Background—Reactive oxygen species (ROS) may mediate pressure overload–induced myocardial hypertrophy. NADPH oxidase may be involved in this process, because its expression and activity are upregulated by pressure overload and because myocardial hypertrophy caused by a subpressor infusion of angiotensin is attenuated in mice deficient in the gp91 catalytic subunit of NADPH oxidase. Methods and ...

During pregnancy, there are several coordinated and dynamic maternal adaptations that take place to meet the demands of the growing and developing fetus. This includes significant physiological, endocrine, and metabolic adaptations that produce a diabetogenic state of progressive insulin resistance. It is thought that these metabolic adaptations occur so that nutrients, such as glucose, are con...

Background: We previously reported that lysophosphatidic acid (LPA) promoted cardiomyocyte hypertrophy in vitro via one of its G protein-coupled receptor subtypes, LPA3. In this study, we examined the role of LPA3 in cardiac hypertrophy induced by isoproterenol (ISO) and myocardial infarction. Methods:In vitro, neonatal rat cardiomyocytes (NRCMs) were subjected to LPA3 knocked-down, or pretreat...

Inducible nitric oxide synthase (iNOS) protein is expressed in cardiac myocytes of patients and experimental animals with congestive heart failure (CHF). Here we show that iNOS expression plays a role in pressure overload-induced myocardial chamber dilation and hypertrophy. In wild-type mice, chronic transverse aortic constriction (TAC) resulted in myocardial iNOS expression, cardiac hypertroph...

A mild to moderate adaptive hypertrophy of a cardiac chamber may be beneficial in increasing the capacity of the heart to cope with an increased work-load. However, in pathological hypertrophy the myocardial muscle cell can hypertrophy to such an extent that myocardial performance deteriorates [ 11. To devise a medical treatment that could modify or even prevent the occurrence of adaptive cardi...

BACKGROUND Cardiac hypertrophy is a major risk factor for morbidity and mortality in a number of cardiovascular diseases. Consequently, the signaling pathways that inhibit cardiac hypertrophy are currently receiving much interest. Among them, nitric oxide (NO), signaling via cGMP and cGMP-dependent protein kinase I, has been recognized as a negative regulator of cardiac hypertrophy. The present...

Hormones and neurotransmitters may mediate common responses through receptors that couple to the same class of heterotrimeric guanine nucleotide-binding (G) protein. For example, several receptors that couple to Gq class proteins can induce cardiomyocyte hypertrophy. Class-specific inhibition of Gq-mediated signaling was produced in the hearts of transgenic mice by targeted expression of a carb...