Cardiac autonomic function in acutely nitric oxide deficient hypertensive rats: role of the sympathetic nervous system and oxidative stress

2011 ◽  
Vol 89 (12) ◽  
pp. 865-874 ◽  
Author(s):  
Meenakshi Chaswal ◽  
Shobha Das ◽  
Jagdish Prasad ◽  
Anju Katyal ◽  
Mohammad Fahim
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
High Frequency ◽  
Spectral Power ◽  
Pressor Response ◽  
Sympathetic Nervous ◽  
And Oxidative Stress

We evaluated the role of the sympathetic nervous system and oxidative stress in hemodynamic and autonomic control after acute inhibition of the synthesis of nitric oxide, using intravenous (i.v.) injection of 30 mg·kg–1 NG-nitro-l-arginine methyl ester (L-NAME) in adult Wistar rats. Baroreflex sensitivity (BRS) and heart rate variability (HRV) were measured as indices of cardiac autonomic control, before and after L-NAME treatment in rats with intact autonomic innervation, and in rats with chemical sympathectomy by 6-hydroxydopamine. Serum malondialdehyde (MDA) was measured as a marker of oxidative stress. In control rats, L-NAME treatment resulted in a significant rise in blood pressure, augmentation of BRS, and enhanced serum MDA. HRV showed an attenuation of total spectral power and high frequency spectral power, along with a rise of the low to high frequency ratio (LF:HF). Administration of L-NAME produced a pressor response even in sympathectomised rats, but augmented BRS was not observed, and the high frequency spectral power showed an increase, in addition to a significant decline of LF:HF and serum MDA. We therefore conclude that even though pressor response was unaffected, reversal of cardiac autonomic responses and decline in oxidative stress following sympathectomy in L-NAME-treated rats reflects a significant role for sympathetic innervation in acute L-NAME-induced hypertension.

Role of vasopressin and sympathetic nervous system during hypertonic NaCl infusion in conscious dog

1985 ◽  
Vol 248 (5) ◽  
pp. H652-H657 ◽  
Author(s):  
E. M. Hasser ◽  
J. R. Haywood ◽  
V. S. Bishop
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Plasma Osmolality ◽  
Ganglionic Blockade ◽  
Osmotic Stimulus ◽  
Sympathetic Nervous ◽  
Subsequent Administration

The contribution of arginine vasopressin (AVP) and the sympathetic nervous system to the pressor response elicited by hypertonic NaCl infusion was investigated in conscious dogs with intact carotid sinus baroreceptors or in dogs subjected to chronic sinoaortic baroreceptor denervation (SAD). Infusion of 6% NaCl at 0.05 ml X kg-1 X min-1 for 60 min increased plasma osmolality an average of 12 +/- 2 mosmol/kg in both intact and SAD dogs. Arterial pressure increased 6 +/- 2 mmHg in intact animals and was normalized by subsequent administration of a specific vascular AVP antagonist. Pretreatment with the AVP antagonist did not alter resting arterial pressure but prevented the increase due to the osmotic stimulus. Pretreatment with ganglionic blockade reduced resting arterial pressure (-17 +/- 2 mmHg). Subsequent infusion of hypertonic NaCl elevated arterial pressure (21 +/- 7 mmHg) to a significantly greater level than that observed with the autonomic nervous system intact. In SAD dogs, the osmotic stimulus increased arterial pressure (16 +/- 1 mmHg) to a significantly greater extent than in intact animals. Subsequent administration of AVP antagonist normalized arterial pressure, and pretreatment with the antagonist prevented any pressor response. Pretreatment with ganglionic blockade did not alter the pressor response (15 +/- 2 mmHg) to hypertonic NaCl. Data suggest that the increase in arterial pressure due to an osmotic stimulus is due to AVP release and does not require a functional sympathetic nervous system. The response is normally buffered by arterial baroreflexes, presumably due to sympathetic withdrawal.

scholarly journals Sympathetic Nervous System Control of Carbon Tetrachloride-Induced Oxidative Stress in Liver throughα-Adrenergic Signaling

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Jung-Chun Lin ◽  
Yi-Jen Peng ◽  
Shih-Yu Wang ◽  
Mei-Ju Lai ◽  
Ton-Ho Young ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Nervous System ◽  
Carbon Tetrachloride ◽  
Sympathetic Nervous System ◽  
Nerve Fibers ◽  
Adrenergic Signaling ◽  
Adrenergic Antagonist ◽  
Sympathetic Nervous

In addition to being the primary organ involved in redox cycling, the liver is one of the most highly innervated tissues in mammals. The interaction between hepatocytes and sympathetic, parasympathetic, and peptidergic nerve fibers through a variety of neurotransmitters and signaling pathways is recognized as being important in the regulation of hepatocyte function, liver regeneration, and hepatic fibrosis. However, less is known regarding the role of the sympathetic nervous system (SNS) in modulating the hepatic response to oxidative stress. Our aim was to investigate the role of the SNS in healthy and oxidatively stressed liver parenchyma. Mice treated with 6-hydroxydopamine hydrobromide were used to realize chemical sympathectomy. Carbon tetrachloride (CCl4) injection was used to induce oxidative liver injury. Sympathectomized animals were protected from CCl4induced hepatic lipid peroxidation-mediated cytotoxicity and genotoxicity as assessed by 4-hydroxy-2-nonenal levels, morphological features of cell damage, and DNA oxidative damage. Furthermore, sympathectomy modulated hepatic inflammatory response induced by CCl4-mediated lipid peroxidation. CCl4induced lipid peroxidation and hepatotoxicity were suppressed by administration of anα-adrenergic antagonist. We conclude that the SNS provides a permissive microenvironment for hepatic oxidative stress indicating the possibility that targeting the hepaticα-adrenergic signaling could be a viable strategy for improving outcomes in patients with acute hepatic injury.

Role of catecholamines in the pathogenesis of diabetic cardiomyopathy

2019 ◽  
Vol 97 (9) ◽  
pp. 815-819 ◽  
Author(s):  
Naranjan S. Dhalla ◽  
Pallab K. Ganguly ◽  
Sukhwinder K. Bhullar ◽  
Paramjit S. Tappia
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Diabetic Cardiomyopathy ◽  
Cardiac Dysfunction ◽  
Oxidation Products ◽  
Sympathetic Nervous ◽  
Myocardial Gene Expression

Although the sympathetic nervous system plays an important role in the regulation of cardiac function, the overactivation of the sympathetic nervous system under stressful conditions including diabetes has been shown to result in the excessive production of circulating catecholamines as well as an increase in the myocardial concentration of catecholamines. In this brief review, we provide some evidence to suggest that the oxidation products of catecholamines such as aminochrome and oxyradicals, lead to metabolic derangements, Ca2+-handling abnormalities, increase in the availability of intracellular free Ca2+, as well as activation of proteases and changes in myocardial gene expression. These alterations due to elevated levels of circulatory catecholamines are associated with oxidative stress, subcellular remodeling, and the development of cardiac dysfunction in chronic diabetes.

Blood pressure maintenance in hypertensive sympathectomized rats. I. Adrenal medullary catecholamines

1991 ◽  
Vol 261 (4) ◽  
pp. R1045-R1051 ◽  
Author(s):  
M. Lo ◽  
C. Julien ◽  
C. Barres ◽  
F. Boomsma ◽  
C. Cerutti ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Pressor Response ◽  
Minor Role ◽  
Plasma Norepinephrine ◽  
The Mean ◽  
Sympathetic Nervous ◽  
A Minor

To assess the role of the sympathetic nervous system in the development of genetic hypertension, blood pressure (BP) was recorded in conscious adult Lyon hypertensive (LH) and normotensive (LN) rats that had received daily injections of saline or guanethidine at 1-13 wk of age. Guanethidine abolished the pressor response to tyramine, decreased plasma norepinephrine by greater than 70% and plasma 3,4-dihydroxyphenylglycol by approximately 90%, and did not change plasma epinephrine. Bilateral adrenalectomy further reduced plasma norepinephrine to 8 and 5% of control levels in LH and LN rats, respectively. BP was lowered (-7%) in sympathectomized rats, but the mean absolute BP difference between LH and LN rats was unaltered. Despite marked supersensitivity to alpha-adrenoreceptor stimulation, phentolamine induced only a small transient depressor response, which was abolished by adrenalectomy in sympathectomized rats. It is concluded that the sympathetic nervous system is not necessary for the development of hypertension in LH rats. After sympathectomy, circulating catecholamines, which mostly derive from the adrenal medulla, play only a minor role in BP maintenance.

scholarly journals Blood pressure variability — regular and irregular waves

2021 ◽  
Vol 26 (6) ◽  
pp. 612-619
Author(s):  
V. A. Tsyrlin ◽  
N. V. Kuzmenko ◽  
M. G. Pliss
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
High Frequency ◽  
Peripheral Resistance ◽  
Baroreceptor Reflex ◽  
Irregular Waves ◽  
Non Invasive ◽  
Sympathetic Nervous

The review presents data on regular and irregular waves of blood pressure (BP) recorded during its invasive (intra-arterial) and non-invasive registration. Regular pulse waves, Traube-Hering waves (second-order waves) and Mayer waves (third-order waves) are described. The characteristic of circadian and ultradian super slow waves is given. The role of the sympathetic nervous system in the origin of regular waves of BP and their relationship with the magnitude of the baroreceptor reflex are shown. Attention is drawn to the role of changes in the minute volume of blood circulation and peripheral resistance to blood flow in the occurrence of fluctuations in BP. We also review the methods and features of BP registration, which enable identification and analysis of irregular high-frequency fluctuations in BP, the relationship of these fluctuations with the magnitude of the baroreceptor reflex and the activity of the sympathetic nervous system. The data on the amplitude of high-frequency irregular fluctuations in BP in animals with simulated hypertension are presented. The review draws attention to the possibility of recording regular fluctuations in BP during its constant non-invasive registration.

The role of the sympathetic nervous system in pressor responses induced by spinal injury

1980 ◽  
Vol 52 (4) ◽  
pp. 473-481 ◽  
Author(s):  
Wise Young ◽  
Vincent DeCrescito ◽  
John J. Tomasula ◽  
Victor Ho
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Spinal Injury ◽  
Pressor Response ◽  
Sham Operation ◽  
Thoracic Sympathectomy ◽  
Cord Injury ◽  
Sympathetic Nervous

✓ Spinal cord injury consistently evokes a transient 3- to 4-minute rise in systemic pressure, followed by prolonged hypotension. Because the role of the sympathetic nervous system in these blood pressure changes is not clear, the pressure responses were studied using systematic ablation of the peripheral sympathetic nervous system. In total, 24 cats were subjected to bilateral thoracic sympathectomy, adrenalectomy, splanchnicectomy, combinations of the preceding, sham operation, or no treatment. Either 3 or 24 hours after the ablations, the blood pressure responses were evoked by 400 gm-cm contusions of the thoracic cord. Although neither thoracic sympathectomy nor adrenalectomy alone abolished the hypertensive phase, the combination of the two procedures did. This suggests that both the thoracic sympathetic ganglia and the adrenal glands participate in the pressor response. Thoracic sympathectomy affected primarily the early part, whereas adrenalectomy diminished the later part of the hypertensive response. This correlates with the function of the former being neurally and the latter being humorally mediated. None of the sympathetic lesions consistently affected the hypotensive phase. Spinal contusion injury produces widespread sympathetic activation, mediating the hypertensive changes.

Thyroid hormone-catecholamine interrelationships during exposure to cold

1981 ◽  
Vol 97 (1) ◽  
pp. 91-97 ◽  
Author(s):  
H. Storm ◽  
C. van Hardeveld ◽  
A. A. H. Kassenaar
Keyword(s):  
Nervous System ◽  
Plasma Concentration ◽  
Thyroid Hormone ◽  
Sympathetic Nervous System ◽  
Plasma Levels ◽  
Surgical Procedure ◽  
Exposure To Cold ◽  
Basal Plasma ◽  
Sympathetic Nervous

Abstract. Basal plasma levels for adrenalin (A), noradrenalin (NA), l-triiodothyronine (T3), and l-thyroxine (T4) were determined in rats with a chronically inserted catheter. The experiments described in this report were started 3 days after the surgical procedure when T3 and T4 levels had returned to normal. Basal levels for the catecholamines were reached already 4 h after the operation. The T3/T4 ratio in plasma was significantly increased after 3, 7, and 14 days in rats kept at 4°C and the same holds for the iodide in the 24-h urine after 7 and 14 days at 4°C. The venous NA plasma concentration was increased 6- to 12-fold during the same period of exposure to cold, whereas the A concentration remained at the basal level. During infusion of NA at 23°C the T3/T4 ratio in plasma was significantly increased after 7 days compared to pair-fed controls, and the same holds for the iodide excretion in the 24-h urine. This paper presents further evidence for a role of the sympathetic nervous system on T4 metabolism in rats at resting conditions.

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