Intracerebroventricular angiotensin II increases arterial blood pressure in rhesus monkeys by stimulation of pituitary hormones and the sympathetic nervous system

Schölkens, Bernward A.; Jung, Wha-Young; Rascher, Wolfgang; Dietz, Rainer; Ganten, Detlev

doi:10.1007/bf01952643

Cited by 28 publications

(7 citation statements)

References 19 publications

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“…Infusions of Ang II into the lateral or third cerebral ventricle increases plasma concentrations of corticosteroids or ACTH in a number of species. 71,108,109 A possible site of action of Ang II to influence the HPA axis is the corticotropin-releasing hormone-containing parvocellular neurons of the PVN. These neurons are rich in AT 1 -receptors.…”

Section: Acth Secretionmentioning

confidence: 99%

Review: AT1-receptors in the central nervous system

Allen

Giles

Lee

et al. 2001

J Renin Angiotensin Aldosterone Syst

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Section: Acth Secretionmentioning

confidence: 99%

Review: AT1-receptors in the central nervous system

Allen

Giles

Lee

et al. 2001

J Renin Angiotensin Aldosterone Syst

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“…Although the central actions of Ang II on autonomic function have long been realized (Scholkens et al . ), the downstream effects, including oxidative stress, neuroinflammation and BBB disruption, have only been uncovered recently.…”

Section: Introductionmentioning

confidence: 99%

The role of the blood–brain barrier in hypertension

Setiadi

Korim

Elsaafien

et al. 2017

Experimental Physiology

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What is the topic of this review? This review highlights the importance of the blood-brain barrier in the context of diseases involving autonomic dysfunction, such as hypertension and heart failure. What advances does it highlight? It highlights the potential role of pro-inflammatory cytokines, leucocytes and angiotensin II in disrupting the blood-brain barrier in cardiovascular diseases. Advances are highlighted in our understanding of neurovascular unit cells, astrocytes and microglia, with a specific emphasis on their pathogenic roles within the brain. The blood-brain barrier (BBB) is a crucial barrier that provides both metabolic and physical protection to an immune-privileged CNS. The BBB has been shown to be disrupted in hypertension. This review addresses the importance of the BBB in maintaining homeostasis in the context of diseases related to autonomic dysfunction, such as hypertension. We highlight the potentially important roles of the immune system and neurovascular unit in the maintenance of the BBB, whereby dysregulation may lead to autonomic dysfunction in diseases such as heart failure and hypertension. Circulating leucocytes and factors such as angiotensin II and pro-inflammatory cytokines are thought ultimately to downregulate endothelial tight junction proteins that are a crucial component of the BBB. The specific mechanisms underlying BBB disruption and their role in contributing to autonomic dysfunction are not yet fully understood but are a growing area of interest. A greater understanding of these systems and advances in our knowledge of the molecular mechanisms causing BBB disruption will allow for the development of future therapeutic interventions in the treatment of autonomic imbalance associated with diseases such as heart failure and hypertension.

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“…In addition to its stimulatory effects on fluid intake, blood pressure and vasopressin secretion, the renin-angiotensin system has been implicated in the autonomic and neuroendocrine responses to stress (2)(3)(4)(5). Immunoreactive A11 and A11 receptors are present in the brain at sites related to the stress responses (6)(7)(8)(9), including the paraventricular nucleus of the hypothalamus (PVN).…”

mentioning

confidence: 99%

Increased Expression of Type 1 Angiotensin II Receptors in the Hypothalamic Paraventricular Nucleus following Stress and Glucocorticoid Administration

Aguilera

Kiss

Luo

1995

J Neuroendocrinology

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Double staining in situ hybridization studies have shown that angiotensin II (AII) type 1 receptors (AT1) in the hypothalamic paraventricular nucleus (PVN) are located primarily in corticotropin releasing hormone (CRH) neurons of the parvicellular subdivision. The purpose of these studies was to investigate the role of AII regulating the hypothalamic-pituitary adrenal (HPA) axis, by correlating AT1 receptor expression levels in the PVN with the known changes in activity of the HPA axis under different stress paradigms, and manipulation of circulating glucocorticoids. AT1 receptor mRNA was measured by in situ hybridization using 35S-labelled cRNA probes and AII binding by autoradiography using 125I[Sar1,Ile8]AII in slide mounted hypothalamic sections. AT1 receptor mRNA levels and AII binding in the PVN were reduced by about 20% 18 h after adrenalectomy remaining at these levels up to 6 days after. This effect was prevented by corticosterone administration in the drinking water, or dexamethasone injection (100 mg, s.c., daily). Conversely, dexamethasone injection in intact rats caused a 20% increase in AT1 receptor mRNA in the PVN. AT1 receptor mRNA and binding in the PVN increased 4 h after exposure to stress paradigms associated with activation of the HPA axis (immobilization for 1 h, or i.p. injection of 1.5 M NaCl), and remained elevated after repeated daily stress for 14 days. Unexpectedly, two osmotic stress models associated with inhibition of the HPA axis (60 h water deprivation or 12 days of 2% saline intake) also resulted in increased AT1 receptor mRNA levels and AII binding in the parvicellular PVN. In intact rats, the stimulatory effect of acute stress on AT1 receptor mRNA in the PVN was significantly enhanced by dexamethasone administration (100 micrograms, s.c., 14 h and 1 h prior to stress), while in adrenalectomized rats, with or without glucocorticoid replacement, stress reduced rather than increased, AT1 receptor mRNA. Dexamethasone, 100 micrograms, injected sc within 1 min the beginning of immobilization in adrenalectomized rats, increased AT1 receptor mRNA in the PVN to levels significantly higher than those after dexamethasone alone, indicating that the stress induced glucocorticoid surge is required for the stimulatory effect of stress on AT1 receptor mRNA. The data suggest that AT1 receptor expression in the PVN is under dual control during stress: stress-activated inhibitory pathways and the stimulatory effect of glucocorticoids. The lack of specificity of the changes in AT1 receptor expression in the PVN following stressors with opposite effects on ACTH secretion (osmotic and physical-psychological stress) does not support a role for AII as a major determinant of the response of the HPA axis during stress.

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Intracerebroventricular angiotensin II increases arterial blood pressure in rhesus monkeys by stimulation of pituitary hormones and the sympathetic nervous system

Cited by 28 publications

References 19 publications

Review: AT1-receptors in the central nervous system

Review: AT1-receptors in the central nervous system

The role of the blood–brain barrier in hypertension

Increased Expression of Type 1 Angiotensin II Receptors in the Hypothalamic Paraventricular Nucleus following Stress and Glucocorticoid Administration

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