Neuropeptide Y and sympathetic control of vascular tone in hypertension

Westfall, Thomas C.

doi:10.1007/3-7643-7417-9_6

Cited by 11 publications

(19 citation statements)

References 103 publications

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“…High doses usually produce tremors, vomiting, tonic-clonic convulsions, agitation/anxiety, dizziness, psychoses (delusions and paranoia), restlessness, hyperthermia, and/or rapid muscle breakdown. Many of psychostimulants also share other adverse side effects such as cardiovascular or hematologic liability and the serotonin syndrome (Boutrel & Koob, 2004;Cami et al, 2000;Foley, 2005;Westfall, 2006). With repeated use at higher doses, some psychostimulants produce SUD in susceptible human individuals (Boutrel & Koob, 2004).…”

Section: Human and Animal Effects Of Psychostimulantsmentioning

confidence: 99%

Psychostimulants

McCreary

Müller

Filip

2015

International Review of Neurobiology

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Section: Human and Animal Effects Of Psychostimulantsmentioning

confidence: 99%

Psychostimulants

McCreary

Müller

Filip

2015

International Review of Neurobiology

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“…Potentially important are the paracrine effects of NPY released from endocardial endothelial cells to affect excitationcontraction coupling [161]. The vasoconstrictive properties of NPY suggest a potential role in the development and / or maintenance of hypertension [28] and ischemic heart disease [35][36][37], whereas angiogenic action could promote revascularization [51]. The progression of compensated / decompensated LVH could be related to hypertrophic actions of the peptide [67].…”

Section: Y 2 Receptorsmentioning

confidence: 99%

“…Much evidence points towards the role of NPY in the development and / or maintenance of hypertension [28]. Furthermore, in LVH, which is an initial compensatory response of the heart to pressure overload precipitated by hypertension [1], NPY has been implicated.…”

Section: Introductionmentioning

confidence: 99%

NPY and Cardiac Diseases

McDermott¹,

Bell²

2007

CTMC

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Hypertension-induced left ventricular hypertrophy (LVH), along with ischemic heart disease, result in LV remodeling as part of a continuum that often leads to congestive heart failure. The neurohormonal model has been used to underpin many treatment strategies, but optimal outcomes have not been achieved. Neuropeptide Y (NPY) has emerged as an additional therapeutic target, ever since it was recognised as an important mediator released from sympathetic nerves in the heart, affecting coronary artery constriction and myocardial contraction. More recent interest has focused on the mitogenic and hypertrophic effects that are observed in endothelial and vascular smooth muscle cells, and cardiac myocytes. Of the six identified NPY receptor subtypes, Y(1), Y(2) and Y(5) appear to mediate the main functional responses in the heart. Plasma levels of NPY become elevated due to the increased sympathetic activation present in stress-related cardiac conditions. Also, NPY and Y receptor polymorphisms have been identified that may predispose individuals to increased risk of hypertension and cardiac complications. This review examines what understanding exists regarding the likely contribution of NPY to cardiac pathology. It appears that NPY may play a part in compensatory or detrimental remodeling of myocardial tissue subsequent to hemodynamic overload or myocardial infarction, and in angiogenic processes to regenerate myocardium after ischemic injury. However, greater mechanistic information is required in order to truly assess the potential for treatment of cardiac diseases using NPY-based drugs.

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“…Increasing evidence suggest that the level of NPY in plasma is significantly elevated in hypertrophy [10], hypertension [11] and myocardial ischemia [12]. Elevated levels of plasma NPY have also been proposed as a prognostic marker for coronary diseases [13], heart failure [14] and myocardial ischemia [15].…”

Section: Introductionmentioning

confidence: 99%

Blockage of Peripheral NPY Y1 and Y2 Receptors Modulates Barorefex Sensitivity of Diabetic Rats

Liu

Wang²,

Xie³

et al. 2013

Cell Physiol Biochem

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Background/Aims: Abnormal baroreceptor reflex sensitivity (BRS) and elevated plasma neuropeptide Y (NPY) are prevalent in diabetic patients. The present study was conducted to determine whether NPY Y1 receptor (Y1R) and NPY Y2 receptor (Y2R) contribute to the regulatin of BRS in diabetic rats. Methods: Diabetes mellitus (DM) rats with hyperlipidemia were developed by an emulsion diet enriched with fat, sucrose and fructose followed by streptozocin (STZ). Y1R and Y2R specific antagonists (BIBP 3226 and BIIE 0246) were administered by a mini-osmotic pump. Systolic blood pressure (SBP), heart rate (HR), BRS and heart functions, as well as the plasma NPY and lipid level were measured after treatment for 4 weeks. Results: Both BIBP 3226 and BIIE 0246 treatment reversed the elevated total cholesterol (TC) and low density lipoprotein (LDL-C) level, and reduced high density lipoprotein (HDL-C) level in DM rats. BIIE 0246 may attenuate the increased triglyceride (TG) level in DM rats. In addition, neither BIBP 3226 nor BIIE 0246 treatment produced significant effects on BRS, SBP or HR (P>0.05) in DM rats, even after PE and SNP challenge. However, BIBP 3226 and BIIE 0246 further impaired LVSP, LVEDP, +dp/dt_max and -dp/dt_max. Conclusion: This study provided us with the evidence that the inhibition of peripheral Y1R and Y2R did not affect impaired BRS but amplified the deterioration of the compromised cardiac function in STZ-induced DM rats with hyperlipidemia.

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Neuropeptide Y and sympathetic control of vascular tone in hypertension

Cited by 11 publications

References 103 publications

Psychostimulants

Psychostimulants

NPY and Cardiac Diseases

Blockage of Peripheral NPY Y1 and Y2 Receptors Modulates Barorefex Sensitivity of Diabetic Rats

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