About this Research Topic
This Research Topic is associated with the 55th Annual Congress of the Brazilian Society of Physiology, exceptionally held online, 4-8 October.
Cardiorespiratory control is continuously adapted to changes in the metabolic, environmental, behavioral and developmental conditions of an organism. Any factor altering cardiorespiratory control can become detrimental to the organism, thus making cardiorespiratory control a core issue in physiology and pathophysiology. This Research Topic will highlight the cellular and network mechanisms that underlie cardiorespiratory control and their clinical implications. Recent advances in neurobiology have provided novel insights into the cellular and network mechanisms that underlie cardiorespiratory control. The use of slices, in situ and in vivo preparations, combined with modern genetic, molecular and optogenetic techniques have lead to a new level of understanding of the mechanisms that govern not only the normal physiological integration of cardiovascular and respiratory functions, but also the mechanisms that lead to pathologies such as those seen in sleep apnea, hypertension, CCHS or Sudden Infant Death Syndrome and Neurological diseases.
The Burden of Systemic Hypertension
It is estimated that worldwide there are 1 billion people with systemic hypertension (i.e., high blood pressure in the arterial vessels throughout the body). Systemic hypertension is a powerful independent predisposing factor for development of cardiovascular diseases, such as coronary heart disease, atrial fibrillation, stroke, peripheral artery disease, and heart failure. Furthermore, systemic hypertension has a relevant impact on other diseases than those of the cardiovascular system. An example is that systemic hypertension is the most common comorbidity of patients with chronic obstructive pulmonary disease, affecting approximately 60% of the patients. Therefore, collectively, available evidence supports that systemic hypertension is an important public-health challenge worldwide, and that its prevention, detection, treatment, and control should receive high priority. However, systemic hypertension remains a difficult condition to adequately control, and there is a pressing need for further understanding of hypertension pathophysiology, as well as for the development of novel therapeutic strategies.
Systemic Hypertension and the Neurogenic Hypothesis
Several mechanisms regulate the arterial pressure. One of the mechanisms is the control of blood vessels by sympathetic nerves. There is accumulating evidence indicating an association between elevated sympathetic vasoconstriction in both humans and primary systemic hypertension (i.e., arterial pressure increases independently of other diseases), as well as secondary systemic hypertension due to a primary kidney dysfunction (i.e., renovascular systemic hypertension). There is also persuasive evidence that sympathetic activation could play a causative role in triggering and sustaining the hypertensive state. Furthermore, sympathetic over-activity has been implicated in the initiation and progression of many pathophysiological processes independent of increases in arterial pressure (e.g., cardiac and vascular hypertrophy, atherosclerosis, and glomerulosclerosis).
Respiratory-sympathetic Coupling
It has been known since the earliest direct recordings that sympathetic nerve activity shows respiratory modulation, which is generated in large part by central neural circuits. Superimposed on these central neuronal circuits are modulatory feedback signals from cardiorespiratory sensory afferents (lung-stretch receptors, baroreceptors, central and peripheral chemoreceptors). Respiratory-sympathetic coupling is predominant in recordings of sympathetic nerve activity in rats, cats, and humans. However, the exact pattern of respiratory modulation of sympathetic nerve activity in both species and target organ specific. This respiratory modulation of vasomotor sympathetic outflow causes phasic changes in arteriolar smooth muscle tone, thus generating Traube–Hering arterial pressure waves. Although variations in arterial pressure with breathing are a normal phenomenon occurring in all vertebrates, excessive arterial pressure variability can cause damage to the delicate blood vessels of the kidneys, brain, and heart. Noteworthy, Dr. Eduardo Colombari’s study showed that dysfunctional respiratory-sympathetic coupling mediates the onset of renovascular systemic hypertension in rats submitted to kidney hypo-perfusion [2 kidneys, 1 clip model (2K1C)].
This Research Topic, as Integrative Physiology, will provide an excellent overview of the integration among systems (Cardiovascular, Respiratory and SNC, for instance) in normal and/or physiological adaptation during “stress” situation such as hypertension, obesity, respiratory syndromes, etc. Indeed, This Research Topic will be much appreciated from basic to clinical researchers, highlighting Frontiers publications and reading.
Cardiorespiratory control is continuously adapted to changes in the metabolic, environmental, behavioral and developmental conditions of an organism. Any factor altering cardiorespiratory control can become detrimental to the organism, thus making cardiorespiratory control a core issue in physiology and pathophysiology. This Research Topic will highlight the cellular and network mechanisms that underlie cardiorespiratory control and their clinical implications. Recent advances in neurobiology have provided novel insights into the cellular and network mechanisms that underlie cardiorespiratory control. The use of slices, in situ and in vivo preparations, combined with modern genetic, molecular and optogenetic techniques have lead to a new level of understanding of the mechanisms that govern not only the normal physiological integration of cardiovascular and respiratory functions, but also the mechanisms that lead to pathologies such as those seen in sleep apnea, hypertension, CCHS or Sudden Infant Death Syndrome and Neurological diseases.
The Burden of Systemic Hypertension
It is estimated that worldwide there are 1 billion people with systemic hypertension (i.e., high blood pressure in the arterial vessels throughout the body). Systemic hypertension is a powerful independent predisposing factor for development of cardiovascular diseases, such as coronary heart disease, atrial fibrillation, stroke, peripheral artery disease, and heart failure. Furthermore, systemic hypertension has a relevant impact on other diseases than those of the cardiovascular system. An example is that systemic hypertension is the most common comorbidity of patients with chronic obstructive pulmonary disease, affecting approximately 60% of the patients. Therefore, collectively, available evidence supports that systemic hypertension is an important public-health challenge worldwide, and that its prevention, detection, treatment, and control should receive high priority. However, systemic hypertension remains a difficult condition to adequately control, and there is a pressing need for further understanding of hypertension pathophysiology, as well as for the development of novel therapeutic strategies.
Systemic Hypertension and the Neurogenic Hypothesis
Several mechanisms regulate the arterial pressure. One of the mechanisms is the control of blood vessels by sympathetic nerves. There is accumulating evidence indicating an association between elevated sympathetic vasoconstriction in both humans and primary systemic hypertension (i.e., arterial pressure increases independently of other diseases), as well as secondary systemic hypertension due to a primary kidney dysfunction (i.e., renovascular systemic hypertension). There is also persuasive evidence that sympathetic activation could play a causative role in triggering and sustaining the hypertensive state. Furthermore, sympathetic over-activity has been implicated in the initiation and progression of many pathophysiological processes independent of increases in arterial pressure (e.g., cardiac and vascular hypertrophy, atherosclerosis, and glomerulosclerosis).
Respiratory-sympathetic Coupling
It has been known since the earliest direct recordings that sympathetic nerve activity shows respiratory modulation, which is generated in large part by central neural circuits. Superimposed on these central neuronal circuits are modulatory feedback signals from cardiorespiratory sensory afferents (lung-stretch receptors, baroreceptors, central and peripheral chemoreceptors). Respiratory-sympathetic coupling is predominant in recordings of sympathetic nerve activity in rats, cats, and humans. However, the exact pattern of respiratory modulation of sympathetic nerve activity in both species and target organ specific. This respiratory modulation of vasomotor sympathetic outflow causes phasic changes in arteriolar smooth muscle tone, thus generating Traube–Hering arterial pressure waves. Although variations in arterial pressure with breathing are a normal phenomenon occurring in all vertebrates, excessive arterial pressure variability can cause damage to the delicate blood vessels of the kidneys, brain, and heart. Noteworthy, Dr. Eduardo Colombari’s study showed that dysfunctional respiratory-sympathetic coupling mediates the onset of renovascular systemic hypertension in rats submitted to kidney hypo-perfusion [2 kidneys, 1 clip model (2K1C)].
This Research Topic, as Integrative Physiology, will provide an excellent overview of the integration among systems (Cardiovascular, Respiratory and SNC, for instance) in normal and/or physiological adaptation during “stress” situation such as hypertension, obesity, respiratory syndromes, etc. Indeed, This Research Topic will be much appreciated from basic to clinical researchers, highlighting Frontiers publications and reading.
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
