Total sleep deprivation inhibits the neuronal nitric oxide synthase and cytochrome oxidase reactivities in the nodose ganglion of adult rats

Abstract

Sleep disorders are a form of stress associated with increased sympathetic activity, and they are a risk factor for the occurrence of cardiovascular disease. Given that nitric oxide (NO) may play an inhibitory role in the regulation of sympathetic tone, this study set out to determine the NO synthase (NOS) reactivity in the primary cardiovascular afferent neurons (i.e. nodose neurons) following total sleep deprivation (TSD). TSD was performed by the disc-onwater method. Following 5 days of TSD, all experimental animals were investigated for quantitative nicotinamine adenine dinucleotide phosphate-diaphorase (NADPH-d, a co-factor of NOS) histochemistry, neuronal NOS immunohistochemistry and neuronal NOS activity assay. In order to evaluate the endogenous metabolic activity of nodose neurons, cytochrome oxidase (COX) reactivity was further tested. All the above-mentioned reactivities were objectively assessed by computerized image analysis. The clinical significance of the reported changes was demonstrated by alterations of mean arterial blood pressure (MAP). The results indicated that in normal untreated rats, numerous NADPH-d/NOS-and COX-reactive neurons were found in the nodose ganglion (NG). Following TSD, however, both the labelling and staining intensity of NADPH-d/NOS as well as COX reactivity were drastically reduced in the NG compared with normal untreated ganglions. MAP was significantly higher in TSD rats (136 ± 4 mmHg) than in normal untreated rats (123 ± 2 mmHg). NO may serve as an important sympathoinhibition messenger released by the NG neurons, and decrease of NOS immunoexpression following TSD may account for the decrease in NOS content. In association with the reduction of NOS activity, a defect in NOS expression in the primary cardiovascular

Blood Pressure Increases During a Simulated Night Shift in Persons at Risk for Hypertension

“…Sleep deprivation can contribute directly to blood pressure dysregulation via increased sympathetic nervous system and adrenocortical excitation independent of sleep apnea. For example, experimentally induced sleep deprivation increases blood pressure and inhibits neuronal nitric oxide synthase in nodose neurons in rats [17]. The authors suggest that reduced expression of nitric oxide synthase in primary cardiovascular neurons could increase the sympathetic nervous system tone and potentially increase the risk for essential hypertension.…”

Sleep deprivation predisposes liver to oxidative stress and phospholipid damage: a quantitative molecular imaging study

“…With the coming of industrialization, sleep disorders are increasingly becoming a major public health issue, affecting millions of people in many countries (Malik & Kaplan, 2005;Lenfent, 2006). In subjects suffering sleep deprivation there is a desynchronization of cellular function, which unavoidably leads to metabolic disturbances (McEwen, 2006;Chang et al 2006). Recent biochemical and physiological studies have indicated that chronic sleep deprivation is an important factor in neurobehavioral, cardiovascular and metabolic morbidity in both developing and adult patients (Copinschi, 2005;Kheirandish & Gozal, 2006;Thase, 2006).…”

Estresse pós-privação de sono: análises morfométricas do fígado

“…Estudos têm demonstrado que a síndrome metabólica [5][6][7][8] está associada ao aumento da morbimortalidade e que também está associada ao aumento do cortisol e intolerância a glicose. Pesquisas têm demonstrado que a diminuição ou privação de sono, em humanos, envolvem alterações metabólicas, problemas na regulação do apetite e diminuição do dispêndio de energia, tornando-se fator de risco para o desenvolvimento de várias doenças tais como doenças cardiovasculares, obesidade, resistência a insulina, intolerância a glicose, dislipidemia e hipertensão e manifestações que alteram a regulação de energia 5,[9][10][11][12][13][14] . Em animais, o estresse pode ser provocado por privação de sono, que por sua vez, ativa o eixo hipotalâmico-pituitário-adrenal 15 .…”