Cardiovascular Neuroendocrinology: Emerging Role for Neurohypophyseal Hormones in Pathophysiology

Aikins, Ato O; Nguyen, Dianna H; Paundralingga, Obed; Farmer, George; Shimoura, Caroline Gusson; Brock, Courtney; Cunningham, J. Thomas

doi:10.1210/endocr/bqab082

Cited by 11 publications

(5 citation statements)

References 183 publications

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“…46 This hormone is produced by magnocellular neurosecretory cells located in the supraoptic and PVN (which house oxytocin-producing neurons). 47 a-sHyp, which encompasses the PVN, exhibits notable volume loss in ALS, 22,23 as shown in our study. These findings support the presence of distinct neuropeptide expression abnormalities that could potentially contribute to the pathogenesis of specific cognitive and behavioral symptoms within the spectrum of this disease.…”

Section: The Involvement Of Hypothalamic Nucleisupporting

confidence: 82%

“…Oxytocin (OXT) is a neuropeptide that plays an important role in the regulation of social cognition and emotional behaviors such as anxiety and depression 46 . This hormone is produced by magnocellular neurosecretory cells located in the supraoptic and PVN (which house oxytocin‐producing neurons) 47 . a‐sHyp, which encompasses the PVN, exhibits notable volume loss in ALS, 22,23 as shown in our study.…”

Section: Discussionsupporting

confidence: 62%

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Volume loss in the left anterior‐superior subunit of the hypothalamus in amyotrophic lateral sclerosis

Ghaderi,

Fatehi,

Kalra

et al. 2024

CNS Neurosci Ther

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Background and ObjectiveAmyotrophic lateral sclerosis (ALS) causes motor neuron loss and progressive paralysis. While traditionally viewed as motor neuron disease (MND), ALS also affects non‐motor regions, such as the hypothalamus. This study aimed to quantify the hypothalamic subregion volumes in patients with ALS versus healthy controls (HCs) and examine their associations with demographic and clinical features.MethodsForty‐eight participants (24 ALS patients and 24 HCs) underwent structural MRI. A deep convolutional neural network was used for the automated segmentation of the hypothalamic subunits, including the anterior‐superior (a‐sHyp), anterior‐inferior (a‐iHyp), superior tuberal (supTub), inferior tuberal (infTub), and posterior (posHyp). The neural network was validated using FreeSurfer v7.4.1, with individual head size variations normalized using total intracranial volume (TIV) normalization. Statistical analyses were performed for comparisons using independent sample t‐tests. Correlations were calculated using Pearson's and Spearman's tests (p < 0.05). The standard mean difference (SMD) was used to compare the mean differences between parametric variables.ResultsThe volume of the left a‐sHyp hypothalamic subunit was significantly lower in ALS patients than in HCs (p = 0.023, SMD = ‐0.681). No significant correlation was found between the volume of the hypothalamic subunits, body mass index (BMI), and ALSFRS‐R in patients with ALS. However, right a‐sHyp (r = 0.420, p = 0.041) was correlated with disease duration, whereas right supTub (r = −0.471, p = 0.020) and left postHyp (r = −0.406, p = 0.049) were negatively correlated with age. There was no significant difference in the volume of hypothalamic subunits between males and females, and no significant difference was found between patients with revised ALS Functional Rating Scale (ALSFRS‐R) scores ≤41 and >41 and those with a disease duration of 9 months or less.Discussion and ConclusionThe main finding suggests atrophy of the left a‐sHyp hypothalamic subunit in patients with ALS, which is supported by previous research as an extra‐motor neuroimaging finding for ALS.

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Section: The Involvement Of Hypothalamic Nucleisupporting

confidence: 82%

Section: Discussionsupporting

confidence: 62%

Volume loss in the left anterior‐superior subunit of the hypothalamus in amyotrophic lateral sclerosis

Ghaderi,

Fatehi,

Kalra

et al. 2024

CNS Neurosci Ther

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“…Expression of vasopressin gene is influenced by changes of body fluid osmolality and blood volume, as well as by constituents of the hypothalamo-hypophysial-adrenal axis, pain, cytokines and inflammation factors, especially those associated with COVID-19 [116,[121][122][123][124][125]. Vasopressin gene expression and AVP mRNA abundance are enhanced by chronic osmotic simulation and are decreased in hypoosmolality.…”

Section: Genomic and Non-genomic Effects Of Vasopressinmentioning

confidence: 99%

Interaction of Vasopressin with Hormones of the Hypothalamo-Pituitary-Adrenal Axis: Significance for Therapeutic Strategies in Cardiovascular and Metabolic Diseases

Szczepańska-Sadowska,

Czarzasta,

Bogacki-Rychlik

et al. 2024

Preprint

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A multiple number of studies provide evidence that vasopressin (AVP) and steroid hormones are frequently secreted together and closely cooperate in the regulation of blood pressure, metabolism, water-electrolyte balance, and behavior, securing thereby survival and comfort of life. Vasopressin interacts with hormones of the hypothalamo-pituitary-adrenal axis (HPA) at several levels through regulation of release of corticotropin-releasing hormone (CRH), adrenocorticotropic hormone ACTH, and multiple steroid hormones, as well as through interactions with steroids in the target organs. The interactions are facilitated by positive and negative feedbacks occurring between specific components of the HPA axis with engagement of other regulatory molecules. Altogether AVP and HPA cooperate closely as a coordinated functional AVP-HPA system. It has been shown that cooperation between AVP and steroid hormones may be affected by the cellular stress combined with hypoxia, and by metabolic, cardiovascular and respiratory disorders, neurogenic stress and inflammation. Growing evidence indicates that central and peripheral interactions of AVP and steroid hormones are reprogrammed in cardiovascular diseases and that the rearrangements play either beneficial or harmful effects. The present review highlights specific mechanisms of interactions of AVP and steroids at cellular and systemic levels and analyses consequences of inappropriate cooperation between various components of the AVP-HPA system for the regulation of the cardiovascular system and energy balance in cardiovascular and metabolic diseases.

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“…It has been reported that the plasma levels of vasopressin are elevated during the development of heart failure [251][252][253]. While the activation of the V 1a receptors via vasopressin results in the development of vasoconstriction, hypertension, cardiac hypertrophy and heart failure, the activation of the V 2 receptors is associated with fluid retention, leading to the development of volume overload, venous congestion, edema and lung congestion [254][255][256][257][258][259]. Vasopressin not only causes water retention but also results in kidney dysfunction in heart failure patients.…”

Section: Role Of Vasopressin In Cardiac Hypertrophy and Heart Failurementioning

confidence: 99%

Role of Vasoactive Hormone-Induced Signal Transduction in Cardiac Hypertrophy and Heart Failure

Dhalla,

Mota,

Elimban

et al. 2024

Cells

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Heart failure is the common concluding pathway for a majority of cardiovascular diseases and is associated with cardiac dysfunction. Since heart failure is invariably preceded by adaptive or maladaptive cardiac hypertrophy, several biochemical mechanisms have been proposed to explain the development of cardiac hypertrophy and progression to heart failure. One of these includes the activation of different neuroendocrine systems for elevating the circulating levels of different vasoactive hormones such as catecholamines, angiotensin II, vasopressin, serotonin and endothelins. All these hormones are released in the circulation and stimulate different signal transduction systems by acting on their respective receptors on the cell membrane to promote protein synthesis in cardiomyocytes and induce cardiac hypertrophy. The elevated levels of these vasoactive hormones induce hemodynamic overload, increase ventricular wall tension, increase protein synthesis and the occurrence of cardiac remodeling. In addition, there occurs an increase in proinflammatory cytokines and collagen synthesis for the induction of myocardial fibrosis and the transition of adaptive to maladaptive hypertrophy. The prolonged exposure of the hypertrophied heart to these vasoactive hormones has been reported to result in the oxidation of catecholamines and serotonin via monoamine oxidase as well as the activation of NADPH oxidase via angiotensin II and endothelins to promote oxidative stress. The development of oxidative stress produces subcellular defects, Ca2+-handling abnormalities, mitochondrial Ca2+-overload and cardiac dysfunction by activating different proteases and depressing cardiac gene expression, in addition to destabilizing the extracellular matrix upon activating some metalloproteinases. These observations support the view that elevated levels of various vasoactive hormones, by producing hemodynamic overload and activating their respective receptor-mediated signal transduction mechanisms, induce cardiac hypertrophy. Furthermore, the occurrence of oxidative stress due to the prolonged exposure of the hypertrophied heart to these hormones plays a critical role in the progression of heart failure.

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Cardiovascular Neuroendocrinology: Emerging Role for Neurohypophyseal Hormones in Pathophysiology

Cited by 11 publications

References 183 publications

Volume loss in the left anterior‐superior subunit of the hypothalamus in amyotrophic lateral sclerosis

Volume loss in the left anterior‐superior subunit of the hypothalamus in amyotrophic lateral sclerosis

Interaction of Vasopressin with Hormones of the Hypothalamo-Pituitary-Adrenal Axis: Significance for Therapeutic Strategies in Cardiovascular and Metabolic Diseases

Role of Vasoactive Hormone-Induced Signal Transduction in Cardiac Hypertrophy and Heart Failure

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