Stress-induced Hypertension Research Articles

S21. Identification of a Novel T-Lymphocyte Inflammatory Protein in Psychological Stress-Induced Hypertension

Post-Traumatic Stress Disorder (PTSD) dysregulates physiological systems leading to elevated sympathetic tone and norepinephrine (NE) outflow, pronounced inflammation, and a >50% increased risk in developing comorbid cardiovascular diseases like hypertension (HTN). We hypothesized that NE increases T-lymphocyte-driven inflammation leading to HTN after trauma exposure.

Central blockade of the AT1 receptor attenuates pressor effects via reduction of glutamate release and downregulation of NMDA/AMPA receptors in the rostral ventrolateral medulla of rats with stress-induced hypertension.

Glutamatergic activity in the rostral ventrolateral medulla (RVLM), which is an important brain area where angiotensin II (Ang II) elicits its pressor effects, contributes to the onset of hypertension. The present study aimed to explore the effect of central Ang II type 1 receptor (AT1R) blockade on glutamatergic actions in the RVLM of stress-induced hypertensive rats (SIHR). The stress-induced hypertension (SIH) model was established by electric foot shocks combined with noises. Normotensive Sprague-Dawley rats (control) and SIHR were intracerebroventricularly infused with the AT1R antagonist candesartan or artificial cerebrospinal fluid for 14 days. Mean arterial pressure (MAP), heart rate (HR), plasma norepinephrine (NE), glutamate, and the expression of N-methyl-D-aspartic acid (NMDA) receptor subunit NR1, and α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptors in the RVLM increased in the SIH group. These increases were blunted by candesartan. Bilateral microinjection of the ionotropic glutamate receptor antagonist kynurenic acid, the NMDA receptor antagonist D-2-amino-5-phosphonopentanoate, or the AMPA/kainate receptors antagonist 6-cyano-7-nitroquinoxaline-2,3-dione into the RVLM caused a depressor response in the SIH group, but not in other groups. NR1 and AMPA receptors expressed in the glutamatergic neurons of the RVLM, and glutamate levels, increased in the intermediolateral column of the spinal cord of SIHR. Central Ang II elicits release of glutamate, which binds to the enhanced ionotropic NMDA and AMPA receptors via AT1R, resulting in activation of glutamatergic neurons in the RVLM, increasing sympathetic excitation in SIHR.

Comparison of Reactivity of the Lipid Peroxidation-Antioxidant Defense System in Normal and Hypertensive Rats at Different Stages of Stress-Reaction.

We compared changes in the parameters of LPO-antioxidant defense system at various stages of the stress response in mature male ISIAH rats (hereditary stress-induced arterial hypertension) and WAG rats in 3 h (stage of anxiety) and 7 days (resistance stage) after a 3-h single immobilization in the supine position. It was found that post-stress reactivity of the nonspecific stress-limiting LPO system is different in normotensive and hypertensive rats. ISIAH rats, irrespective of the stage of the stress-reaction, demonstrated more intense LPO reactions (accumulation of TBA-reactive products) and reduced antioxidant defense parameters (low content of lipid-soluble vitamins, increased oxidized glutathione content) in comparison with the corresponding parameters in WAG rats.

Peripheral Sensory Nerve Tissue but Not Connective Tissue Is Involved in the Action of Acupuncture.

Acupuncture has been used to treat a variety of diseases and symptoms for more than 2,500 years. While a number of studies have shown that nerves are responsible for initiating the effects of acupuncture, several lines of study have emphasized the role of connective tissue in the initiation of acupuncture signals. To determine whether nerves or connective tissue mediate the action of acupuncture, we constructed a robotic acupuncture needle twister that mimicked the twisting of the needle by an acupuncturist, and we examined the role of nerves and connective tissues in the generation of acupuncture effects in rat cocaine-induced locomotion, stress-induced hypertension, and mustard oil-induced visceral pain models. Robotic or manual twisting of acupuncture needles effectively suppressed cocaine-induced hyperactivity, elevated systemic blood pressure or mustard oil-induced visceral pain in rats. These acupuncture effects were completely abolished by injecting bupivacaine, a local anesthetic, into acupoints. However, disruption of connective tissue by injecting type I collagenase into acupoints did not affect these acupuncture effects. Our findings suggest that nerve tissue, but not connective tissue, is responsible for generating the effects of acupuncture.

Upregulation of AT1 Receptor Mediates a Pressor Effect Through ROS-SAPK/JNK Signaling in Glutamatergic Neurons of Rostral Ventrolateral Medulla in Rats With Stress-Induced Hypertension.

The present study examined whether angiotensin II (Ang II) mediates the pressor effect through nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-derived reactive oxygen species (ROS)-mitogen-activated protein kinase (MAPK) signaling in the glutamatergic neurons of the rostral ventrolateral medulla (RVLM) in stress-induced hypertensive rats (SIHR). The SIHR model was established using electric foot-shocks combined with noises for 15 days. We observed that Ang II type 1 receptor (AT1R) and the glutamatergic neurons co-localized in the RVLM of SIHR. Furthermore, glutamate levels in the intermediolateral column of the spinal cord were higher in SIHR than in controls. Microinjection of Ang II into the RVLM of SIHR activated stress-activated protein kinase/Jun N-terminal kinase (SAPK/JNK), extracellular signal-regulated protein kinase (ERK) 1/2, and p38MAPK. Compared with controls, the activation of SAPK/JNK, ERK1/2, p38MAPK, and ROS in the RVLM were higher in SIHR, an effect that was blocked by an NADPH oxidase inhibitor (apocynin) and an AT1R antagonist (candesartan). RVLM microinjection of apocynin or a SAPK/JNK inhibitor (SP600125), but not an ERK1/2 inhibitor (U0126) or a p38MAPK inhibitor (SB203580), decreased AT1R mRNA and mean arterial blood pressure (MABP) in SIHR. The increase of AT1R protein expression and MABP was inhibited by intracerebroventricular infusion (ICV), for 14 days, of SP600125, but not U0126 or SB203580 in SIHR. We conclude that Ang II modulates the pressor effect through AT1R-dependent ROS-SAPK/JNK signaling in glutamatergic neurons in the RVLM of SIHR.

Upregulation of Nav1.6 expression in the rostral ventrolateral medulla of stress-induced hypertensive rats.

The rostral ventrolateral medulla (RVLM) plays a key role in mediating the development of stress-induced hypertension (SIH) by excitation and/or inhibition of sympathetic preganglionic neurons. The voltage-gated sodium channel Nav1.6 has been found to contribute to neuronal hyperexcitability. To examine the expression of Nav1.6 in the RVLM during SIH, a rat model was established by administering electric foot-shocks and noises. We found that Nav1.6 protein expression in the RVLM of SIH rats was higher than that of control rats, peaking at the tenth day of stress. Furthermore, we observed changes in blood pressure correlating with days of stress, with systolic blood pressure (SBP) found to reach a similarly timed peak at the tenth day of stress. Percentages of cells exhibiting colocalization of Nav1.6 with NeuN, a molecular marker of neurons, indicated a strong correlation between upregulation of Nav1.6 expression in NeuN-positive cells and SBP. The level of RSNA was significantly increased after 10 days of stress induction than control group. Compared with the SIHR, knockdown of Nav1.6 in RVLM of the SIHR decreased the level of SBP, heart rate (HR) and renal sympathetic nerve activity (RSNA). These results suggest that upregulated Nav1.6 expression within neurons in the RVLM of SIH rats may contribute to overactivation of the sympathetic system in response to SIH development.

Worksite hypertension as a model of stress-induced arterial hypertension

The review presents a modern view on stress as a risk factor for the development of arterial hypertension (AH). A variety pathogenic mechanisms responsible for increase of blood pressure during stress exposure are described in detail. The importance of the sympathetic activation as a key link in the development of stress-induced AH and initiation of a cascade of pathophysiological reactions that realize their adverse effects at the level of the whole organism is underlined. Particular attention is paid to worksite AH as a variant of stress-induced hypertension due to its wide prevalence and association with an increased risk of cardiovascular complications, primarily myocardial infarction and stroke. Epidemiological data and results of recent metanalysis are presented, indicating the high significance of job strain as a risk factor for adverse cardiovascular events. The actual psychological stress reduction programs are described. Possibilities of using β-blockers in patients with stress-induced hypertension as drugs affecting the central pathogenetic trigger of this disease are considered. The advantages of using bisoprolol as a highly selective β-blocker are considered taking into account the available body of evidence for its effectiveness in patients with worksite AH, as well as its metabolic neutrality and target-organ protective properties.

Abstract 023: Redox-Driven T-Lymphocyte Inflammation Sensitizes Mice to Psychological Stress-Mediated Hypertension

Post-traumatic stress disorder (PTSD) is a debilitating psychological disease that increases sympathoexcitation, norepinephrine (NE) outflow, and the risk of cardiovascular diseases like hypertension by >50%, but the mechanisms remain unclear. Hypertension is regulated in part due to immune system-driven inflammation, and our laboratory has previously reported that exposure to NE can modulate levels of T-lymphocyte pro-inflammatory cytokines by redox signaling mechanisms. Therefore, we hypothesized that psychological stress-induced sympathoexcitation leads to a redox-regulated increase in pro-inflammatory cytokine production from T-lymphocytes, which may impact the development of hypertension. Utilizing a mouse-model of PTSD-like psychological stress ( i.e. social defeat), increased sympathoexcitation was confirmed by a 2.5 fold increase in splenic NE content and 4.1 fold increase in tyrosine hydroxylase (TH; p<0.05). Splenic and peripheral T-lymphocytes demonstrated increased reactive oxygen species (ROS) levels as evidenced by enhanced dihydroethidium and MitoSOX Red oxidation (p<0.05). Increases in ROS were correlated with elevated pro-inflammatory cytokines IL-17A, IL-6, and IL-2 in circulation as well as specifically within T-lymphocytes (p<0.05). Examination of hemodynamics elucidated a progressive increase in mean arterial pressure (15 mmHg, p<0.05) over the stress-induction period, correlating with the elevation of T-lymphocyte driven inflammation. This hypertension was not associated with an increase in circulating renin levels. To investigate the causal contribution of T-lymphocytes in driving this hypertension, recombination activating gene 2 (Rag2) knock-out animals, which are devoid of mature lymphocytes, were utilized. Rag2 -/- mice showed no changes in pro-inflammatory cytokines, a 75% decrease in splenic TH levels (p<0.05), and decreased blood pressure after stress, suggesting T-lymphocytes may regulate the stress-induced hypertension. Overall, our data suggest the potential for a new paradigm involving redox control of T-lymphocytes in the regulation of psychological stress-driven hypertension.

Role of microglia M1/M2 polarisation in the paraventricular nucleus: New insight into the development of stress-induced hypertension in rats.

The lack of precise therapies for stress-induced hypertension highlights the need to explore the process of blood pressure changes. Studies have shown that neuroinflammation in the central nervous system is associated with hypertension, although the mechanisms remain elusive. Microglia, are known to play dualistic protective and destructive roles, representing logical but challenging targets for improving stress-induced hypertension. Here, as a model, we used rats with stress-induced hypertension, and found that a switch from an immunoregulatory (M2) to a pro-inflammatory (M1) dominant response occurred in microglia during development of stress-induced hypertension. Administration of minocycline, which is commonly used to inhibit microglial M1 polarisation, attenuated the increase in activated microglia and M1 microglial markers expression in the hypothalamic paraventricular nucleus of rats with stress-induced hypertension. To shed further light on development of stress-induced hypertension, we examined changes in pro- and anti-inflammatory cytokines, and found increased expression of M2 microglial markers during early pathogenesis. Based on these results, we propose the possibility that M1/M2 microglia are related to development of stress-induced hypertension. Consequently, a target molecule that skews M2 polarisation of microglia may be a beneficial therapy for this disease.

Coupling of Lipoperoxidation Reactions with Changes in Arterial Blood Pressure in Hypertensive ISIAH Rats under Conditions of Chronic Stress.

Mature normotensive male WAG rats and stress-sensitive hypertensive ISIAH rats were exposed to "everyday life stress" modelled by alternation of immobilization and adaptation. Increased LPO intensity (increased content of substrates with unsaturated double bonds and primary and secondary LPO products) and reduced content of some antioxidant protection components (reduced retinol level and GSH/GSSG ratio) were revealed in the blood of ISIAH rats. These changes correlated with elevated mean BP. The results can reflect the significant role of LPO changes in the pathogenesis of stress-induced arterial hypertension.

Alteration of serum immunoglobins, C-reactive protein, vitamin D, and electrolyteby atenolol and amlodipine in stress-induced hypertensive rats.

The present study is designed for the assessment of various pathological changes like immunoglobins, C-reactive protein, vitamin D, sodium, potassium, calcium in stress-induced hypertensive rats. Albino Wistar rats of sex male were grouped into six. Each group consists of six animals. Groups were Group I (normal control), Group II (disease control), Group III (amlodipine control), Group IV (atenolol control), Group V (amlodipine treatment), and Group VI (atenolol treatment). Group II, V, and VI animals exposed to regular stress by placing them in cages individually and giving foot electric shocks (1mA, 50ms duration with 0.5-1min of intervals regulated randomly by a computer)along withforced swimming (30 min) in order to induce hypertension in rats. This stress was given two times daily (morning and evening) for regular 15 days. Induction of hypertension was confirmed by measuring the tail arterial pressure of blood and angiotensin II. For next 1 month, Group III and V animals are treated with amlodipine with 1mg/kg, s.c. dose while Group IV and VI animals were given 10mg/kg, s.c. the dose of atenolol once daily. At the end of the experimental work, blood collected, rats sacrificed, and serum separated. Serum sodium, potassium, immunoglobins, C-reactive protein, vitamin D, and calcium were measured by semi-auto-analyzer. Stress-induced hypertension in rats produced altered serum sodium, potassium, immunoglobins, C-reactive protein, vitamin D, and calcium level which is restored by atenolol. Administration of amlodipine in animals without hypertension shows alteration in the level of immunoglobins, calcium, vitamin D, and electrolytes.

Social stress-induced blood pressure increase in borderline hypertensive rats is associated with endothelial dysfunction in the resistant arteries

ObjectivesSeveral studies have observed that altered endothelial function is involved in the development of stress-induced hypertension. The aim of this study was to investigate the effects of chronic social stress (crowding) on endothelium-dependent relaxation (EDR) of the superior mesenteric artery (SMA) and of small resistant mesenteric arteries (MA) as well as on neurogenic contractions of SMA in adult borderline hypertensive rats (BHR).MethodsTwelve-week-old BHR (offspring of spontaneously hypertensive dams and Wistar-Kyoto sires) males were exposed to crowding (living space: 200 cm2/rat) for eight weeks. Control BHR were kept in the groups of four rats per cage (living space: 480 cm2/rat). Systolic blood pressure (sBP) was determined by the tail-cuff method.Vascular function was investigated in the isolated arteries at isometric conditions.EDR was assessed using acetylcholine test.ResultsCrowding significantly increased sBP of BHR to the hypertensive values. Results showed that stress did not affect total acetylcholine-induced relaxation and its nitric oxide (NO)-dependent and NO-independent components in the SMA. In the resistant MA, stress reduced total acetylcholine-induced relaxation by reducing NO-independent component, without the alterations of its NO-dependent component.However, stress failed to affect significantly neurogenic contractions of SMA elicited by electrical stimulation of perivascular sympathetic nerves and vasoconstriction induced by exogenous noradrenaline in SMA.ConclusionIn conclusion, chronic social stress can accelerate the development of hypertension in BHR, which seems to be associated with NO-independent endothelial dysfunction in small resistant arteries.Supported by the grants VEGA No. 2/0190/17 and APVV-16-0263.

GW28-e0055 The Management Manner and Reasons Analysis for Stress-induced Hypertension in Adults with Aortic Dissection (Stanford type A) after Bentall or Improved-Cabrol of Cardiac Surgery

GW28-e0055 The Management Manner and Reasons Analysis for Stress-induced Hypertension in Adults with Aortic Dissection (Stanford type A) after Bentall or Improved-Cabrol of Cardiac Surgery

Behavioral activity and immune effects of the stress exposures and susceptibility to glucocorticoid drug in inherited stress-induced arterial hypertension rat strain with stress-sensitive arterial hypertension

Behavioral activity and immune effects of the stress exposures and susceptibility to glucocorticoid drug in inherited stress-induced arterial hypertension rat strain with stress-sensitive arterial hypertension

Abstract P218: Role of UCP2 on Mitochondrial Dysfunction and Blood Pressure Regulation in the Renal Oxidative Stress-mediated Hypertension Associated With Dj-1 Depletion

DJ-1 and uncoupling protein 2 (UCP2) exert protective roles against mitochondrial (MT) oxidative stress. DJ-1 -/- mice have increased systolic blood pressure (BP) (+30±3% vs WT, n=6). This study determined the mechanisms involved in the oxidative stress-mediated hypertension due to DJ-1 germline deletion. There were no differences in sodium excretion, renal renin expression, NADPH oxidase activity and serum creatinine between DJ-1 -/- and WT mice (n=5). However, renal expression of nitro-tyrosine was increased in DJ-1 -/- mice (+176.8±31% vs WT mice, n=5). Tempol, a radical scavenger, normalized the BP (tempol: 118±2% vs 100±1% vs WT, n=4) and renal malondialdehyde (tempol: 160±23% vs 109±15% vs WT, n=4) in DJ-1 -/- mice. Tempol-treated DJ-1 -/- mice had higher serum nitrite/nitrate levels than placebo-treated (172±30% vs WT, n=4). Heat shock protein mtHSP60 was increased in DJ-1 -/- mice (2.9±0.1-fold increase vs WT, n=4), indicating MT stress. However, there were no changes in the renal mRNA expression of mitophagy, MT fusion and MT biosynthesis markers indicating that MT function was not altered. Renal expression of UCP2 was increased in DJ-1 -/- mice (4.1±1.1-fold change vs WT, n=4), and was partially normalized by tempol (1.8±0.2-fold change vs WT, n=4), UCP2 may have a protective role on MT function in this model. UCP2 was selectively silenced via sub-capsular infusion of UCP2 siRNA in the kidney (WT: 63%±7 vs control: DJ-1 -/- :60%±6 vs control; n=4). mRNA expression of mitophagy markers BNIP3 (-0.65±6-fold) and PINK1 (1.55±0.3-fold), MT fusion markers FIS1 (-0.29±0.03-fold) and NFN2 (1.42±0.06-fold), and MT biosynthesis marker PPRC1 (1.71±0.07-fold) were altered by UCP2 silencing in DJ-1 -/- mice (n=4). Renal-selective silencing of UCP2 normalized BP in DJ-1 -/- mice ( DJ-1 -/- mice: 122±5 vs 98±7 mmHg, n=4), and the serum nitrite and nitrate concentrations (-40±9% vs WT, n=4). In conclusion, deletion of DJ-1 leads to oxidative stress-induced hypertension associated with down-regulation of NO synthesis. UCP2 has protective properties against the development of MT dysfunction in MT oxidative stress conditions . However, excessive and chronic over expression of UCP2 could have deleterious consequences on BP regulation.

Neuroinflammation contributes to autophagy flux blockage in the neurons of rostral ventrolateral medulla in stress-induced hypertension rats

BackgroundNeuroinflammation plays hypertensive roles in the uninjured autonomic nuclei of the central nervous system, while its mechanisms remain unclear. The present study is to investigate the effect of neuroinflammation on autophagy in the neurons of the rostral ventrolateral medulla (RVLM), where sympathetic premotor neurons for the maintenance of vasomotor tone reside.MethodsStress-induced hypertension (SIH) was induced by electric foot-shock stressors with noise interventions in rats. Systolic blood pressure (SBP) and the power density of the low frequency (LF) component of the SAP spectrum were measured to reflect sympathetic vasomotor activity. Microglia activation and pro-inflammatory cytokines (PICs (IL-1β, TNF-α)) expression in the RVLM were measured by immunoblotting and immunostaining. Autophagy and autophagic vacuoles (AVs) were examined by autophagic marker (LC3 and p62) expression and transmission electron microscopy (TEM) image, respectively. Autophagy flux was evaluated by RFP-GFP-tandem fluorescent LC3 (tf-LC3) vectors transfected into the RVLM. Tissue levels of glutamate, gamma aminobutyric acid (GABA), and plasma levels of norepinephrine (NE) were measured by using high-performance liquid chromatography (HPLC) with electrochemical detection. The effects of the cisterna magna infused minocycline, a microglia activation inhibitor, on the abovementioned parameters were analyzed.ResultsSIH rats showed increased SBP, plasma NE accompanied by an increase in LF component of the SBP spectrum. Microglia activation and PICs expression was increased in SIH rats. TEM demonstrated that stress led to the accumulation of AVs in the RVLM of SIH rats. In addition to the Tf-LC3 assay, the concurrent increased level of LC3-II and p62 suggested the impairment of autophagic flux in SIH rats. To the contrary, minocycline facilitated autophagic flux and induced a hypotensive effect with attenuated microglia activation and decreased PICs in the RVLM of SIH rats. Furthermore, SIH rats showed higher levels of glutamate and lower level of GABA in the RVLM, while minocycline attenuated the decrease in GABA and the increase in glutamate of SIH rats.ConclusionsCollectively, we concluded that the neuroinflammation might impair autophagic flux and induced neural excitotoxicity in the RVLM neurons following SIH, which is involved in the development of SIH.

The prevalence of risk factors of cardiovascular diseases in persons with arterial hypertension exposed to occupational
 stress

Based on the literature data and the results of their own research, the authors emphasize the importance of studying adverse effects of high emotional load during stress-induced hypertension and draw attention to the high prevalence of modifiable risk factors of cardiovascular disease among servicemen exposed to occupational stress. It has been shown that lifestyle of hypertensive subjects under heavy stress is characterized by irrational changes in eating behavior, high prevalence of smoking, increased alcohol consumption, and low physical activity. The leading role of long-term emotional stress was demonstrated as an independent risk factor of hypertension in servicemen exposed to long-term occupational psycho-emotional stress. Analysis of the intima-media complex thickness in brachiocephalic arteries, depending on the level of psychosocial stress demonstrated that the group of the examined servicemen with hypertension showed changes that might be due to the development of atherosclerotic process, the response to increased flow, and arterial wall tension at a high level of stress. These changes are unidirectional regardless of the duration of hypertension history. Results of evaluation of the overall risk of developing cardiovascular complications based on the SCORE scale in the servicemen with established and newly diagnosed hypertension under heavy stress suggest its enhancement in the next 10 years which makes necessary implementation of a system of measures for preventing and correcting pathological conditions caused by stressful loads. Stratification of risk factors is essential for early diagnosis of hypertension and the choice of adequate therapy in subjects undergoing high psycho-emotional stress.

A violation of emotion regulation as a central link in pathogenesis of stress-induced hypertension

IntroductionEssential hypertension (EH) is one of the most common diseases of the cardiovascular system. Today, scientists discover more and more patients whose BP values during work appear to be higher than those values during free time. This form of EH is called “hypertension at work”.ObjectiveTo study the role emotion dysregulation in the pathogenesis of EH.Materials and methodsA projective study of emotion regulation was undertaken with our modified version of Rosenzweig Picture-Frustration Test (Zinchernko, Pervichko). At the second stage of the study, the simulation of emotional stress with the aspiration level modelling was carried out. The level of state anxiety, BP values and levels of catecholamines, renin and angiotonin I were taken before and after the experiment. Eighty-five patients with “hypertension at work” (mean age: 45.9 ± 2.8), 85 patients with “classical” EH (mean age: 47.4 ± 4.5 years) and 82 healthy subjects (mean age: 44.9 ± 3.1) took part in the study.Results“Hypertension at work” patients significantly more frequently than patients from the second group and healthy subjects are more prone to rumination, disasterization and repression of their emotions. They will seldom employ the strategy of subjective-objective interactive transformations; their edibility to actualize new meanings in traumatic situations is diminished. We showed that emotion regulation strategies in “hypertension in the work” patients were ineffective in overcoming the emotional tension and created the conditions for chronization of high blood pressure, and could be considerded as the central link in pathogenesis of stress-induced hypertension.ConclusionThe results contributes to enrich our understanding of etiology and pathogenesis of EH.Disclosure of interestThe authors have not supplied their declaration of competing interest.

The Orexin System and Hypertension.

In this review, we focus on the role of orexin signaling in blood pressure control and its potential link to hypertension by summarizing evidence from several experimental animal models of hypertension. Studies using the spontaneously hypertensive rat (SHR) animal model of human essential hypertension show that pharmacological blockade of orexin receptors reduces blood pressure in SHRs but not in Wistar-Kyoto rats. In addition, increased activity of the orexin system contributes to elevated blood pressure and sympathetic nerve activity (SNA) in dark-active period Schlager hypertensive (BPH/2J) mice, another genetic model of neurogenic hypertension. Similar to these two models, Sprague-Dawley rats with stress-induced hypertension display an overactive central orexin system. Furthermore, upregulation of the orexin receptor 1 increases firing of hypothalamic paraventricular nucleus neurons, augments SNA, and contributes to hypertension in the obese Zucker rat, an animal model of obesity-related hypertension. Finally, we propose a hypothesis for the implication of the orexin system in salt-sensitive hypertension. All of this evidence, coupled with the important role of elevated SNA in increasing blood pressure, strongly suggests that hyperactivity of the orexin system contributes to hypertension.

Early diagnosis of stress-induced hypertension in young employees of state law enforcement agencies

Psychoemotional stress is one of the leading cardiovascular risk factors. The aim of this study was to explore manifestations of arterial hypertension (AH) in young men employed in the stress associatedfield works. Material and methods. A total of 68 young men, exposed to job stress (JS) of different severity during 1 to 5 years were surveyed. The control group was formed of persons whose daily work was unrelated to operational activities. The study included ambulatory monitoring (AM) blood pressure (BP) on different days of the week, comparing the results of the office and DMBP determination and assessment of resistance to a variety of diagnostic loads. Results. The study revealed an increase of AMBP indicators during the working day and their normalization at weekend. The comparison of the results of office and ambulatory determination of BP demonstrated that different forms of stressful AH (stable, isolated office and latent) occurred significantly more often than in the control group. These changes almost completely disappeared at weekends. The tolerance ofpsychoemotional testing was much worse than that of traditional exercises. It is proposed to more extensively use AMBP during regular medical examinations of young men exposed to JS in order to establish a timely differential diagnosis of various forms of stressful hypertension.