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Biomedical subjects

C Polidori

Publications and source records attributed to C Polidori.

66 records · Page 4Linked to original sources
PubMed1989

[Effects of eledoisin on water intake induced by subcutaneous injection of hypertonic NaCl in the rat].

Intracerebroventricular administration of eledoisin, the tachykinin peptide of the salivary glands of Eledone Moschata, exerts a potent and long-lasting inhibition of water intake induced by the subcutaneous administration of hypertonic NaCl in the rat. The inhibitory effect is statistically significant up to 6 hr following eledoisin treatment, while the 24 hr water intake in control and treated rats is essentially identical. The results of the present study demonstrate that the long-lasting effect is not due to increased renal excretion of the osmotic load, nor, likely, to larger production of metabolic water. Probably, eledoisin exerts an inhibitory effect of such a long duration by means of central actions which last well beyond its half-life, or, alternatively, by promoting an increased excretion of the osmotic load through elimination routes different from the kidney.

Animals↗
PubMed1988

The tachykinin NH2-senktide, a selective neurokinin B receptor agonist, is a very potent inhibitor of salt appetite in the rat.

The tachykinin peptide [Asp5.6, MePhe8]substance P(5-11) (NH2-senktide), a senktide analogue lacking the N-terminal succinyl group, is a selective and metabolically stable NK-3 receptor agonist. In the present study it potently inhibited salt appetite induced by sodium depletion in rats. Argo-neurokinin B, too, inhibited salt appetite, but was less potent than NH2-senktide. Neither peptide inhibited drinking behaviour induced by subcutaneous hypertonic NaCl. NH2-senktide slightly inhibited angiotensin-induced drinking, while Argo-neurokinin B was ineffective. On the other hand, eledoisin was a potent inhibitor in the 3 behavioural tests. Present results indicate that activation of NK-3 receptors is involved in the antinatriorexic action of tachykinins, and that different receptor subtypes might be involved in the different effects of tachykinins on the rat ingestive behaviour.

Animals↗
PubMed1988

Neurokinin A selectively inhibits water intake in the rat.

The results of the present study show that the intracerebroventricular injection of neurokinin A elicited a selective antidipsogenic effect in the rat. Neurokinin A proved to be an extremely potent inhibitor of drinking elicited by subcutaneous administration of hypertonic NaCl, and produced also a statistically-significant inhibition of food-associated drinking. On the other hand, it did not affect drinking evoked by other dipsogenic determinants, such as water deprivation and intracerebroventricular injection of carbachol or of angiotensin II. Thus, neurokinin A shows a spectrum of antidipsogenic activity clearly different from that of substance P, the other mammalian tachykinin so far tested on drinking behaviour in the rat, which appears to be a non-selective antidipsogenic agent. The findings of the present study suggest that different tachykinins, endogenous to the brain of the rat, might subserve distinct roles in the control of drinking behaviour.

Angiotensin II↗
PubMed1988

Vasopressin release induced by intracranial injection of eledoisin is mediated by central angiotensin II.

Pulse intracerebroventricular injection of eledoisin, but not of substance P, markedly increases plasma vasopressin levels in the rat. Intracerebroventricular pretreatment with sarcosine1, alanine8-angiotensin II, 1 microgram/rat, completely suppresses the effect of eledoisin, suggesting that it is mediated by angiotensin release and angiotensin II receptor activation. The vasopressin releasing effect of eledoisin is neither due to peripheral haemodynamic alterations, nor to activation of the peripheral renin-angiotensin system. It is apparently related to central angiotensin release in a specific neuronal pathway subserving vasopressin release. This effect is not secondary to inhibition by tachykinins of the brain mechanisms for angiotensin-induced drinking, but is probably expression of direct activation of specific tachykinin receptors controlling vasopressin release.

Angiotensin II↗
PubMed1987

Effect of kassinin, neurokinin A and neurokinin B on drinking behaviour in the pigeon.

Intracerebroventricular (i.c.v.) injection of kassinin produced a prompt and copious drinking response at doses of 10-1000 ng/pigeon, in the absence of other behavioural alterations or of changes in core temperature. Neurokinin A and B evoked drinking, but they were respectively 10 and 100 times less potent than kassinin. Intraperitoneal injection of kassinin elicited drinking, but at doses about 1000 X larger than the i.c.v. ones. The angiotensin antagonist [Sar1, Leu8]angiotensin II did not reduce drinking induced by i.c.v. kassinin, suggesting that its effect is not due to interaction with the central renin-angiotensin system. Moreover, the effect is apparently independent of the mechanisms controlling hypovolaemic and hyperosmotic thirst since exact additivity was found in the dipsogenic response when i.c.v. kassinin was administered in the presence of a hypovolaemic (subcutaneous (s.c.), polyethylene glycol) or hyperosmotic (s.c. hypertonic NaCl) dipsogenic stimulus. The present findings show that kassinin, neurokinin A and B share with the tachykinins already tested (eledoisin, physalaemin, substance P) a common dipsogenic action in pigeons. However, marked differences exist in their dipsogenic potency. This order of potency, eledoisin = kassinin = physalaemin greater than neurokinin A = substance P greater than neurokinin B, is not consistent with the tachykinin receptor subtypes so far proposed.

Angiotensin II↗
PubMedDate not supplied

Age-related changes in the visual cortex: a review.

The main age related changes in visual cortex are reviewed. The visual cortex (occipital cortex, areas 17-19) undergoes a variety of anatomical, biochemical and functional changes with aging. From a morphological point of view the visual cortex loses nerve cells mainly in the last period of life. From a biochemical point of view cholinergic, serotonergic, and GABAergic neurotransmissions seem to be the most remarkably affected. In terms of functional correlates, a decline of several activities of the visual cortex has been documented in the elderly. Due to the importance of visual cortex in the realization of visual function, the influence of aging on this cerebrocortical area requires a more detailed analysis.

Journal Article↗
PubMedDate not supplied

Hypotensive effect of intravenous injection of tachykinins in conscious, freely moving spontaneously hypertensive and Wistar Kyoto rats.

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.

Amino Acid Sequence↗
PubMedDate not supplied

Release of atrial natriuretic factor induced by the A1 adenosine receptor agonist 2-chloro-N6-cyclopentyl-adenosine in the rat.

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.

Adenosine↗