scholarly journals Mechanisms responsible for postmenopausal hypertension in a rat model: Roles of the renal sympathetic nervous system and the renin-angiotensin system

2016 ◽  
Vol 4 (2) ◽  
pp. e12669 ◽  
Author(s):  
Rodrigo O. Maranon ◽  
Jane F. Reckelhoff
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Rat Model ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Sympathetic Nervous ◽  
Renal Sympathetic

scholarly journals Role of the renin-angiotensin system in cardiac hypertrophy induced in rats by hyperthyroidism

1997 ◽  
Vol 273 (2) ◽  
pp. H593-H599 ◽  
Author(s):  
H. Kobori ◽  
A. Ichihara ◽  
H. Suzuki ◽  
T. Takenaka ◽  
Y. Miyashita ◽  
...  
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Cardiac Hypertrophy ◽  
Weight Ratio ◽  
Renin Angiotensin System ◽  
Sympathetic Denervation ◽  
Sprague Dawley ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Sympathetic Nervous

This study was conducted to examine whether the renin-angiotensin system contributes to hyperthyroidism-induced cardiac hypertrophy without involving the sympathetic nervous system. Sprague-Dawley rats were divided into control-innervated, control-denervated, hyperthyroid-innervated, and hyperthyroid-denervated groups using intraperitoneal injections of thyroxine and 6-hydroxydopamine. After 8 wk, the heart-to-body weight ratio increased in hyperthyroid groups (63%), and this increase was only partially inhibited by sympathetic denervation. Radioimmunoassays and reverse transcription-polymerase chain reaction revealed increased cardiac levels of renin (33%) and angiotensin II (53%) and enhanced cardiac expression of renin mRNA (225%) in the hyperthyroid groups. These increases were unaffected by sympathetic denervation or 24-h bilateral nephrectomy. In addition, losartan and nicardipine decreased systolic blood pressure to the same extent, but only losartan caused regression of thyroxine-induced cardiac hypertrophy. These results suggest that thyroid hormone activates the cardiac renin-angiotensin system without involving the sympathetic nervous system or the circulating renin-angiotensin system; the activated renin-angiotensin system contributes to cardiac hypertrophy in hyperthyroidism.

The contribution of the renin-angiotensin system to limb vasoregulation in patients with heart failure: observations during orthostasis and α-adrenergic blockade

1985 ◽  
Vol 68 (6) ◽  
pp. 659-667 ◽  
Author(s):  
Mark A. Creager ◽  
David P. Faxon ◽  
Susan M. Rockwell ◽  
Haralambos Gavras ◽  
Jay D. Coffman
Keyword(s):  
Heart Failure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Vascular Resistance ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Patients With Heart Failure ◽  
Sympathetic Nervous ◽  
Forearm Vascular Resistance

1. In patients with congestive heart failure, both the sympathetic nervous system and renin-angiotensin system are often stimulated. In order to assess the contribution of the renin-angiotensin system to limb vascular resistance, the forearm haemodynamic response to captopril was studied in 13 patients with heart failure. 2. Seven subjects were studied while supine and during 60° head-up tilt. To eliminate α-adrenergic effects, six additional patients with heart failure were pretreated with intra-arterial phentolamine and then given captopril. Venous occlusion plethysmography was used to determine forearm blood flew and forearm vascular resistance. 3. Tilt did not significantly increase pretreatment plasma renin activity or plasma noradrenaline concentration, nor did it decrease forearm blood flow. Furthermore, captopril did not alter forearm vascular resistance during supine or upright posture. During the phentolamine infusion, however, captopril reduced forearm vascular resistance by 19% (P < 0.05). 4. Despite increased plasma renin activity, captopril did not cause forearm vasodilatation during supine or upright posture in these patients with heart failure. When the contribution of the sympathetic nervous system was eliminated, captopril decreased forearm vascular resistance. Therefore, in patients with congestive heart failure, the sympathetic nervous system is important in limb vasoregulation, and the contribution of the renin-angiotensin system is apparent only after α-adrenergic blockade.

scholarly journals Nifedipine-Sensitive Blood Pressure Component in Hypertensive Models Characterized by High Activity of Either Sympathetic Nervous System or Renin-Angiotensin System

2014 ◽  
pp. 13-26 ◽  
Author(s):  
J. ZICHA ◽  
Z. DOBEŠOVÁ ◽  
M. BEHULIAK ◽  
M. PINTÉROVÁ ◽  
J. KUNEŠ ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Spontaneously Hypertensive ◽  
Renin Angiotensin ◽  
Wide Range ◽  
Voltage Dependent ◽  
Sympathetic Nervous

High blood pressure (BP) of spontaneously hypertensive rats (SHR) is maintained by enhanced activity of sympathetic nervous system (SNS), whereas that of Ren-2 transgenic rats (Ren-2 TGR) by increased activity of renin-angiotensin system (RAS). However, both types of hypertension are effectively attenuated by chronic blockade of L-type voltage-dependent calcium channel (L-VDCC). The aim of our study was to evaluate whether the magnitude of BP response elicited by acute nifedipine administration is proportional to the alterations of particular vasoactive systems (SNS, RAS, NO) known to modulate L-VDCC activity. We therefore studied these relationships not only in SHR, in which mean arterial pressure was modified in a wide range of 100-210 mm Hg by chronic antihypertensive treatment (captopril or hydralazine) or its withdrawal, but also in rats with augmented RAS activity such as homozygous Ren-2 TGR, pertussis toxin-treated SHR or L-NAME-treated SHR. In all studied groups the magnitude of BP response to nifedipine was proportional to actual BP level and it closely correlated with BP changes induced by acute combined blockade of RAS and SNS. BP response to nifedipine is also closely related to the degree of relative NO deficiency. This was true for both SNS- and RAS-dependent forms of genetic hypertension, suggesting common mechanisms responsible for enhanced L-VDCC opening and/or their upregulation in hypertensive animals. In conclusions, BP response to nifedipine is proportional to the vasoconstrictor activity exerted by both SNS and RAS, indicating a key importance of these two pressor systems for actual L-VDCC opening necessary for BP maintenance.

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