Inter-Relationship of Sympathetic Nervous System and Renin-Angiotensin-Aldosterone System in three Renin Subgroups of Borderline and Persistent Essential Hypertension

1981 ◽  
Vol 3 (6) ◽  
pp. 1091-1107 ◽  
Author(s):  
Keiji Mikami ◽  
Tetsuo Nishikawa ◽  
Yasushi Tamura ◽  
Akira Kumagai
Keyword(s):  
Nervous System ◽  
Essential Hypertension ◽  
Sympathetic Nervous System ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Sympathetic Nervous ◽  
Relationship Of

scholarly journals MicroRNAs Regulating Renin–Angiotensin–Aldosterone System, Sympathetic Nervous System and Left Ventricular Hypertrophy in Systemic Arterial Hypertension

Biomolecules ◽  
2021 ◽  
Vol 11 (12) ◽  
pp. 1771
Author(s):  
Alex Cleber Improta-Caria ◽  
Marcela Gordilho Aras ◽  
Luca Nascimento ◽  
Ricardo Augusto Leoni De Sousa ◽  
Roque Aras-Júnior ◽  
...  
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Left Ventricular Hypertrophy ◽  
Signaling Pathways ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Gene And Protein Expression ◽  
Sympathetic Nervous

MicroRNAs are small non-coding RNAs that regulate gene and protein expression. MicroRNAs also regulate several cellular processes such as proliferation, differentiation, cell cycle, apoptosis, among others. In this context, they play important roles in the human body and in the pathogenesis of diseases such as cancer, diabetes, obesity and hypertension. In hypertension, microRNAs act on the renin–angiotensin–aldosterone system, sympathetic nervous system and left ventricular hypertrophy, however the signaling pathways that interact in these processes and are regulated by microRNAs inducing hypertension and the worsening of the disease still need to be elucidated. Thus, the aim of this review is to analyze the pattern of expression of microRNAs in these processes and the possible associated signaling pathways.

Control of Sodium Excretion: The Kidney Produces Under Pressure

Physiology ◽  
1987 ◽  
Vol 2 (1) ◽  
pp. 26-29
Author(s):  
FG Knox ◽  
JP Granger
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Sodium Excretion ◽  
Sodium Intake ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Regulatory Systems ◽  
Sympathetic Nervous ◽  
Effector Mechanisms

Sodium excretion is controlled by an integration of physical, neural, and hormonal regulatory systems. The major systems involved in retention of sodium include the renin-angiotensin-aldosterone system and the sympathetic nervous system. In response to increased sodium intake, the sodium-retaining systems are inhibited and natriuretic hormones are activated. Pressures and flows within the microcirculation of the kidney, in concert with neural and hormonal systems, are important effector mechanisms that work to regulate sodium excretion.

scholarly journals Neurohormonal Regulation of I Ks in Heart Failure: Implications for Ventricular Arrhythmogenesis and Sudden Cardiac Death

2020 ◽  
Vol 9 (18) ◽  
Author(s):  
Tyler Shugg ◽  
Andy Hudmon ◽  
Brian R. Overholser
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Potassium Current ◽  
Slow Component ◽  
Delayed Rectifier ◽  
Electrical Remodeling ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Delayed Rectifier Potassium Current ◽  
Sympathetic Nervous

Abstract Heart failure (HF) results in sustained alterations in neurohormonal signaling, including enhanced signaling through the sympathetic nervous system and renin‐angiotensin‐aldosterone system pathways. While enhanced sympathetic nervous system and renin‐angiotensin‐aldosterone system activity initially help compensate for the failing myocardium, sustained signaling through these pathways ultimately contributes to HF pathophysiology. HF remains a leading cause of mortality, with arrhythmogenic sudden cardiac death comprising a common mechanism of HF‐related death. The propensity for arrhythmia development in HF occurs secondary to cardiac electrical remodeling that involves pathological regulation of ventricular ion channels, including the slow component of the delayed rectifier potassium current, that contribute to action potential duration prolongation. To elucidate a mechanistic explanation for how HF‐mediated electrical remodeling predisposes to arrhythmia development, a multitude of investigations have investigated the specific regulatory effects of HF‐associated stimuli, including enhanced sympathetic nervous system and renin‐angiotensin‐aldosterone system signaling, on the slow component of the delayed rectifier potassium current. The objective of this review is to summarize the current knowledge related to the regulation of the slow component of the delayed rectifier potassium current in response to HF‐associated stimuli, including the intracellular pathways involved and the specific regulatory mechanisms.

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