Specific Respiratory Neuron Types Have Increased Excitability That Drive Presympathetic Neurones in Neurogenic Hypertension

Autor(es)

Moraes, Davi J. A. ^{[1, 2]} ; Machado, Benedito H. ^[2] ; Paton, Julian F. R. ^[1]

Afiliação do(s) autor(es)

^[1] Univ Bristol, Sch Physiol & Pharmacol, Bristol Heart Inst, Bristol BS8 1TD, Avon - England

^[2] Univ Sao Paulo, Sch Med Ribeirao Preto, Dept Physiol, BR-14049900 Ribeirao Preto, SP - Brazil

• Tipo de documento: Artigo Científico
• Fonte: Hypertension; v. 63, n. 6, p. 1309-1318, JUN 2014.
• Citações Web of Science: 44

Resumo

Hyperventilation and reduced cerebral blood flow velocity can occur in postural tachycardia syndrome (POTS). We studied orthostatically intolerant patients, with suspected POTS, with a chief complaint of upright dyspnea. On the basis of our observations of an immediate reduction of cerebral blood flow velocity with orthostasis, we hypothesize that the resulting ischemic hypoxia of the carotid body causes chemoreflex activation, hypocapnic hyperpnea, sympathetic activation, and increased heart rate and blood pressure in this subset of POTS. We compared 11 dyspneic POTS subjects with 10 healthy controls during a 70 degrees head-up tilt. In POTS subjects during initial orthostasis before blood pressure recovery; central blood volume and mean arterial pressure were reduced (P<0.025), resulting in a significant (P<0.001) decrease in cerebral blood flow velocity, which temporally preceded (17 +/- 6 s; P<0.025) a progressive increase in minute ventilation and decrease in end tidal CO2 (P<0.05) when compared with controls. Sympathoexcitation, measured by muscle sympathetic nerve activity, was increased in POTS (P<0.01) and inversely proportional to end tidal CO2 and resulted in an increase in heart rate (P<0.001), total peripheral resistance (P<0.025), and a decrease in cardiac output (P<0.025). The decrease in cerebral blood flow velocity and mean arterial pressure during initial orthostasis was greater (P<0.025) in POTS. Our data suggest that exaggerated initial central hypovolemia during initial orthostatic hypotension in POTS results in reduced cerebral blood flow velocity and postural hypocapnic hyperpnea that perpetuates cerebral ischemia. We hypothesize that sustained hypocapnia and cerebral ischemia produce sympathoexcitation, tachycardia, and a statistically significant increase in blood pressure. (AU)

• Processo FAPESP: 09/50113-0 - Transmissão sináptica em neurônios envolvidos na geração e modulação das atividades simpática e respiratória na hipoxia
• Beneficiário: Benedito Honorio Machado
• Linha de fomento: Auxílio à Pesquisa - Temático
• Processo FAPESP: 11/24050-1 - Caracterização dos mecanismos celulares no tronco encefálico envolvidos nas alterações simpática e respiratória de ratos jovens submetidos à hipóxia crônica intermitente
• Beneficiário: Davi José de Almeida Moraes
• Linha de fomento: Bolsas no Brasil - Pós-Doutorado