Trilostane, FAD286, and the role of aldosterone in the central regulation of blood pressure: focus on “Role of central nervous system aldosterone synthase and mineralocorticoid receptors in salt-induced hypertension in Dahl salt-sensitive rats”

2009 ◽  
Vol 296 (4) ◽  
pp. R992-R993 ◽  
Author(s):  
John W. Funder
Keyword(s):  
Blood Pressure ◽  
Central Nervous System ◽  
Nervous System ◽  
Mineralocorticoid Receptors ◽  
Central Regulation ◽  
Aldosterone Synthase ◽  
Induced Hypertension ◽  
Regulation Of Blood Pressure

scholarly journals Missing pieces of the Piezo1/Piezo2 baroreceptor hypothesis: an autonomic perspective

2019 ◽  
Vol 122 (3) ◽  
pp. 1207-1212 ◽  
Author(s):  
Sean D. Stocker ◽  
Alan F. Sved ◽  
Michael C. Andresen
Keyword(s):  
Blood Pressure ◽  
Central Nervous System ◽  
Arterial Blood Pressure ◽  
Tissue Perfusion ◽  
Cellular Mechanism ◽  
Baroreceptor Function ◽  
Arterial Blood ◽  
The Central Nervous System ◽  
Regulation Of Blood Pressure

Baroreceptors play a pivotal role in the regulation of blood pressure through moment to moment sensing of arterial blood pressure and providing information to the central nervous system to make autonomic adjustments to maintain appropriate tissue perfusion. A recent publication by Zeng and colleagues (Zeng WZ, Marshall KL, Min S, Daou I, Chapleau MW, Abboud FM, Liberles SD, Science 362: 464–467, 2018) suggests the mechanosensitive ion channels Piezo1 and Piezo2 represent the cellular mechanism by which baroreceptor nerve endings sense changes in arterial blood pressure. However, before Piezo1 and Piezo2 are accepted as the sensor of baroreceptors, the question must be asked of what criteria are necessary to establish this and how well the report of Zeng and colleagues (Zeng WZ, Marshall KL, Min S, Daou I, Chapleau MW, Abboud FM, Liberles SD, Science 362: 464–467, 2018) satisfies these criteria. We briefly review baroreceptor function, outline criteria that a putative neuronal sensor of blood pressure must satisfy, and discuss whether the recent findings of Zeng and colleagues suitably meet these criteria. Despite the provocative hypothesis, there are significant concerns regarding the evidence supporting a role of Piezo1/Piezo2 in arterial baroreceptor function.

scholarly journals Role of the Renin-Angiotensin-Aldosterone System in Various Disease Processes: An Overview

2021 ◽  
Author(s):  
Volkan Gelen ◽  
Abdulsamed Kükürt ◽  
Emin Şengül
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Electrolyte Balance ◽  
Physiological System ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Working Principle ◽  
Kidney Liver ◽  
Regulation Of Blood Pressure

The renin-angiotensin-aldosterone system is a physiological system that plays an important role in the regulation of blood pressure and body water-electrolyte balance, in which the kidney, liver and lungs play a role in its activation. This system comes into play in various diseases such as the cardiovascular, renal, pulmonary and nervous system where blood pressure and fluid-electrolyte balance may change. The purpose of this study, which is presented in line with this information, is to explain the working principle of this system, how this system is activated, how it comes into play in the mentioned diseases, and what kind of results occur.

Cocaine inhibits baroreflex control of blood pressure by actions at arterial baroreceptors

1990 ◽  
Vol 258 (4) ◽  
pp. H1244-H1249 ◽  
Author(s):  
M. C. Andresen ◽  
M. Yang ◽  
S. H. Nelson ◽  
O. S. Steinsland
Keyword(s):  
Blood Pressure ◽  
Central Nervous System ◽  
Nervous System ◽  
Aortic Arch ◽  
Local Anesthetic ◽  
Carotid Sinus ◽  
Cardiovascular Responses ◽  
Baroreflex Control ◽  
Baroreceptor Function

Blood pressure and heart rate often increase during cocaine intoxication, but the mechanisms of these cardiovascular responses are poorly understood. The most often suggested theories are central nervous system mechanisms involving the blockade of neuronal transmitter uptake. Cocaine also has potent local anesthetic properties, and in this study we tested the possible role of peripheral actions of cocaine at baroreceptor afferents. Single fiber baroreceptors were recorded using an in vitro preparation of the rat aortic arch. Diameter, pressure, and baroreceptor discharge were recorded. Cocaine perfused through the lumen of the aortic arch at a suprathreshold pressure reduced baroreceptor discharge within 90 s of entering the lumen of the aorta. Slow ramps of pressure elicited complete pressure- and diameter-discharge curves every 5 min. Beginning at about 1 microM, cocaine inhibited baroreceptor function; threshold increased, the maximum discharge decreased, and at 100 microM cocaine, all discharge ceased. The vasodilator nitroprusside or the alpha 1-adrenoreceptor antagonist prazosin did not affect baroreceptor responses to cocaine. In in vivo tests in rabbits, cocaine that perfused through a vascularly isolated carotid sinus reduced the slope of the baroreflex relationship between carotid sinus pressure and systemic mean arterial pressure. Significant depression of baroreceptor function was found at concentrations similar to the plasma cocaine levels measured in clinical studies. The local anesthetic properties of cocaine may be involved in baroreceptor effects. Our studies suggest a possible contributing role of a new site of action of cocaine outside the central nervous system. Compromise of baroreceptor reflexes could facilitate the development of serious cardiovascular complications associated with cocaine abuse.

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