NO-synthase inhibitor. Vasodilatation induced by capsaicin remained unchanged, while that induced by acetylcholine, used as control, was significantly reduced. The results indicate that in the mesenteric bed, capsaicin-induced vasodilatation is probably independent of the NO-synthesis mechanism and possibly mediated by CGRP.

Amino Acid Oxidoreductases↗

PubMedDate not supplied

Involvement of nitric oxide in hyporeactivity of rat mesenteric vascular bed during endotoxic shock: effect of dexamethasone and endothelin-I.

The present study was carried out on mesenteric vascular bed from LPS-injected rats in order to investigate the cause of hyporesponsiveness in resistance blood vessels, during septic shock syndrome. The involvement of L-Arg/NO pathway was evaluated by administration of L-Arg, which produced a decrease in perfusion pressure in LPS-treated rats, whereas it was ineffective in control rats. Furthermore, DEX-pretreatment in endotoxaemic rats significantly reduced the vasorelaxation by L-Arg, whereas it was ineffective to reverse vascular hyporeactivity occurring in septic shock. In order to evaluate whether hyporesponsiveness could be due to defects in contraction mechanisms, we tested the effect of ET-I. This peptide was able to markedly enhance the contractile response to NA in LPS-treated rats. Our findings suggest that vascular hyporesponsiveness during septic shock may depend on both activation of the L-Arg/NO pathway and alterations in post-receptor mechanisms involving calcium handling.

Animals↗