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

1. We examined interactions between haemodynamic and autonomic neural oscillations during passive upright tilt, to gain better insight into human autonomic regulatory mechanisms. 2. We recorded the electrocardiogram, finger photoplethysmographic arterial pressure, respiration and peroneal nerve muscle sympathetic activity in nine healthy young adults. Subjects breathed in time with a metronome at 12 breaths min-1 (0.2 Hz) for 5 min each, in supine, and 20, 40, 60, 70 and 80 deg head-up positions. We performed fast Fourier transform (and autoregressive) power spectral analyses and integrated low-frequency (0.05-0.15 Hz) and respiratory-frequency (0. 15-0.5 Hz) spectral powers. 3. Integrated areas of muscle sympathetic bursts and their low- and respiratory-frequency spectral powers increased directly and significantly with the tilt angle. The centre frequency of low-frequency sympathetic oscillations was constant before and during tilt. Sympathetic bursts occurred more commonly during expiration than inspiration at low tilt angles, but occurred equally in expiration and inspiration at high tilt angles. 4. Systolic and diastolic pressures and their low- and respiratory-frequency spectral powers increased, and R-R intervals and their respiratory-frequency spectral power decreased progressively with the tilt angle. Low-frequency R-R interval spectral power did not change. 5. The cross-spectral phase angle between systolic pressures and R-R intervals remained constant and consistently negative at the low frequency, but shifted progressively from positive to negative at the respiratory frequency during tilt. The arterial baroreflex modulus, calculated from low-frequency cross-spectra, decreased at high tilt angles. 6. Our results document changes of baroreflex responses during upright tilt, which may reflect leftward movement of subjects on their arterial pressure sympathetic and vagal response relations. The intensity, but not the centre frequency of low-frequency cardiovascular rhythms, is modulated by the level of arterial baroreceptor input. Tilt reduces respiratory gating of sympathetic and vagal motoneurone responsiveness to stimulatory inputs for different reasons; during tilt, sympathetic stimulation increases to a level that overwhelms the respiratory gate, and vagal stimulation decreases to a level below that necessary for maximal respiratory gating to occur.

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1111/j.1469-7793.1999.0617t.x

Human responses to upright tilt: a window on central autonomic integration

In patients with autonomic failure orthostatic hypotension results from an impaired capacity to increase vascular resistance during standing. This fundamental defect leads to increased downward pooling of venous blood and a consequent reduction in stroke volume and cardiac output that exaggerates the orthostatic fall in blood pressure. The location of excessive venous blood pooling has not been established so far, but present data suggest that the abdominal compartment and perhaps leg skin vasculature are the most likely candidates. To improve the orthostatic tolerance in patients with autonomic failure, protective measures that reduce excessive orthostatic blood pooling have been developed and evaluated. These measures include physical counter-manoeuvres and abdominal compression.

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1111/j.1469-7793.1999.0001o.x

Pathophysiological basis of orthostatic hypotension in autonomic failure

Background Baroreflexes originate in the great vessels of the neck and thorax and prevent arterial pressure from rising or falling excessively. Methods This study was undertaken to clarify the cause, clinical spectrum, and therapy of this disorder. We studied 11 patients with baroreflex failure presenting as severe, labile hypertension and hypotension, often with headache, diaphoresis, and emotional instability, and characterized by the failure of exogenous vasoactive substances to alter heart rate. Each underwent hemodynamic monitoring and biochemical, physiologic, and pharmacologic testing. Results The patients' maximal systolic blood pressures ranged from 164 to 280 mm Hg, and their minimal systolic pressures ranged from 58 to 96 mm Hg. Plasma norepinephrine and epinephrine concentrations were sometimes many times normal during blood-pressure surges. All the patients had excessive pressor and tachycardic responses to the mental-arithmetic and cold pressor tests and marked hypersensitivity to clonidine....

The diagnosis and treatment of baroreflex failure.

Hypertension, heart failure (HF), type II diabetes mellitus, and chronic kidney disease represent significant and growing global health issues.1 The rates of control of blood pressure and the therapeutic efforts to prevent progression of HF, chronic kidney disease, diabetes mellitus, and their sequelae remain unsatisfactory.2–5 Although patient nonadherence and nonpersistence with medications participate in this failure, especially in asymptomatic disorders, the inherent complexity of drug titration, drug interactions, and both the real and perceived adverse events collectively contribute to the failure of lifelong polypharmacy. Furthermore, therapy targeting the potentially unique contribution of autonomic imbalance is limited by the poorly tolerated systemic adverse effects of adrenergic blocking agents. Recent introduction of medical procedures, such as renal denervation,6,7 and devices such as deep brain stimulation,8 baroreceptor stimulation,9 and direct vagus nerve stimulation10 begin to address these gaps in selective patients.

The contribution of excessive sympathetic nerve activity to the development and progression of hypertension, insulin resistance, and HF has been demonstrated in both preclinical and human experiments. Preclinical experiments in models of these diseases have successfully used sympathetic or parasympathetic modifications to alter the time course of their progression.11,12 Reduction of blood pressure after dorsal rhizotomy in rats with renal hypertension and reduced total body noradrenaline and muscle sympathetic nerve activity in humans after renal denervation confirm that the afferent signals from the kidney underlie some of the excessive sympathetic drive seen in these states.13,14 However, additional afferent signals may arise from sites elsewhere in the body and in particular the carotid body (CB). We propose targeting the CB in patients with increased chemosensitivity to address the underlying autonomic imbalance seen in hypertension, HF, insulin resistance, and chronic kidney disorders.

### The CB: A Peripheral Chemosensor

The CB (Figure 1), the dominant …

The Carotid Body as a Therapeutic Target for the Treatment of Sympathetically Mediated Diseases

The subjects were two hospital patients with long-established bronchial asthma. Their histories and clinical condition have been described elsewhere (Wood, Frankland & Eastcott, 1965). The clinical details are largely irrelevant to the present paper since each subject was tested before operation and thus provided control observations. Subject A (patient 2 of Wood et al. 1965) was a woman of 53 and subject B (patient 3 of Wood et al. 1965) was a man of 44. A box bag respirator (Donald & Christie, 1949) was used to administer gas mixtures for periods of up to 4 min each and to record tidal volume and respiratory frequency. The gas mixtures were saturated with water vapour at room temperature and had the following composition: room air, 100% oxygen, 10% oxygen in nitrogen, 3% carbon dioxide in air and 6% carbon dioxide in air. 10% oxygen was usually administered twice on each occasion. On some occasions arterial oxygen saturation was recorded with an Atlas ear oximeter which was calibrated against samples of arterial blood analysed by manometric Van Slyke estimations and was accurate to within + 4 %. Arterial blood pressure and pulse rate were measured at frequent intervals by auscultation and palpation respectively or by a Sanborn pressure transducer and recorder through a needle in the brachial artery. The frequency response was accurate from 0.5 to 15 c/s. Passive changes in posture were produced by tilting the subject on an Eve rocker which had been modified to allow a vertical position. Valsalva mannsuvres were performed by the subject blowing against a mercury column.

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1113/jphysiol.1965.sp007767

The effects of bilateral removal of the carotid bodies and denervation of the carotid sinuses in two human subjects.

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The effects of bilateral removal of the carotid bodies and denervation of the carotid sinuses in two human subjects.