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C Verrecchia

Publications and source records attributed to C Verrecchia.

23 records · Page 2Linked to original sources
PubMed1985

Perivascular peptides relax cerebral arteries concomitant with stimulation of cyclic adenosine monophosphate accumulation or release of an endothelium-derived relaxing factor in the cat.

Calcitonin gene-related peptide (CGRP), substance P (SP) and vasoactive intestinal polypeptide (VIP) have been proposed to be neurotransmitters/neuromodulators in cerebral perivascular nerve fibers. Here, we present pharmacological and biochemical evidence showing that these peptides have different modes of relaxing cerebral blood vessels in the cat. CGRP causes pronounced relaxation, this occurs simultaneously with stimulation of cyclic adenosine monophosphate (cAMP) accumulation. The strong VIP-induced dilatation is parallelled by cAMP accumulation, albeit of a lower magnitude than with CGRP. The SP-induced relaxation was much weaker than that of CGRP and VIP, and it was not associated with cAMP accumulation. Only at concentrations of SP where maximum relaxation had occurred, was a nonsignificant cAMP accumulation seen. The responses to SP and acetylcholine were absent in arteries where the endothelium had been removed, whereas the relaxations induced by CGRP and VIP persisted.

Adenylyl Cyclases↗
PubMed1985

Vascular monoamine oxidase activity in the rat brain: variation with the substrate and the vascular segment.

Brain vascular monoamine oxidase (MAO) was assayed in order to determine (a) whether microvessel MAO is more or less specific for certain substrates and (b) if the extraparenchymal, pial arteries possess an MAO activity as high as that in the microvessels. Rat brain microvessels were prepared by gentle homogenisation of grey matter, followed by filtration and differential centrifugation of the matter retained. Pial arteries were carefully freed of the meninges and cut into small segments. For comparison, rat mesenteric arteries were also dissected out and cut up. MAO was assayed by measuring the rate of oxygen consumption in a small cell with a Clark electrode. Although a high microvessel MAO activity (2.2 +/- 0.3 nmol min-1 mg prot.-1) was found using noradrenaline as substrate, significantly higher rates were found with tyramine, serotonin and beta-phenyl-ethylamine. By contrast, both pial and mesenteric arteries showed a 6-7 fold lower activity (substrate tyramine). These results indicate first, that a certain specialisation of the microvessel MAO activity exists which is apparently independent of the classical A or B-form category of the substrates, and second, that the extraparenchymal vessels (pial arteries) appear to possess significantly lower MAO activity, in accordance with the concept that blood-brain properties are induced by the cerebral parenchyma.

Animals↗
PubMed1985

Pial artery responses to norepinephrine potentiated by endothelium removal.

The effect of endothelium removal on pial artery constriction in response to norepinephrine (NE) was studied in vitro using a perfused vessel setup in which pressure increases indicate vasoconstriction. In deenodothelialized rabbit arteries, the reaction to extraluminal NE was found to be characterized by a much higher Emax (2.0 times) and a slight (but significant) leftward shift of the concentration-response curve (lower EC50) compared with control vessels. In cat arteries subjected to either extra- or intraluminal NE, the Emax was also substantially higher in deendothelialized preparations (4.4 and 5.1 times, respectively), but there was no significant difference in the EC50 values. Anatomical verification and functional tests (acetylcholine-induced dilatation) confirmed the presence and the absence of the endothelium in control and lesioned arteries, respectively. This modulatory influence of the endothelium may be of importance in cerebrovascular pathology.

Animals↗
PubMedDate not supplied

Influence of endothelium on noradrenaline-induced vasoconstriction in rabbit central ear artery.

The effects of removing the endothelium of the rabbit central ear artery on the response to noradrenaline have been examined in vitro. A 10 mm segment of this artery was cannulated and connected to a constant flow perfusion circuit; the endothelium of some arteries was first removed mechanically. Vasomotor activity was determined by measuring the pressure at the input to the artery. Scanning electron microscopy, light microscopy and functional test with acetylcholine on intact and rubbed arteries showed that the endothelium had been effectively removed in lesioned arteries and remained intact in control arteries throughout the experiment. Internal or external noradrenaline-induced a concentration-dependent constriction which was significantly greater in the rubbed arteries. In contrast, there was no significant difference in the pressure/flow curves of control and rubbed arteries whether preconstricted with K+ or not. We conclude that the endothelium in the rabbit isolated ear artery greatly influences the response to internal or external noradrenaline, and that this effect cannot be explained by changes in the physical characteristics of de-endothelialized arteries. The endothelium thus may play an inhibitory role in noradrenaline-induced vasoconstrictions.

Animals↗