Differential effects of high salt intake on neuropeptide Y and adrenergic markers in hearts of dahl rats

Nyquist-Battie, Cynthia; Cochran, P. K.; Chronwall, Bibie M.

doi:10.1016/s0196-9781(98)00101-6

Cited by 2 publications

(2 citation statements)

References 23 publications

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“…Similarly, transgenic TG(mREN2)27 rats overexpressing the mouse renin gene causing fulminant hypertension with cardiac hypertrophy, have reduced myocardial NPY concentrations; these are restored along with normalisation of blood pressure and left ventricular weight by inhibition of the renin angiotensin system using quinapril or losartan [74]. In another model of hypertension-induced LVH produced in Dahl rats sensitive to high salt intake, ventricular NPY is also reduced [75]. In diabetic cardiomyopathy produced by administration of streptozotocin (STZ), diabetic rats in an uncompensated state have decreased NPY levels in atria at twelve months and in ventricles at six months after the onset of diabetes; partial spontaneous recovery of diabetes is associated with increased NPY levels in the atria [76].…”

Section: Npy In the Heartmentioning

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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Section: Npy In the Heartmentioning

confidence: 99%

NPY and Cardiac Diseases

McDermott¹,

Bell²

2007

CTMC

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“…Nyquist-Battie et al [46] previously showed that in Dahl salt-sensitive rats with cardiac hypertrophy induced by high-salt diet, NGF and p75 NTR were elevated in the LV. Our findings that among AC groups p75 NTR mRNA was augmented while simultaneously TrkA decreased suggest that p75 NTR may mediate the biological effects of NGF when TrkA is insufficient.…”

Section: Discussionmentioning

confidence: 94%

Exogenous nerve growth factor supplementation elevates myocardial immunoreactivity and attenuates cardiac remodeling in pressure-overload rats

He¹,

Ye²,

Zhou³

et al. 2012

ABBS

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It is postulated that supplementation of exogenous nerve growth factor (NGF) might mediate improvement of the cardiac sympathetic nerve function in heart failure (HF). Local intramuscular injection of NGF near the cardiac sympathetic ganglia could influence the innervation pattern, norepinephrine transporter (NET) gene expression, and improve the cardiac remodeling in experimental HF animals. In this study, we injected NGF into the scalenus medius muscles of Sprague-Dawley rats with abdominal aortic constriction (AC). The nerve innervated pattern, left ventricular morphology, and function following injection in rats with AC were investigated respectively by immunohistochemistry and echocardiography. Levels of mRNA expression of NET, growth associated protein 43 (GAP 43), NGF and its receptors TrkA and p75 NTR , and brain natriuretic peptide (BNP) were measured by realtime polymerase chain reaction. The results showed that myocardial NGF mRNA levels were comparable in rats with AC. Short-term supplementation of exogenous NGF raised the myocardial NGF immunoreactivity, but did not cause hyperinnervation and NET mRNA upregulation in the AC rats. Furthermore, myocardial TrkA mRNA was found to be remarkably decreased and p75 NTR mRNA was increased. Myocardial TrkA downregulation may play a beneficial effect for avoiding the hyperinnervation, and it is reasonable to postulate that p75 NTR can function as an NGF receptor in the absence of TrkA. Interestingly, local NGF administration into the neck muscles near the ganglia could attenuate cardiac remodeling and downregulate BNP mRNA. These results suggest that exogenous NGF can reach the target tissue along the axons anterogradely, and improve the cardiac remodeling.

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Differential effects of high salt intake on neuropeptide Y and adrenergic markers in hearts of dahl rats

Cited by 2 publications

References 23 publications

NPY and Cardiac Diseases

NPY and Cardiac Diseases

Exogenous nerve growth factor supplementation elevates myocardial immunoreactivity and attenuates cardiac remodeling in pressure-overload rats

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