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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Post-mortem studies of the carotid bodies of 62 humans were carried out using light microscopic and morphometric methods. According to the clinical and autopsic data the subjects were divided into 5 groups: normotensives, essential hypertensives, renal hypertensives, chronically hypoxic persons with severe lung diseases, and people who suffered from both lung diseases and essential hypertension. Carotid body volume showed age-dependence in the normotensive group; the biggest glomera carotici were found at an age of 40-60 years, whereas younger and older people exhibited smaller carotid bodies. In the group with the essential hypertensives only old patients exhibited enlarged carotid bodies. In younger essential hypertensives but also in the renal hypertensives an increase of carotid body size was not demonstrable. The people with severe lung diseases regularly had greater carotid bodies when compared with age-matched normotensive subjects. In addition, chronically hypoxic patients had a proliferation of type II cells, perhaps with involvement of Schwann cells and fibrocytes. This increases of elongated cells was only seldom observed in the other groups. The results are discussed with respect to the alterations known so far of arterial chemoreceptor function and reflex effects in systemic arterial hypertension.
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PMID:Morphological findings at the carotid bodies of humans suffering from different types of systemic hypertension or severe lung diseases. 375 31

Lung ventilation fluctuates widely with behavior but arterial PCO2 remains stable. Under normal conditions, the chemoreflexes contribute to PaCO2 stability by producing small corrective cardiorespiratory adjustments mediated by lower brainstem circuits. Carotid body (CB) information reaches the respiratory pattern generator (RPG) via nucleus solitarius (NTS) glutamatergic neurons which also target rostral ventrolateral medulla (RVLM) presympathetic neurons thereby raising sympathetic nerve activity (SNA). Chemoreceptors also regulate presympathetic neurons and cardiovagal preganglionic neurons indirectly via inputs from the RPG. Secondary effects of chemoreceptors on the autonomic outflows result from changes in lung stretch afferent and baroreceptor activity. Central respiratory chemosensitivity is caused by direct effects of acid on neurons and indirect effects of CO2 via astrocytes. Central respiratory chemoreceptors are not definitively identified but the retrotrapezoid nucleus (RTN) is a particularly strong candidate. The absence of RTN likely causes severe central apneas in congenital central hypoventilation syndrome. Like other stressors, intense chemosensory stimuli produce arousal and activate circuits that are wake- or attention-promoting. Such pathways (e.g., locus coeruleus, raphe, and orexin system) modulate the chemoreflexes in a state-dependent manner and their activation by strong chemosensory stimuli intensifies these reflexes. In essential hypertension, obstructive sleep apnea and congestive heart failure, chronically elevated CB afferent activity contributes to raising SNA but breathing is unchanged or becomes periodic (severe CHF). Extreme CNS hypoxia produces a stereotyped cardiorespiratory response (gasping, increased SNA). The effects of these various pathologies on brainstem cardiorespiratory networks are discussed, special consideration being given to the interactions between central and peripheral chemoreflexes.
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PMID:Regulation of breathing and autonomic outflows by chemoreceptors. 2542 53