Vasopressin dysregulation: Hyponatremia, fluid retention and congestive heart failure

LeJemtel, Thierry H.; Serrano, Claudia

doi:10.1016/j.ijcard.2006.11.113

Cited by 23 publications

(19 citation statements)

References 56 publications

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“…ROC analyses demonstrated that a cutoff level of plasma AVP for all-cause survival over 2 years was identically speculated. 5, 13 Uretsky et al's data that demonstrated a significant negative correlation between changes in systemic blood pressure and plasma AVP levels after intravenous infusion of vasodilator accompanied by non-significant increases in CO would support our result, 7 although the correlation between blood pressure and AVP levels barely reached statistical significance in our analysis.…”

Section: Clinical Prognosis Stratified By Plasma Avp Levels In Patiensupporting

confidence: 82%

Low Cardiac Output Stimulates Vasopressin Release in Patients With Stage D Heart Failure

Imamura

Kinugawa

Hatano

et al. 2014

Circ J

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Section: Clinical Prognosis Stratified By Plasma Avp Levels In Patiensupporting

confidence: 82%

Low Cardiac Output Stimulates Vasopressin Release in Patients With Stage D Heart Failure

Imamura

Kinugawa

Hatano

et al. 2014

Circ J

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“…113 The prevalence of atrial fibrillation, atherosclerosis, and CHF is also high among patients with COPD. 114,115 Although some of the association between COPD and atherosclerosis may be the result of common risk factors such as tobacco use, epidemiological evidence suggests that impaired lung function is a risk factor for increased cardiovascular death independent of tobacco use. Analysis of participants in the National Health and Nutrition Examination Survey revealed that patients in the lowest FEV 1 quintile had the highest risk of cardiovascular death, with a relative risk of 3.36 after adjusting for Framingham risk factors such as smoking status, blood pressure, body mass index, and diabetes.…”

Section: Atherosclerosis and Copdmentioning

confidence: 99%

Pulmonary Diseases and the Heart

et al. 2007

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Abstract-The complex nature of interactions between the pulmonary and cardiovascular systems is becoming increasingly appreciated. Pulmonary vascular abnormalities are frequently present in patients with respiratory disorders, including chronic obstructive pulmonary disease, idiopathic pulmonary fibrosis, sarcoidosis, neuromuscular or chest wall disorders, and disorders of ventilatory control including sleep apnea syndromes and obesity hypoventilation syndrome. Pulmonary hypertension, classified as group III in the World Health Organization classification scheme for pulmonary hypertension, may result in severe right ventricular dysfunction caused by lung disease, also known as cor pulmonale. The development of cor pulmonale is generally associated with poorer prognosis and increased death. Systemic manifestations of lung disease, particularly obstructive disorders, are also particularly relevant because they are associated with increased cardiac death and impaired health status. This article will discuss the most common pulmonary diseases and disorders of ventilatory control that cause pulmonary vascular abnormalities and cor pulmonale, with particular concentration on how treatment of these diseases may affect the heart. In addition, the complex nature of cardiac and lung disease will also be explored, particularly with respect to the relationship between chronic obstructive pulmonary disease, systemic inflammation, atherosclerosis, and cardiovascular death, which is currently a very active focus of research. Key Words pulmonary heart disease Ⅲ pulmonary disease, chronic obstructive Ⅲ hypertension, pulmonary Ⅲ inflammation S ystemic manifestations have become increasingly recognized in lung diseases, particularly obstructive disorders. 1 Cardiovascular involvement is particularly relevant because it is associated with impaired health status and worsened mortality. In the present targeted review we will discuss evolving data regarding pulmonary vascular abnormalities in the most common respiratory disorders, including chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis, sarcoidosis, neuromuscular or chest wall disorders, and disorders of ventilatory control. We will also explore the relationship between COPD and systemic inflammation, atherosclerosis, and cardiovascular death. Pulmonary Vascular Disease in Respiratory IllnessThe classification of pulmonary hypertension (PH) has recently been revised, and PH associated with hypoxemic pulmonary disorders falls into World Health Organization group III. 2 Cor pulmonale was defined by the World Health Organization in 1963 as "hypertrophy of the right ventricle (RV) resulting from diseases affecting the function and/or structure of the lungs, except when these pulmonary alterations are the result of diseases that primarily affect the left side of the heart, as in congenital heart disease." 3 Since then the definition has come to encompass both right ventricular hypertrophy, dilation, or both secondary to PH caused by pulmonary disorders. 4 Betw...

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“…Physiologically, hyperosmolality increases, whereas hypoosmolality decreases plasma AVP concentration (4). However, in diverse pathological syndromes, such as hepatic cirrhosis (35), congestive heart failure (37,38), and nephrogenic syndrome (23,26,48), a decrease in osmolality fails to inhibit AVP release. This AVP release leads to water retention and contributes to the morbidity and mortality associated with these diseases (1, 22, 24, 37, 38).…”

Section: R952 Ang II Induces Trpv4 Trafficking In 4b Cellsmentioning

confidence: 99%

Angiotensin II induces membrane trafficking of natively expressed transient receptor potential vanilloid type 4 channels in hypothalamic 4B cells

Saxena

Bachelor

Park

et al. 2014

American Journal of Physiology-Regulatory, Integrative and Comp

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We previously reported that in the rodent, a model of dilutional hyponatremia associated with hepatic cirrhosis, TRPV4 expression is increased in lipid rafts from the hypothalamus and that this effect may be angiotensin dependent. In this study, we utilized the immortalized neuroendocrine rat hypothalamic 4B cell line to more directly test the effects of angiotensin II (ANG II) on TRPV4 expression and function. Our results demonstrate the expression of corticotropin-releasing factor (CRF) transcripts, for sex-determining region Y (SRY) (male genotype), arginine vasopressin (AVP), TRPV4, and ANG II type 1a and 1b receptor in 4B cells. After a 1-h incubation in ANG II (100 nM), 4B cells showed increased TRPV4 abundance in the plasma membrane fraction, and this effect was prevented by the ANG II type 1 receptor antagonist losartan (1 M) and by a Src kinase inhibitor PP2 (10 M). Ratiometric calcium imaging experiments demonstrated that ANG II incubation potentiated TRPV4 agonist (GSK 1016790A, 20 nM)-induced calcium influx (control 18.4 Ϯ 2.8% n ϭ 5 and ANG II 80.5 Ϯ 2.4% n ϭ 5). This ANG II-induced increase in calcium influx was also blocked by 1 M losartan and 10 M PP2 (losartan 26.4 Ϯ 3.8% n ϭ 5 and PP2 19.7 Ϯ 3.9% n ϭ 5). Our data suggests that ANG II can increase TRPV4 channel membrane expression in 4B cells through its action on AT1R involving a Src kinase pathway.angiotensin; TRPV4; hypothalamus; 4B; SRC kinase; SRY TRANSIENT RECEPTOR POTENTIAL (TRP) channel superfamily plays a central role in sensory physiology (47, 54). The TRP subfamily vanilloid member 4 (TRPV4) is a nonselective cation channel that is calcium permeable and shows polymodal activation by diverse stimuli including, but not limited to, moderate heat, cell swelling, and endogenous ligands (51,55,69). Functionally, it is strongly implicated in a number of physiological systems that include endothelial function and vascular tone (21, 64), renal function (56), central osmosensation (41, 46), and regulating hydromineral homeostasis (51, 55, 69). Mutations of TRPV4 are linked to a number of motor and sensory neuropathies and skeletal dysplasias (51, 69).TRPV4 is expressed in central nervous system (CNS) regions involved in neuroendocrine function including neurosecretory cells in the supraoptic nucleus (SON) and the paraventricular nuclei of the hypothalamus (PVN) (3, 9). In a rodent model of cirrhosis, we have previously reported increased TRPV4 trafficking to lipid rafts in hypothalamic samples that contained the SON, the PVN, and the organum vasculosum of the lamina terminalis (9). Importantly, we also found that increased TRPV4 trafficking correlated with activation of renin-angiotensin system (RAS) and was reversed after RAS inhibition (9).Angiotensin II (ANG II) is an effector molecule of RAS (25). Circulating ANG II is known to contribute to water and electrolyte homeostasis peripherally and centrally through its actions on blood-brain barrier-deficient circumventricular organs in the forebrain and dorsal hindbrain (31, 43). As part of the ...

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Vasopressin dysregulation: Hyponatremia, fluid retention and congestive heart failure

Cited by 23 publications

References 56 publications

Low Cardiac Output Stimulates Vasopressin Release in Patients With Stage D Heart Failure

Low Cardiac Output Stimulates Vasopressin Release in Patients With Stage D Heart Failure

Pulmonary Diseases and the Heart

Angiotensin II induces membrane trafficking of natively expressed transient receptor potential vanilloid type 4 channels in hypothalamic 4B cells

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