The role of sympathetic nervous system in the development of neurogenic pulmonary edema in spinal cord-injured rats

2012 ◽  
Vol 112 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Jiří Šedý ◽  
Josef Zicha ◽  
Jara Nedvídková ◽  
Jaroslav Kuneš
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Neurogenic Pulmonary Edema ◽  
Spinal Pathways ◽  
Adrenoceptor Blocker ◽  
Sympathetic Nervous ◽  
Spinal Cord Injured

The pronounced activation of sympathetic nervous system is a necessary prerequisite for the development of neurogenic pulmonary edema (NPE) in rats with balloon compression of spinal cord. In this study we examined whether this is a consequence of rapid activation of spinal pathways leading to sympathetic venoconstriction, blood pressure rise, and reflex bradycardia. We found that NPE development can be prevented by epidural upper thoracic anesthesia or by transection of the upper spinal cord. This indicates an important role of spinal pathways activation. NPE development can also be prevented by moderate blood loss, supporting the role of blood redistribution to pulmonary circulation. In rats developing NPE the catecholamine surge following spinal cord compression involved not only a dramatic increase of circulating norepinephrine but also of epinephrine levels. The pretreatment of rats with α-1 adrenoceptor blocker prazosin, α-2 adrenoceptor blocker yohimbine, or calcium channel blocker nifedipine prevented NPE development, whereas the effect of β-adrenoceptor blockade with propranolol was less convincing. In conclusion, considerable activation of thoracic spinal pathways, followed by marked catecholamine secretion, play a major role in the development of NPE in spinal cord-injured rats. Enhanced α-adrenergic nifedipine-sensitive vasoconstriction is responsible for observed blood pressure changes, subsequent baroreflex bradycardia, and blood volume redistribution, which represent major pathogenetic mechanisms of NPE development.

scholarly journals Role of Sympathetic Nervous System in Cyclosporine-Induced Rise in Blood Pressure

Hypertension ◽  
1999 ◽  
Vol 34 (1) ◽  
pp. 102-106 ◽  
Author(s):  
Mario J. Carvalho ◽  
Anton H. van den Meiracker ◽  
Frans Boomsma ◽  
Joao Freitas ◽  
Arie J. Man in ‘t Veld ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Sympathetic Nervous

Role of the sympathetic nervous system in CCl4 hepatotoxicity

1960 ◽  
Vol 198 (3) ◽  
pp. 669-676 ◽  
Author(s):  
Deane N. Calvert ◽  
Theodore M. Brody
Keyword(s):  
Spinal Cord ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Liver Mitochondria ◽  
Central Vein ◽  
Fat Depots ◽  
Sympathetic Nervous ◽  
Adrenergic Blocking ◽  
Stimulation Of

An hypothesis is proposed which states that the characteristic hepatic changes seen after the administration of carbon tetrachloride are the result of stimulation of central sympathetic areas which produce a massive discharge of the peripheral sympathetic nervous system. Stimulation of the sympathetic supply to the blood vessels of the liver results in restriction of blood flow in the liver, leading to anoxia and the characteristic necrosis around the central vein of the hepatic lobule. Similarly the discharge causes the release of unesterified fatty acids from the peripheral fat depots and the consequent deposition of lipid in the liver. This hypothesis is based upon experimental evidence using the following physiologic and pharmacologic maneuvers: adrenergic blocking agents, pretreatment with reserpine, adrenalectomy and section of the spinal cord—all are effective to a greater or lesser extent in preventing the changes characteristically seen in oxidative phosphorylation of the liver mitochondria, activation of a Mg-dependent ATPase and deposition of lipid in the liver. Transection of the spinal cord is the most effective treatment and prevents entirely the characteristic changes seen in the above-mentioned functions.

scholarly journals Insulin and Blood Pressure Regulation : Role of Sodium Retention and Sympathetic Nervous System

1993 ◽  
Vol 57 (supplementIV) ◽  
pp. 1154-1156
Author(s):  
Toshio Kushiro ◽  
Hirofumi Tomiyama ◽  
Katsuo Kanmatsuse ◽  
Nagao Kajiwara
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Blood Pressure Regulation ◽  
Sodium Retention ◽  
Pressure Regulation ◽  
Sympathetic Nervous

Chronic antioxidant therapy lowers blood pressure in adult but not in young Dahl salt hypertensive rats: the role of sympathetic nervous system

2013 ◽  
Vol 208 (4) ◽  
pp. 340-349 ◽  
Author(s):  
I. Vaněčková ◽  
M. Vokurková ◽  
H. Rauchová ◽  
Z. Dobešová ◽  
O. Pecháňová ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Antioxidant Therapy ◽  
Hypertensive Rats ◽  
Sympathetic Nervous

Aging and Insulin Sensitivity: Role of Blood Pressure and Sympathetic Nervous System Activity

1993 ◽  
Vol 48 (6) ◽  
pp. M237-M243 ◽  
Author(s):  
M. A. Supiano ◽  
R. V. Hogikyan ◽  
L. A. Morrow ◽  
F. J. Ortiz-Alonso ◽  
W. H. Herman ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Insulin Sensitivity ◽  
Sympathetic Nervous System ◽  
Sympathetic Nervous System Activity ◽  
System Activity ◽  
Nervous System Activity ◽  
Sympathetic Nervous

Nighttime blood pressure dipping: the role of the sympathetic nervous system

2002 ◽  
Vol 15 (2) ◽  
pp. 111-118 ◽  
Author(s):  
A. Sherwood ◽  
P. R. Steffen ◽  
J. A. Blumenthal ◽  
C. Kuhn ◽  
A. L. Hinderliter
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Nighttime Blood Pressure ◽  
Blood Pressure Dipping ◽  
Sympathetic Nervous

scholarly journals Contribution of Sympathetic Nervous System to High Blood Pressure in Salt Hypertensive Dahl Rats

2021 ◽  
pp. 117-118
Author(s):  
Josef Zicha
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Salt Intake ◽  
Adrenergic Blockade ◽  
Control Groups ◽  
Adrenergic Mechanisms ◽  
Salt Hypertension ◽  
Sympathetic Nervous

The important participation of sympathetic nervous system in various forms of experimental hypertension is well known. This is also true for salt hypertension elicited by excess salt intake in Dahl salt-sensitive rats (for review see Zicha et al. 2012). Two recent studies in Dahl rats (Zicha et al. 2019, Puleo et al. 2020) evaluated the hypothesis on the role of β-adrenergic WNK4-NCC pathway in salt-sensitive hypertension which has been proposed by Mu et al. (2011). Although these studies differed in many experimental details, both of them demonstrated a major importance of α1- rather than β adrenergic mechanisms for the development of salt hypertension in this rat strain. Zicha et al. (2019) demonstrated that chronic β adrenergic blockade by propranolol did not lower blood pressure (BP) in Dahl salt-sensitive rats developing salt hypertension. It also did not modify their sympathetic component or natriuretic response to acute hydrochlorothiazide administration which inhibited the activity of sodium-chloride cotransporter (NCC). Puleo et al. (2020) reported that chronic β-adrenergic blockade failed to affect salt hypertension development or to reduce renal WNK4-NCC pathway. On the other hand, their study demonstrated the important influence of α1 adrenergic pathway on the activity, expression and phosphorylation of NCC. Chronic α1-adrenergic antagonism by terazosin treatment in Dahl salt-sensitive rats, which started before the onset of high salt intake, considerably attenuated the development of salt hypertension. This treatment diminished BP difference between the salt-loaded Dahl salt-sensitive rats and their control groups by 70-75 %. However, terazosin-treated Dahl salt-sensitive animals fed a high-salt diet had not only suppressed renal NCC activity but they also did not respond to acute phenylephrine administration. This suggests that chronic α1-adrenergic blockade affected both renal sodium retention mechanisms and α1-adrenergic vasoconstriction (Puleo et al. 2020). It remains to determine how these two mechanisms contribute to salt hypertension in Dahl rats. We found that the acute ganglionic blockade lowered substantially BP of salt hypertensive Dahl rats, abolishing 45-55 % of the BP difference between salt-loaded Dahl salt-sensitive rats and their control groups (Zicha et al. 2019). If we consider the results of both above studies, it seems that the renal contribution might be responsible for about 25 % of BP elevation seen in Dahl salt-sensitive rats developing salt hypertension, whereas α1-adrenergic vasoconstriction contributes to this BP change by about 50 %. Of course, this consideration is highly speculative. Nevertheless, it might stimulate further effort to distinguish the role of kidney and brain in the pathogenesis of salt hypertension. Perhaps even more promising could be the estimation of renal and extrarenal effects of central sympathoexcitation in Dahl rats (Mark 1991, Gabor and Leenen 2012, Fujita et al. 2009) which is related to central α2-adrenergic mechanisms (Wainford et al. 2015). As far as the role of kidney in the pathogenesis of salt hypertension is concerned (Frame et al. 2019), some attention should also be paid to participation of renal vascular and tubular effects of increased sympathetic tone in these salt hypertensive animals.

Blood pressure response to chronic episodic hypoxia: role of the sympathetic nervous system

1997 ◽  
Vol 83 (1) ◽  
pp. 95-101 ◽  
Author(s):  
Gang Bao ◽  
Naira Metreveli ◽  
Rena Li ◽  
Addison Taylor ◽  
Eugene C. Fletcher
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Renal Artery ◽  
Adrenal Medulla ◽  
Blood Pressure Response ◽  
Episodic Hypoxia ◽  
Sympathetic Nervous ◽  
Renal Artery Denervation

Bao, Gang, Naira Metreveli, Rena Li, Addison Taylor, and Eugene C. Fletcher. Blood pressure response to chronic episodic hypoxia: role of the sympathetic nervous system. J. Appl. Physiol. 83(1): 95–101, 1997.—Previous studies in several strains of rats have demonstrated that 35 consecutive days of recurrent episodic hypoxia (7 h/day) cause an 8- to 13-mmHg persistent increase in diurnal systemic blood pressure (BP). Carotid chemoreceptors and the sympathetic nervous system have been shown to be necessary for development of this BP increase. The present study was undertaken to further define the role of renal artery sympathetic nerves and the adrenal medulla in this BP increase. Male Sprague-Dawley rats had either adrenal medullectomy, bilateral renal artery denervation, or sham surgery. Rats from each of these groups were subjected to episodic hypoxia for 35 days. Control groups received either compressed air or were left unhandled. Adrenal demedullation or renal artery denervation eliminated the chronic diurnal mean BP response (measured intra-arterially) to episodic hypoxia, whereas sham-operated controls continued to showed persistent elevation of systemic BP. Plasma and renal tissue catecholamine levels at the end of the experiment confirmed successful adrenal demedullation or renal denervation in the respective animals. The chronic episodic hypoxia-mediated increase in diurnal BP requires both intact renal artery nerves as well as an intact adrenal medulla.

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