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

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

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

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

Influence of the sympathetic nervous system and vasopressin on the blood pressure lowering effect of nifedipine in deoxycorticosterone acetate–salt hypertensive rats

1987 ◽  
Vol 73 (3) ◽  
pp. 253-258 ◽  
Author(s):  
Yutaka Takata ◽  
Yoshiaki Yamashita ◽  
Shuichi Takishita ◽  
Masatoshi Fujishima
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Calcium Influx ◽  
Hypotensive Effect ◽  
Ang Ii ◽  
Hypertensive Rats ◽  
Blood Pressure Lowering Effect ◽  
Hypotensive Action ◽  
Sympathetic Nervous

1. The role of the sympathetic nervous system and the effect of vasopressin (AVP) on the hypotensive action of nifedipine (Nf) were evaluated in conscious, unrestrained normotensive and DOCA–salt hypertensive rats. 2. The hypotensive response to Nf was much greater in DOCA rats than in the controls. 3. Solitary blockade of the sympathetic nervous system or AVP, did not alter the Nf effect in either DOCA or control rats. However, a combination clearly diminished the effect of Nf in the DOCA group, but enhanced it in the controls. The inhibition of angiotensin II (ANG II) augmented the hypotensive effect of Nf in control animals, but not in the DOCA rats. The percentage fall in blood pressure with Nf was much the same in both groups after the combined inhibition of the sympathetic nervous system and AVP. 4. The enhanced hypotensive action of Nf in DOCA rats may be dependent on the hyperactivity of the sympathetic nervous system and AVP, which facilitates calcium influx, and in the normotensive animals the depressor response to Nf may relate to blockade of the calcium influx, independent of the sympathetic nervous system, AVP and ANG II.

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.

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