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M L M Barreto-Chaves, N Senger, M R Fevereiro, A C Parletta and A P C Takano

( 5 , 6 , 7 , 8 ). Cardiac hypertrophy, driven by TH, is triggered by both direct action on cardiac cells and indirect mechanisms through interaction with other endocrine systems, such as the sympathetic nervous system (SNS) and the renin

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Frans H H Leenen, Mordecai P Blaustein and John M Hamlyn

lowers the setpoint for sympathetic tone but may also inhibit responsiveness to acute stresses. In contrast, slow-acting CNS pathways involve signal transduction over seconds to minutes. In the case of angiotensinergic pathways, Ang II released into the

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Stephen A Martin, Kenneth A Philbrick, Carmen P Wong, Dawn A Olson, Adam J Branscum, Donald B Jump, Charles K Marik, Jonathan M DenHerder, Jennifer L Sargent, Russell T Turner and Urszula T Iwaniec

reduced osteoclast number at other skeletal sites. Taken together, these findings are consistent with the hypothesis that 32°C abolishes the requirement for adaptive thermogenesis, which likely diminishes sympathetic signaling in bone, resulting in an

Open access

Masatada Watanabe, Shuji Ohno and Hiroshi Wachi

healthy subjects ( 18 ). An increase in salivary cortisol concentration reflects the response of the hypothalamus–pituitary–adrenal axis (HPA) to stress, whereas an increase in plasma catecholamine concentration reflects the response of the (hypothalamus)–sympathetic

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Michaela Keuper

catecholamine in WAT and brown adipose tissue (BAT): One mechanism proposes the inhibition of neuronal innervation. BAT-specific MΦ inhibit sympathetic neuronal innervation and thereby impair catecholamine signaling in BAT, while WAT innervation is not affected

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Maria Angela D'amico, Barbara Ghinassi, Pascal Izzicupo, Lamberto Manzoli and A Di Baldassarre

derived peptides. The 5′-UTR (259 bp) of the CgA mRNA and most of the signal peptide of CgA correspond to the exon I. The β-granin represents the highly conserved amino-terminal domain of CgA encoded by exons II–V and few amino acids encoded by the exon

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Esben Thyssen Vestergaard, Morten B Krag, Morten M Poulsen, Steen B Pedersen, Niels Moller, Jens Otto Lunde Jorgensen and Niels Jessen

increased expression of the hepatic gluconeogenic enzyme phosphoenolpyruvate carboxykinase and impaired skeletal muscle insulin signaling (17) . Moreover, genetic deletion or reduced serum concentrations of RBP4 by pharmacological remedies increase insulin

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Antonia Ertelt, Ann-Kristin Barton, Robert R Schmitz and Heidrun Gehlen

. Furthermore, omental fat and fat in muscles are suspected of playing an important role in the development of a proinflammatory state, because expression of TNF is increased and suppression of cytokine signaling 3 (SOCS3) and Toll-like receptor 4 (TLR4) is

Open access

Trevor Lewis, Eva Zeisig and Jamie E Gaida

HPA ( 16 ). Interestingly, there is an additional level of control whereby the suprachiasmatic nucleus of the hypothalamus acts via the sympathetic nervous system to set the sensitivity of the adrenal cortex to the incoming hormonal signal ( 17

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Tsuneo Ogawa and Adolfo J de Bold

sharp decline to baseline. This transient increased secretion of ANF and BNP is not due to the cNPs pool depletion but due to the decreased sensitivity to the stimulating signal for regulated release (36) . ET1 and phenylephrine (PE) also increase ANF