Origin and Actions of Neuropeptide Y in the Cardiovascular System

1993 ◽  
pp. 315-388 ◽  
Author(s):  
Zofia Zukowska-Grojec ◽  
Claes Wahlestedt
Keyword(s):  
Neuropeptide Y ◽  
Cardiovascular System

Distribution and activity of dogfish NPY and peptide YY in the cardiovascular system of the common dogfish

1993 ◽  
Vol 264 (6) ◽  
pp. R1119-R1124 ◽  
Author(s):  
C. Bjenning ◽  
N. Hazon ◽  
A. Balasubramaniam ◽  
S. Holmgren ◽  
J. M. Conlon
Keyword(s):  
Neuropeptide Y ◽  
Cardiovascular System ◽  
Peptide Yy ◽  
Nerve Fibers ◽  
Dependent Manner ◽  
Cardiovascular Tissue ◽  
Y1 Receptor ◽  
Selective Agonist ◽  
Y2 Receptor ◽  
The Common

Neuropeptide Y is present in sympathetic nerves in the mammalian cardiovascular system. This study has investigated the distribution of neuropeptide Y in the cardiovascular and gastrointestinal systems and the effect of dogfish neuropeptide Y and related peptides on cardiovascular tissue of an elasmobranch fish, the common dogfish (Scyliorhinus canicula). Neuropeptide Y-like immunoreactivity is present in varicose nerve fibers innervating dogfish gut and cardiovascular tissue and in endocrine cells of the dogfish spiral intestine. Dogfish neuropeptide Y, dogfish peptide YY, and porcine neuropeptide Y contract the dogfish afferent branchial artery in a concentration-dependent manner. The effect is not inhibited by the presence of tetrodotoxin or by removal of the endothelium. The mammalian Y1 receptor selective agonist [Leu31Pro34]NPY but not the mammalian Y2 receptor selective agonist neuropeptide Y-(13-36) peptide has vasoconstrictor properties in this system, suggesting that the receptor mediating the vasoconstriction resembles the mammalian Y1 receptor more than the Y2 receptor.

Hemodynamic effects of posterior hypothalamic injection of neuropeptide Y in awake rats

1991 ◽  
Vol 261 (3) ◽  
pp. H814-H824 ◽  
Author(s):  
J. R. Martin ◽  
M. M. Knuepfer ◽  
T. C. Westfall
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Neuropeptide Y ◽  
Cardiovascular System ◽  
Peripheral Resistance ◽  
Hypothalamic Nucleus ◽  
Initial Increase ◽  
System Control ◽  
Posterior Hypothalamic Nucleus ◽  
Freely Moving

Unilateral microinjection of neuropeptide Y (NPY) into the posterior hypothalamic nucleus was previously found to evoke a sympathoexcitatory-mediated increase in mean arterial pressure (MAP) in urethan-anesthetized rats. In this study, the effect of unilateral injection of NPY into the posterior hypothalamic nucleus on the cardiovascular system of conscious, freely moving rats was determined. Microinjection of NPY (0.2-2.4 nmol) or the cholinergic agonist carbachol (0.5-5.5 nmol) resulted in concentration-dependent increases in MAP. Pretreatment of animals with 7.5 mg/kg iv of the ganglionic blocker pentolinium resulted in a blockade of the increase in MAP evoked by microinjection of NPY (2.4 nmol) or carbachol (3.3 nmol). Despite their similarity of effects on MAP, NPY and carbachol evoked different changes in heart rate. NPY increased heart rate, whereas carbachol evoked a biphasic change in heart rate that consisted of an initial increase followed by a decrease. In addition, carbachol caused increases in both hindquarter and mesenteric vascular resistances, whereas NPY caused a short-lasting increase in mesenteric resistance and a tendency toward an increase in hindquarter resistance. Both NPY and carbachol increased total peripheral resistance while NPY decreased stroke volume. Cardiac output was not significantly affected by either NPY or carbachol, although NPY had a tendency to decrease cardiac output. These results suggest that microinjection of NPY or carbachol into the posterior hypothalamic nucleus of conscious rats evokes an increase in MAP primarily as a result of sympathoexcitation and that NPY and carbachol selectively affect autonomic nervous system control of the cardiovascular system.

Localisation of neuropeptide Y in nerves of the rat cardiovascular system and the effect of 6-hydroxydopamine

1985 ◽  
Vol 19 (9) ◽  
pp. 570-577 ◽  
Author(s):  
J. M ALLEN ◽  
J. M POLAK ◽  
J. RODRIGO ◽  
K. DARCY ◽  
S. R BLOOM
Keyword(s):  
Neuropeptide Y ◽  
Cardiovascular System ◽  
6 Hydroxydopamine

Effects of neuropeptide Y on the cardiovascular system

1987 ◽  
Vol 8 (6) ◽  
pp. 231-235 ◽  
Author(s):  
L. Edvinsson ◽  
R. Håkanson ◽  
C. Wahlestedt ◽  
R. Uddman
Keyword(s):  
Neuropeptide Y ◽  
Cardiovascular System

Neuropeptide Y is present in the sympathetic nerves of the cardiovascular system

1985 ◽  
Vol 14 (1) ◽  
pp. 108
Author(s):  
J.M. Allen ◽  
J. Rodrigo ◽  
J.M. Polak ◽  
S.R. Bloom
Keyword(s):  
Neuropeptide Y ◽  
Cardiovascular System ◽  
Sympathetic Nerves

Chemical sympathectomy reveals pre-and postsynaptic effects of neuropeptide Y (NPY) in the cardiovascular system

1987 ◽  
Vol 43 (9) ◽  
pp. 1018-1020 ◽  
Author(s):  
Y. Mabe ◽  
R. Pérez ◽  
K. Tatemoto ◽  
J. P. Huidobro-Toro
Keyword(s):  
Neuropeptide Y ◽  
Cardiovascular System ◽  
Chemical Sympathectomy

Origin and Actions of Neuropeptide Y in the Cardiovascular System

2003 ◽  
pp. 315-388 ◽  
Author(s):  
Zofia Zukowska-Grojec ◽  
Claes Wahlestedt
Keyword(s):  
Neuropeptide Y ◽  
Cardiovascular System

Do we need another echo ‘window to the cardiovascular system’?

2000 ◽  
Vol 99 (2) ◽  
pp. 149
Author(s):  
ANDREW KELION
Keyword(s):  
Cardiovascular System

Inflammageing in the cardiovascular system: mechanisms, emerging targets, and novel therapeutic strategies

2020 ◽  
Vol 134 (17) ◽  
pp. 2243-2262
Author(s):  
Danlin Liu ◽  
Gavin Richardson ◽  
Fehmi M. Benli ◽  
Catherine Park ◽  
João V. de Souza ◽  
...  
Keyword(s):  
Cardiovascular Diseases ◽  
Cardiovascular System ◽  
Nlrp3 Inflammasome ◽  
Molecular Mechanisms ◽  
Molecular Targets ◽  
Therapeutic Interventions ◽  
Low Grade ◽  
Cardiovascular Research ◽  
Inflammatory Processes ◽  
Ach Receptors

Abstract In the elderly population, pathological inflammation has been associated with ageing-associated diseases. The term ‘inflammageing’, which was used for the first time by Franceschi and co-workers in 2000, is associated with the chronic, low-grade, subclinical inflammatory processes coupled to biological ageing. The source of these inflammatory processes is debated. The senescence-associated secretory phenotype (SASP) has been proposed as the main origin of inflammageing. The SASP is characterised by the release of inflammatory cytokines, elevated activation of the NLRP3 inflammasome, altered regulation of acetylcholine (ACh) nicotinic receptors, and abnormal NAD+ metabolism. Therefore, SASP may be ‘druggable’ by small molecule therapeutics targeting those emerging molecular targets. It has been shown that inflammageing is a hallmark of various cardiovascular diseases, including atherosclerosis, hypertension, and adverse cardiac remodelling. Therefore, the pathomechanism involving SASP activation via the NLRP3 inflammasome; modulation of NLRP3 via α7 nicotinic ACh receptors; and modulation by senolytics targeting other proteins have gained a lot of interest within cardiovascular research and drug development communities. In this review, which offers a unique view from both clinical and preclinical target-based drug discovery perspectives, we have focused on cardiovascular inflammageing and its molecular mechanisms. We have outlined the mechanistic links between inflammageing, SASP, interleukin (IL)-1β, NLRP3 inflammasome, nicotinic ACh receptors, and molecular targets of senolytic drugs in the context of cardiovascular diseases. We have addressed the ‘druggability’ of NLRP3 and nicotinic α7 receptors by small molecules, as these proteins represent novel and exciting targets for therapeutic interventions targeting inflammageing in the cardiovascular system and beyond.

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