Biomedical subjects
Publications and source records attributed to M Massi.
Eledoisin, administered to dogs by intra-carotid route, potently stimulated salivary secretion. The effect was not due to stimulation of cholinergic, adrenergic, histaminergic or 5-hydroxytryptaminergic receptors but was direct on salivary glands.
Eledoisin, administered to dogs by conjunctival route, potently stimulated lacrimal secretion. The effect did not depend on activation of adrenergic, histaminergic or 5-hydroxytryptaminergic receptor and was only in part due to stimulation of cholinergic receptors.
Eledoisin cured corneal lesions produced in the rabbit by cocaine but failed to heal those produced by sodium hydroxide. The effect was probably due to accelerated epithelial proliferation.
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1. The effect on water intake of intracranial injections of Substance P was studied in the rat. 2. Substance P strongly inhibited drinking elicited by Angiotensin II, Carbachol water deprivation or sodium chloride load, in that order. 3. The peptide was particularly effective when water intake was induced by injections of Angiotensin II into the preoptic area. In these experiments, drinking was inhibited by doses of Substance P as low as 1 ng. 4. The results suggest that in the rat Substance P may play a role in the brain in the regulation of water intake, acting as a thirst inhibitor.
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The effects on ingestive behavior of the naturally occurring bombesin-like peptides ranatensin and litorin were studied in comparison to those of bombesin by intracerebroventricular pulse injection or by continuous infusion in the rat. Ranatensin and litorin, like bombesin, proved to inhibit drinking and feeding behavior. Marked differences, however, were observed in their effects. In particular our results indicate that these peptides possess different selectivity of action on drinking elicited by different dipsogenic stimuli and different potency and effectiveness in inhibiting food intake induced by food deprivation. Moreover, the effects of the three peptides were markedly affected also by the modality of administration (pulse injection or continuous infusion). On the basis of these results it seems possible to hypothesize that the endogenous bombesin-like peptides may differently affect rat ingestive behavior according to their structure and to the rate and modality of their release in the brain.
The present study investigated the sensitivity of 12 forebrain and midbrain structures to the antidipsogenic effect of eledoisin, physalaemin and substance P on angiotensin-induced drinking. The three tachykinins elicited the most potent effects when injected into the nucleus preopticus medialis, the nucleus anterior hypothalami and the subfornical organ. In other sites (nuclei lateralis, ventromedialis and posterior hypothalami, nucleus septi lateralis, nucleus interpeduncularis and substantia grisea periventricularis) the effect was lower, and most of these sites showed different sensitivity to the three tachykinins. Finally, the nucleus septi medialis, the nucleus preopticus lateralis and the substantia nigra were refractory to the three tachykinins. These results show that: (1) the antidipsogenic effect of tachykinins can be elicited not only in forebrain, but also in midbrain structures such as the substantia grisea periventricularis and the nucleus interpeduncularis; (2) the distribution of brain sites sensitive to the antidipsogenic effect of substance P and physalaemin is always overlapping, while this is not true for eledoisin. This probably reflects selective distribution and/or activation of distinct subtypes of tachykinin receptors.
In infant rats, kassinin exerts its antidipsogenic effect in the very early stages of neonatal life (2nd-3rd day). The inhibition of cell-dehydration drinking appears in rats of 2 days, and attains adult levels in pups of 9 days. Instead, the thirsts induced by suckling deprivation or by intracerebroventricular angiotensin II are inhibited by kassinin precociously (3rd day), but are unaffected by it in rats of 12-15 days. Kassinin also inhibits milk intake very early (3rd day) and this effect also disappears at 12 days of age. The pattern of ontogenetic results described here may be that of a brain kassinin-like tachykinin that, in the course of the development of the neural structures on which it acts, gains potent and selective control of cell-dehydration thirst.
Neurokinin A (NKA), which selectively inhibits only cellular dehydration (CD)-induced drinking in adult rats, exerts a more general antidipsogenic effect in pups in which it also inhibits drinking induced by angiotensin II (AII) or suckling deprivation (SD). The inhibition of drinking is precocious (1st-3rd day) and never involves the intake of milk. The inhibition of CD-induced drinking increases with age, while that of AII- or SD-induced drinking progressively decreases and disappears on day 12-15. In the rat, NKA is therefore a precocious and selective inhibitor of drinking behavior and its selectivity is achieved ontogenetically.
The present study evaluated the sensitivity of spontaneously hypertensive (SHR) and of Wistar Kyoto (WKY) rats to the hypotensive effect of tachykinins (TKs). Eledoisin, substance P, and the NK-1-selective agonist [Sar9,Met(O2)11]substance P evoked a smaller hypotensive response in SHR than in WKY rats. The hypotensive effect of NKA was slightly smaller in SHR, but no significant strain difference was observed. The NK-2-selective agonist [beta Ala8]NKA(4-10) was a very weak hypotensive agent in WKY rats, while being completely inactive in SHR. The NK-3-selective agonists [Asp5,6,MePhe8]substance P(5-11) and [MePhe7]NKB did not modify blood pressure in both strains. Heart rate was essentially unmodified following the NK-3 agonists, while it was increased after injection of substance P, [Sar9,Met(O2)11]substance P, and neurokinin A, the increase being greater in WKY than in SHR. Surprisingly, eledoisin increased heart rate in SHR, but not in WKY rats, despite the greater hypotensive effect elicited in the latter strain. The present results confirm that the hypotensive effect of peripheral TKs is mediated by NK-1 receptors and show that SHR are less sensitive than WKY rats to this effect.
Intravenous (i.v. 320 and 640 micrograms/kg) and intracerebroventricular (i.c.v.; 1 microgram/rat) injection of Escherichia coli lipopolysaccharide (LPS) powerfully inhibited drinking induced by 24 h water deprivation. Pretreatment with acetylsalicylic acid (ASA) into the preoptic area (POA) completely abolished the effect induced by i.v. LPS, but did not modify that elicited by i.c.v. LPS. Intraperitoneal ASA injections significantly reduced the antidipsogenic effect of i.c.v. LPS. Electrolytic ablation of the subfornical organ (SFO) did not modify the effect induced by either i.v. or i.c.v. LPS. Present findings indicate that: (1) the antidipsogenic effect of i.v. LPS is mediated by prostaglandin synthesis into the POA, (2) the SFO is not involved in this effect, and (3) prostaglandins in other brain areas, besides POA, modulate the effect of i.c.v. LPS. It is suggested that at least two different brain sites, inside the blood-brain barrier, might be involved in the antidipsogenic effect of LPS.
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The effect of the adenosine receptor agonists, 2-chloro-N6-cyclopentyladenosine (CCPA) and 2-hexynyl-adenosine-5'-N-ethylcarboxamide (HENECA) on atrial natriuretic factor (ANF) release was investigated. The A1 adenosine receptor agonist CCPA markedly increased plasma ANF levels, following subcutaneous (s.c.), but not intracerebroventricular injection. ANF release evoked by the s.c. injection of CCPA was completely abolished by s.c. pretreatment with the selective A1 adenosine receptor antagonist, 1,3-dipropyl-8-cyclopentylxanthine. The A2 adenosine receptor agonist HENECA did not produce ANF release. The results of the present study suggest that peripheral adenosine mechanisms might be involved in the control of ANF secretion, through the activation of A1 adenosine receptors. Preliminary results show that CCPA produces ANF release also from isolated atria, thus suggesting that its action on ANF release is, at least in part, direct, and not only a consequence of cardiovascular modifications.