Long-term blood pressure control: is there a set-point in the brain?

Nishida, Yasuhiro; Tandai-Hiruma, Megumi; Kemuriyama, Takehito; Hagisawa, Kohsuke

doi:10.1007/s12576-012-0192-0

Cited by 16 publications

(7 citation statements)

References 72 publications

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“…BP regulation is an integrative process that involves complex interactions between the structures of the nervous system, cardiovascular system, hormones, and renal balance of fluids, which are in continuous feedback with specialized receptors related to monitoring the volume and hemodynamic parameters of blood circulation [ 134 ]. ET-1 can raise BP by disturbing some of these regulatory mechanisms (Figure 5), and in particular, maintaining intravascular fluid volume [ 24 , 25 , 135 ], peripheral vascular resistance [ 22 , 136 , 137 ], and cardiac contractility [ 138 , 139 , 140 ].…”

Section: Role Of Et-1 In the Pathogenesis Of Htnmentioning

confidence: 99%

The Causal Relationship between Endothelin-1 and Hypertension: Focusing on Endothelial Dysfunction, Arterial Stiffness, Vascular Remodeling, and Blood Pressure Regulation

Kostov

2021

Life

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Hypertension (HTN) is one of the most prevalent diseases worldwide and is among the most important risk factors for cardiovascular and cerebrovascular complications. It is currently thought to be the result of disturbances in a number of neural, renal, hormonal, and vascular mechanisms regulating blood pressure (BP), so crucial importance is given to the imbalance of a number of vasoactive factors produced by the endothelium. Decreased nitric oxide production and increased production of endothelin-1 (ET-1) in the vascular wall may promote oxidative stress and low-grade inflammation, with the development of endothelial dysfunction (ED) and increased vasoconstrictor activity. Increased ET-1 production can contribute to arterial aging and the development of atherosclerotic changes, which are associated with increased arterial stiffness and manifestation of isolated systolic HTN. In addition, ET-1 is involved in the complex regulation of BP through synergistic interactions with angiotensin II, regulates the production of catecholamines and sympathetic activity, affects renal hemodynamics and water–salt balance, and regulates baroreceptor activity and myocardial contractility. This review focuses on the relationship between ET-1 and HTN and in particular on the key role of ET-1 in the pathogenesis of ED, arterial structural changes, and impaired vascular regulation of BP. The information presented includes basic concepts on the role of ET-1 in the pathogenesis of HTN without going into detailed analyses, which allows it to be used by a wide range of specialists. Also, the main pathological processes and mechanisms are richly illustrated for better understanding.

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Section: Role Of Et-1 In the Pathogenesis Of Htnmentioning

confidence: 99%

The Causal Relationship between Endothelin-1 and Hypertension: Focusing on Endothelial Dysfunction, Arterial Stiffness, Vascular Remodeling, and Blood Pressure Regulation

Kostov

2021

Life

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“…There may also be an indirect effect, as input from baroreceptors (in addition to that from the chemoreceptors) influences the amount of parasympathetic and sympathetic tonic activity upon which breathing can exert its influence [152]. In this context, the effects of baroreceptor stimulation on respiration [153] and the short and long term effects on BP [20, 154, 155] have recently been described in greater detail. The role of low pressure baroreceptors in onset and progression of hypertension in OSA patients remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Chemoreflexes, Sleep Apnea, and Sympathetic Dysregulation

Mansukhani¹,

Kára

Caples

et al. 2014

Curr Hypertens Rep

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Obstructive sleep apnea (OSA) and hypertension are closely linked conditions. Disordered breathing events in OSA are characterized by increasing efforts against an occluded airway whilst asleep, resulting in a marked sympathetic response. This is predominantly due to hypoxemia activating the chemoreflexes, resulting in reflex increases in sympathetic neural outflow. In addition, apnea, and the consequent lack of inhibition of the sympathetic system that occurs with lung inflation during normal breathing, potentiates central sympathetic outflow. Sympathetic activation persists into the daytime, and is thought to contribute to hypertension and other adverse cardiovascular outcomes. This review discusses chemoreflex physiology and sympathetic modulation during normal sleep, as well as the sympathetic dysregulation seen in OSA, its extension into wakefulness, and changes after treatment. Evidence supporting the role of the peripheral chemoreflex in the sympathetic dysregulation seen in OSA, including in the context of co-morbid obesity, metabolic syndrome and systemic hypertension is reviewed. Finally, alterations in cardiovascular variability and other potential mechanisms that might play a role in the autonomic imbalance seen in OSA are also discussed.

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“…Cumulative research over an extensive time span will be necessary to elucidate the changes induced in long-term mechanisms of blood-pressure regulation [ 38 – 40 ] and short-term circulatory functions by these effects of +Gz load and the trained G-load tolerance. Understanding endogenous physiological responses will in turn provide new information and materials leading to further investigations.…”

Section: Discussionmentioning

confidence: 99%

Effects and biological limitations of +Gz acceleration on the autonomic functions-related circulation in rats

Nishida

Maruyama²,

Shouji

et al. 2016

J Physiol Sci

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The effects of gravitational loading (G load) on humans have been studied ever since the early 20th century. After the dangers of G load in the vertical head-to-leg direction (+Gz load) became evident, many animal experiments were performed between 1920 and 1945 in an effort to identify the origins of high G-force-induced loss of consciousness (G-LOC), which led to development of the anti-G suit. The establishment of norms and training for G-LOC prevention resulted in a gradual decline in reports of animal experiments on G load, a decline that steepened with the establishment of anti-G techniques in humans, such as special breathing methods and skeletal muscle contraction, called an anti-G straining maneuver, which are voluntary physiological functions. Because the issue involves humans during flight, the effects on humans themselves are clearly of great importance, but ethical considerations largely preclude any research on the human body that probes to any depth the endogenous physiological states and functions. The decline in reports on animal experiments may therefore signify a general decline in research into the changes seen in the various involuntary, autonomic functions. The declining number of related reports on investigations of physiological autonomic systems other than the circulatory system seems to bear this out. In this review, we therefore describe our findings on the effects of G load on the autonomic nervous system, cardiac function, cerebral blood flow, tissue oxygen level, and other physiological autonomic functions as measured in animal experiments, including denervation or pharmacological blocking, in an effort to present the limits and the mechanisms of G-load response extending physiologically. We demonstrate previously unrecognized risks due to G load, and also describe fundamental research aimed at countering these effects and development of a scientific training measure devised for actively enhancing +Gz tolerance in involuntary, autonomic system functions. The research described here is rough and incomplete, but it is offered as a beginning, in the hope that researchers may find it of reference and carry the effort toward completion. The advances described here include (1) a finding that cerebral arterial perfusion pressure decreases to nearly zero under +5.0 Gz loads, (2) indications that G load may cause myocardial microinjuries, (3) detection of differences between cerebral regions in tissue-oxygen level under +3.0 Gz load, (4) discovery that hypotension is deeper under decreasing +Gz loads than increasing +Gz loads with use of an anti-G system, due in part to suppression of baroreceptor reflex, and (5) revelations and efforts investigating new measures to reduce cerebral hypotension, namely the “teeth-clenching pressor response” and preconditioning with slight but repeated G loads.

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Long-term blood pressure control: is there a set-point in the brain?

Cited by 16 publications

References 72 publications

The Causal Relationship between Endothelin-1 and Hypertension: Focusing on Endothelial Dysfunction, Arterial Stiffness, Vascular Remodeling, and Blood Pressure Regulation

The Causal Relationship between Endothelin-1 and Hypertension: Focusing on Endothelial Dysfunction, Arterial Stiffness, Vascular Remodeling, and Blood Pressure Regulation

Chemoreflexes, Sleep Apnea, and Sympathetic Dysregulation

Effects and biological limitations of +Gz acceleration on the autonomic functions-related circulation in rats

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