Angiotensin II-based hypertension and the sympathetic nervous system: the role of dose and increased dietary salt in rabbits

2007 ◽  
Vol 92 (5) ◽  
pp. 831-840 ◽  
Author(s):  
Fiona D. McBryde ◽  
Sarah-Jane Guild ◽  
Carolyn J. Barrett ◽  
John W. Osborn ◽  
Simon C. Malpas
Keyword(s):  
Nervous System ◽  
Angiotensin Ii ◽  
Sympathetic Nervous System ◽  
Dietary Salt ◽  
Sympathetic Nervous

Selective renal medullary damage and hypertension in the rat: The role of vasopressin

1986 ◽  
Vol 71 (2) ◽  
pp. 167-171 ◽  
Author(s):  
G. I. Russell ◽  
N. P. Godfrey ◽  
M. L. Forsling ◽  
R. F. Bing ◽  
H. Thurston ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Angiotensin Ii ◽  
Sympathetic Nervous System ◽  
Response Curve ◽  
Elevated Blood ◽  
Plasma Vasopressin ◽  
Normal Rat ◽  
Sympathetic Nervous

1. The induction of selective renal medullary damage by 2-bromoethylamine hydrobromide (BEA) results in polyuria and raised blood pressure. In view of the likely elevation of plasma vasopressin we have investigated the role of vasopressin (AVP) in the elevated blood pressure in this model. 2. Plasma vasopressin levels in BEA pretreated rats were raised significantly (2 ± 0.6 pg/ml vs 0.8 ± 0.1 in normal rat, P < 0.05) but not to pressor levels. 3. In addition, pressor responsiveness was investigated in renal medullary damaged rats. There was a reduced response to vasopressin and noradrenaline but no alteration with angiotensin II. A specific V1 receptor AVP antagonist [d(CH2)5Tyr(Me)AVP] produced no fall in blood pressure but returned the noradrenaline dose-response curve to normal. This suggests an interaction between vasopressin and the sympathetic nervous system in this model. 4. Thus there is no evidence that vasopressin contributes to the rise in blood pressure produced by chemical renal medullectomy and other mechanisms have to be sought.

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.

Neurovascular Role of Sympathetic Nervous System and Beta-Adrenoceptor Polymorphisms in Obesity and Hypertension

2008 ◽  
Vol 4 (2) ◽  
pp. 121-130 ◽  
Author(s):  
Kazuko Masuo ◽  
Gavin Lambert ◽  
Hiromi Rakugi ◽  
Toshio Ogihara ◽  
Murray Esler
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Beta Adrenoceptor ◽  
Sympathetic Nervous

scholarly journals Pathophysiology of Resistant Hypertension: The Role of Sympathetic Nervous System

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Costas Tsioufis ◽  
Athanasios Kordalis ◽  
Dimitris Flessas ◽  
Ioannis Anastasopoulos ◽  
Dimitris Tsiachris ◽  
...  
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Resistant Hypertension ◽  
Antihypertensive Treatment ◽  
Treatment Options ◽  
Treatment Resistance ◽  
Obstructive Sleep ◽  
Cardiovascular Morbidity And Mortality ◽  
Sympathetic Nervous

Resistant hypertension (RH) is a powerful risk factor for cardiovascular morbidity and mortality. Among the characteristics of patients with RH, obesity, obstructive sleep apnea, and aldosterone excess are covering a great area of the mosaic of RH phenotype. Increased sympathetic nervous system (SNS) activity is present in all these underlying conditions, supporting its crucial role in the pathophysiology of antihypertensive treatment resistance. Current clinical and experimental knowledge points towards an impact of several factors on SNS activation, namely, insulin resistance, adipokines, endothelial dysfunction, cyclic intermittent hypoxaemia, aldosterone effects on central nervous system, chemoreceptors, and baroreceptors dysregulation. The further investigation and understanding of the mechanisms leading to SNS activation could reveal novel therapeutic targets and expand our treatment options in the challenging management of RH.

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