The discovery of the sensory nature of the carotid body dates back to the beginning of the 20th century. Following these seminal discoveries, research into carotid body mechanisms moved forward progressively through the 20th century, with many descriptions of the ultrastructure of the organ and stimulus-response measurements at the level of the whole organ. The later part of 20th century witnessed the first descriptions of the cellular responses and electrophysiology of isolated and cultured type I and type II cells, and there now exist a number of testable hypotheses of chemotransduction. The goal of this article is to provide a comprehensive review of current concepts on sensory transduction and transmission of the hypoxic stimulus at the carotid body with an emphasis on integrating cellular mechanisms with the whole organ responses and highlighting the gaps or discrepancies in our knowledge. It is increasingly evident that in addition to hypoxia, the carotid body responds to a wide variety of blood-borne stimuli, including reduced glucose and immune-related cytokines and we therefore also consider the evidence for a polymodal function of the carotid body and its implications. It is clear that the sensory function of the carotid body exhibits considerable plasticity in response to the chronic perturbations in environmental O2 that is associated with many physiological and pathological conditions. The mechanisms and consequences of carotid body plasticity in health and disease are discussed in the final sections of this article.

Peripheral Chemoreceptors: Function and Plasticity of the Carotid Body

The sections in this article are:


1
Spontaneous Respiratory Variations in the Cardiovascular System
1.1
Arterial Blood Pressure

1.2
Heart Rate

1.3
Cardiac Output

1.4
Systemic Vascular Resistance

1.5
Pulmonary Hemodynamics




2
Central Nervous Control of Respiration and the Cardiovascular System
2.1
Receptors and Afferent Pathways

2.2
Cell Bodies and Efferent Pathways

2.3
Central Control of Sympathetic Efferent Activity

2.4
Descending Pathways to Spinal Sympathetic Outflow




3
Central and Local Peripheral Circulatory Control by Blood Gases
3.1
Central Effects

3.2
Peripheral Effects




4
Some Reflex Neural Control Mechanisms
4.1
Arterial Baroreceptors

4.2
Peripheral Arterial Chemoreceptors

4.3
Upper Airway Receptors

4.4
Facial Receptors

4.5
Cardiopulmonary Receptors

4.6
Overall Involvement of Cardiopulmonary Receptors




5
Reflex Cardiovascular Effects of Lung Inflation
5.1
Cardiac Responses

5.2
Changes in Systemic Vascular Resistance

5.3
Coronary Circulation

5.4
Nature of Pulmonary Receptors




6
Mechanisms of Respiratory Modulation
6.1
Pulmonary Vagal Reflex

6.2
Central Respiratory Neuronal Activity

6.3
Hypocapnia




7
Phasic Respiratory Modulation of Reflex Responses
7.1
Respiration

7.2
Heart Rate




8
Respiratory Modulation of Specific Inputs to Nervous System
8.1
Modulation by Hyperventilation

8.2
Modulation by Reflex Hypoventilation and Apnea

8.3
Interactions Between Carotid Baroreceptors and Chemoreceptors




9
Respiratory Modulation of Vagal and Sympathetic Efferent Fiber Activity
9.1
Activity in Cardiac Vagal Efferent Fibers

9.2
Activity in Sympathetic Efferent Nerves

9.3
Mechanisms of Central Integration




10
Respiratory Sinus Arrhythmia
10.1
Mechanisms




11
Some Examples of Respiratory-Circulatory Integrative Control
11.1
Effects of Deep Breath

11.2
Valsalva Maneuver

11.3
Acute Hypoxia

11.4
Hypocapnia

11.5
Hypercapnia

11.6
Asphyxia and Breath Holding

11.7
Breath-Hold Diving




12
Effects of Changes in the Cardiovascular System on Respiration
12.1
Respiration, Metabolism, and Cardiac Output

12.2
Hemorrhagic Hypotension




13
Medical Implications of Respiratory-Cardiovascular Interactions
13.1
Diving Response

13.2
Protective Effects of Defense Mechanisms

13.3
Exaggerated Defense Responses

13.4
Restoration of Normal Cardiac Rhythm

13.5
Sudden Infant Death Syndrome

Interactions Between Respiration and Circulation

During dynamic exercise, mechanisms controlling the cardiovascular apparatus operate to provide adequate oxygen to fulfill metabolic demand of exercising muscles and to guarantee metabolic end-products washout. Moreover, arterial blood pressure is regulated to maintain adequate perfusion of the vital organs without excessive pressure variations. The autonomic nervous system adjustments are characterized by a parasympathetic withdrawal and a sympathetic activation. In this review, we briefly summarize neural reflexes operating during dynamic exercise. The main focus of the present review will be on the central command, the arterial baroreflex and chemoreflex, and the exercise pressure reflex. The regulation and integration of these reflexes operating during dynamic exercise and their possible role in the pathophysiology of some cardiovascular diseases are also discussed.

/pdf/neural-regulation-of-cardiovascular-response-to-exercise-wpfcnhbha6.pdf

Neural regulation of cardiovascular response to exercise: role of central command and peripheral afferents.

The pattern of breathing during a hyperthermia-induced hyperventilation varies across different species. Thermal tachypnea is a first phase panting response adopted during hyperthermia when tidal volume is minimized and the frequency of breathing is maximized. Blood-gas tensions and pH are maintained during this hyperventilation, and the associated heat loss helps the animal regulate its body temperature. A second pattern of breathing adopted in hyperthermia is thermal hyperpnea; this response is the focus of this review. This form of hyperventilation is evident after an increase in core temperature and it is apparent in humans. Increases of tidal volume as well as frequency of breathing are evident during this response that results in a respiratory alkalosis. The cause of thermal hyperpnea is not resolved; evidence of the potential mechanisms underlying this response support that modulators of the response act in either a multiplicative or additive manner with body temperatures. The details of the designs and methodologies of the studies supporting or refuting these two views are discussed. A physiological rationale for thermal hyperpnea is presented in which it is suggested this response serves a heat-loss role and contributes to selective brain cooling in hyperthermic humans. Ongoing research in this area is focused on resolving the mechanisms underlying thermal hyperpnea and its contribution to cranial thermoregulation. The direct application of this research is for the care of febrile and hyperthermic patients.

Components and mechanisms of thermal hyperpnea

The influence of severe passive heat stress and hypohydration (Hypo) on cardiorespiratory and cerebrovascular function is not known. We hypothesized that 1) heating-induced hypocapnia and periphera...

https://www.physiology.org/doi/pdf/10.1152/japplphysiol.00010.2008

Human cardiorespiratory and cerebrovascular function during severe passive hyperthermia: effects of mild hypohydration.

Effects of temperature on carotid chemoreceptor and baroreceptor activity.

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Effects of temperature on carotid chemoreceptor and baroreceptor activity.