NO Balance

Badorff, Cornel; Dimmeler, Stefanie

doi:10.1161/01.cir.0000057859.91134.ad

Cited by 10 publications

(4 citation statements)

References 23 publications

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“…Furthermore, NO inhibits proliferation and migration of smooth muscle cells, reduces platelet adhesion, decreases lipoxygenase activity and oxidized LDL-cholesterol [60-69]. Recently, NO has been shown to modulate cardiac cytoskeletal functions by altering calcium myofilament responsiveness [70]. In addition, IGF-1 may cause vasorelaxation both by enhancing Na + /K + ATPase activity [71] and regulating gene expression of K ATP channel in vascular smooth cells [72].…”

Section: Cardiovascular Effectsmentioning

confidence: 99%

“…Treatment with GH normalizes NO production, thereby reducing peripheral vascular resistance and modulating cardiac cytoskeletal functions by altering calcium myofilament responsiveness [70, 157]. Moreover, GH replacement improves body composition, which is an important factor for reducing cardiovascular risk [176, 177], induces beneficial effects on lipid profile [178, 179] and reduces arterial intima-media thickness [152, 155, 178, 179].…”

Section: Gh Deficiencymentioning

confidence: 99%

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The GH/IGF-1 Axis and Heart Failure

Castellano¹,

Affuso²,

Conza³

et al. 2009

CCR

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The growth hormone (GH)/insulin-like growth factor 1 (IGF-1) axis regulates cardiac growth, stimulates myocardial contractility and influences the vascular system. The GH/IGF-1 axis controls intrinsic cardiac contractility by enhancing the intracellular calcium availability and regulating expression of contractile proteins; stimulates cardiac growth, by increasing protein synthesis; modifies systemic vascular resistance, by activating the nitric oxide system and regulating non-endothelial-dependent actions. The relationship between the GH/IGF-1 axis and the cardiovascular system has been extensively demonstrated in numerous experimental studies and confirmed by the cardiac derangements secondary to both GH excess and deficiency. Several years ago, a clinical non-blinded study showed, in seven patients with idiopathic dilated cardiomyopathy and chronic heart failure (CHF), a significant improvement in cardiac function and structure after three months of treatment with recombinant GH plus standard therapy for heart failure. More recent studies, including a small double-blind placebo-controlled study on GH effects on exercise tolerance and cardiopulmonary performance, have shown that GH benefits patients with CHF secondary to both ischemic and idiopathic dilated cardiomyopathy. However, conflicting results emerge from other placebo-controlled trials. These discordant findings may be explained by the degree of CHF-associated GH resistance. In conclusion, we believe that more clinical and experimental studies are necessary to exactly understand the mechanisms that determine the variable sensitivity to GH and its positive effects in the failing heart.

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Section: Cardiovascular Effectsmentioning

confidence: 99%

Section: Gh Deficiencymentioning

confidence: 99%

The GH/IGF-1 Axis and Heart Failure

Castellano¹,

Affuso²,

Conza³

et al. 2009

CCR

View full text Add to dashboard Cite

show abstract

“…Potential signaling molecules in this cascade include heat shock proteins, which have been shown to protect microtubules during simulated ischemia in cardiac myocytes. 28 …”

Section: Microtubulinmentioning

confidence: 99%

Pretreatment With Angiotensin Receptor Blockade Prevents Left Ventricular Dysfunction and Blunts Left Ventricular Remodeling Associated With Acute Myocardial Infarction

et al. 2006

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“…Chronic heart failure is associated with enhanced NOS2 myocardial expression; however, the contribution of NOS2 and sustained NO production to the development of heart failure is an area of intense debate. 11 In any case, the multiple adverse effects of high NO levels produced by NOS2 overexpression in vivo appear to be attenuated by myoglobin, which effectively metabolizes NO. 12,13 The observation that cardiac-specific NOS2 overexpression in myoglobin-deficient mice leads to cardiac hypertrophy, ventricular dilatation, and interstitial fibrosis indicates that the effect of NO on cardiomyocyte growth is dependent on spatial confinement and/or level of production.…”

Section: Cardiac Cgmp and Nitric Oxide Formationmentioning

confidence: 99%

Putting the Brakes on Cardiac Hypertrophy

Booz

2005

Hypertension

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Abstract-We know a great deal about the receptors and signaling pathways in cardiomyocytes that contribute to hypertrophic growth. Although drugs that target them have proven effective in substantially reducing left ventricular hypertrophy and associated mortality, cardiovascular disease remains the leading cause of death in the West. Another approach may rest with exploiting naturally occurring regulators of maladaptive cardiac hypertrophy that have been identified in the past few years. These endogenous negative regulators can be grouped, for the most part, into those constitutively active but whose activity is decreased by hypertrophic stimulation, and those with little or no baseline activity that are activated by hypertrophic stimulation. Spanning both groups are 4 systems that converge on cyclic guanosine 3Ј, 5Ј-monophosphate (cGMP) generation, namely natriuretic peptides (ANP and BNP), kinins, nitric oxide (NO), and the angiotensin II type 2 receptor (AT 2 ). Although holding promise as a means for restricting hypertrophy, each of these signaling molecules has certain limitations that need to be overcome. What follows is an overview of research over the past 2 years, much of it published in Hypertension, which has dealt with the antihypertrophic action of this particular group of endogenous signaling molecules. Understanding the function and regulation of the antihypertrophic NO-cGMP system offers the promise of novel therapeutic strategies for treating cardiac hypertrophy and heart failure. Key Words: adrenergic antagonists Ⅲ angiotensin II Ⅲ kinins Ⅲ natriuretic peptides Ⅲ nitric oxide synthase Ⅲ statins V arious disease states that impose an additional workload on the heart, including hypertension and myocardial infarction, lead to left ventricular (LV) hypertrophy. 1 The increase in LV mass is largely caused by increased size and protein content of cardiomyocytes and was once viewed as an adaptive response for maintaining cardiac output and tissue perfusion. After more than a decade of study, however, LV hypertrophy is recognized as a maladaptive response associated with untoward events, such as cardiomyocyte fetal gene re-expression, apoptosis, and interstitial fibrosis. 1 Untreated, LV hypertrophy generally progresses to ventricular dilatation, systolic and diastolic contractile dysfunction, and heart failure. In fact, LV hypertrophy represents a well-established risk factor for cardiovascular mortality. 2 Even the premise that cardiac hypertrophy is required to preserve heart function and normalize wall stress under conditions of pressure overload is challenged by recent studies. 1,3,4 Drugs targeting receptors and signaling pathways that couple to cardiomyocyte hypertrophic growth are highly effective in reducing LV hypertrophy and associated mortality. Yet cardiovascular disease remains the leading cause of death in the West. 5 Is there another strategy that could be used to control or reverse LV hypertrophy? An answer may rest with naturally occurring regulators of cardiac hypertrophy identified...

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NO Balance

Cited by 10 publications

References 23 publications

The GH/IGF-1 Axis and Heart Failure

The GH/IGF-1 Axis and Heart Failure

Pretreatment With Angiotensin Receptor Blockade Prevents Left Ventricular Dysfunction and Blunts Left Ventricular Remodeling Associated With Acute Myocardial Infarction

Putting the Brakes on Cardiac Hypertrophy

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