Angiotensin II mediates catecholamine and neuropeptide Y secretion in human adrenal chromaffin cells through the AT1 receptor

Cavadas, Cláudia; Grand, Daniela; Mosimann, F; Cotrim, Maria Dulce; Ribeiro, Carlos; Brunner, Hans R.; Grouzmann, Eric

doi:10.1016/s0167-0115(02)00253-7

Cited by 28 publications

(17 citation statements)

References 25 publications

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“…Other neuronal elements including sensory and parasympathetic neurons, expressing opioid peptides, vasoactive intestinal polypeptide (VIP) or substance P (SP), as well as Type I and II intramedullary ganglionic cells, play a role in the physiological regulation of this gland (Mravec 2005). Additional factors such as angiotensin II, histamine, glucocorticoids and gonadal steroids act as endocrine or paracrine/autocrine modulators of adrenomedullary activity (Cavadas et al 2003;Marley 2003;Schinner and Bornstein 2005). Signalling from the activated immune system is little explored, despite being a potentially important non-neural adrenomedullary regulator.…”

Section: Introductionmentioning

confidence: 99%

Cytokine Interactions with Adrenal Medullary Chromaffin Cells

et al. 2010

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It is generally accepted that a bi-directional or reciprocal interaction occurs between the immune and neuroendocrine systems, and that this relationship is important for the appropriate physiological functioning of both systems. Similarly, an imbalance in this relationship may contribute to a number of pathologies, most notably those relating to stress. The aim of this article is to consider the interaction of cytokines with the adrenal medulla, a potentially important player in this relationship. The chromaffin cells of the adrenal medulla release catecholamines and a range of biologically active peptides in response to a wide variety of stress-related signals. A growing body of evidence indicates that this stress response is influenced by, and in turn has influence upon, immune signalling. This brief review will focus primarily on the best-described adrenal medullary active cytokines, namely interferon-α, interleukin-6, interleukin-1α/β and tumour necrosis factor-α. In each case, three key issues will be addressed: the physiologically relevant source of the cytokine; the intracellular signalling events arising from activation of its receptor and finally the cellular consequences of such activation in terms of modulation of gene expression and the secretory output of the chromaffin cells.

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Section: Introductionmentioning

confidence: 99%

Cytokine Interactions with Adrenal Medullary Chromaffin Cells

et al. 2010

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“…though the AT1 receptor has been implicated in mediating catecholamine secretion from mammalian chromaffin cells (9), the specific ANG II receptor subtype has not yet been identified in any fish species, although there is evidence that the piscine receptor is AT1-like (15,57). Once the specific chromaffin cell ANG II receptor is identified in rainbow trout, future studies should be directed at quantifying their expression levels in response to dietary salt loading.…”

Section: Catecholamine Secretion In Hypertensive Fishmentioning

confidence: 99%

Effects of chronic dietary salt loading on the renin angiotensin and adrenergic systems of rainbow trout (Oncorhynchus mykiss)

Perry

Ellis

Russell

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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NJ, Montpetit C. Effects of chronic dietary salt loading on the renin angiotensin and adrenergic systems of rainbow trout (Oncorhynchus mykiss). Am J Physiol Regul Integr Comp Physiol 301: R811-R821, 2011. First published June 22, 2011 doi:10.1152/ajpregu.00244.2011.-Previous studies have demonstrated that chronic dietary salt loading causes hypertension and a decreased sensitivity of the systemic vasculature to ␣-adrenergic stimulation and other hypertensive stimuli (e.g. hypercapnia) in rainbow trout (Oncorhynchus mykiss). This reduced sensitivity to hypertensive stimuli is consistent with a possible blunting of homeostatic responses normally aimed at raising blood pressure. To test this idea, we examined the consequences of long-term salt feeding and the associated hypertension on the interactive capacities of the renin angiotensin system (RAS) and adrenergic systems to elevate blood pressure in trout. Secretion of catecholamines in response to a range of doses of homologous ANG II in vivo and in situ (using a perfused posterior cardinal vein preparation) was reduced in the salt-fed fish. The reduced sensitivity to ANG II could not be explained by alterations in stored catecholamine (adrenaline or noradrenaline) levels or the general responsiveness of the chromaffin cells to depolarizing stimuli (60 mmol/l KCl). Despite the decreased responsiveness of the chromaffin cells to ANG II, plasma catecholamines were increased to a greater extent in the salt-fed fish during acute hypoxia (a condition that activates the RAS). Interestingly, the pressor effects of ANG II in vivo were actually heightened in the salt-fed fish. The increased pressor response to exogenous ANG II was likely attributable to its direct interaction with vascular ANG II receptors because the effect persisted even after blockade of ␣-adrenergic receptors. Treating fish with the vascular smooth muscle relaxant papaverine caused similar reductions in blood pressure and increases in plasma ANG II levels regardless of diet. Similarly, inhibition of angiotensin converting enzyme with lisinopril reduced blood pressure equally in control and salt-fed fish. These results indicate that, while long-term dietary salt loading blunts the response of trout chromaffin cells to ANG II, the RAS itself appears to be unaffected. Indeed, the capacity of ANG II to elevate blood pressure is not compromised nor do fish exhibit a reduced capacity to mount an acute humoral adrenergic stress response during acute hypoxia. high dietary salt; hypertension; catecholamines; chromaffin cells; angiotensin II; hypoxia; control of blood pressure ALTHOUGH EPIDEMIOLOGICAL studies (21) have revealed a significant correlation between dietary salt intake and blood pressure in humans, the underlying mechanisms have not been clearly identified (for reviews see Refs. 6 and 30). In most individuals, the vascular volume expansion associated with moderately increased levels of ingested salt is restored rapidly by increased urine production, and thus the related increases in blood pressur...

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“…Catecholamine secretion in human chromaffin cells is regulated by NPY, presumably acting via the putative y3 receptor (Cavadas et al 2001), though factors such as angiotensin II (Cavadas et al 2003) or interleukin-1b (Rosmaninho-Salgado et al 2009) have also been found to regulate the release of catecholamines and NPY.…”

Section: Chromaffin Vesiclesmentioning

confidence: 99%

Past, Present and Future of Human Chromaffin Cells: Role in Physiology and Therapeutics

2010

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Chromaffin cells are neuroendocrine cells mainly found in the medulla of the adrenal gland. Most existing knowledge of these cells has been the outcome of extensive research performed in animals, mainly in the cow, cat, mouse and rat. However, some insight into the physiology of this neuroendocrine cell in humans has been gained. This review summarizes the main findings reported in human chromaffin cells under physiological or disease conditions and discusses the clinical implications of these results.

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Angiotensin II mediates catecholamine and neuropeptide Y secretion in human adrenal chromaffin cells through the AT1 receptor

Cited by 28 publications

References 25 publications

Cytokine Interactions with Adrenal Medullary Chromaffin Cells

Cytokine Interactions with Adrenal Medullary Chromaffin Cells

Effects of chronic dietary salt loading on the renin angiotensin and adrenergic systems of rainbow trout (Oncorhynchus mykiss)

Past, Present and Future of Human Chromaffin Cells: Role in Physiology and Therapeutics

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