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Lateral Parafacial Neurons Evoked Expiratory Oscillations Driving Neurogenic Hypertension
Karolyne S Magalhães1, Renato W Martins Sá1, Nathalia Salim1
1Department of Physiology, School of Medicine of Ribeirão Preto (K.S.M., R.W.M.S., N.S., T.M.S., B.H.M.), University of São Paulo, Brazil.
Excessive sympathetic activity contributes to uncontrolled hypertension. Silencing specific medullary neurons (pFL) reduced blood pressure in hypertensive rats, suggesting a therapeutic target.
Area of Science:
- Neuroscience
- Cardiovascular Physiology
- Hypertension Research
Background:
- Hypertension is a major cardiovascular risk factor with poor control in 40% of treated patients.
- Excessive sympathetic activity is implicated as a key contributor to uncontrolled hypertension.
- Neuronal expiratory oscillations in the medullary lateral parafacial (pFL) region are hypothesized to be activated in neurogenic hypertension.
Purpose of the Study:
- To investigate the role of pFL neuronal activity in neurogenic hypertension.
- To determine if silencing pFL neurons exerts an antihypertensive effect.
Main Methods:
- pFL neurons were manipulated using optogenetics and pharmacogenetics in rats.
- Sympathetic activity, respiratory motor outputs, and arterial pressure were recorded in normotensive and hypertensive rats.
- Neurogenic hypertension was induced via chronic intermittent hypoxia.
Main Results:
- Activation of pFL neurons increased sympathetic activity and blood pressure.
- pFL neurons project to and excite RVLM and A5 presympathetic neurons.
- Inhibition of pFL neurons normalized arterial pressure in hypertensive rats by reducing sympatho-excitation.
Conclusions:
- Heightened sympathetic activity in hypoxia-induced hypertension involves pFL expiratory oscillations.
- pFL neurons drive RVLM and A5 sympathetic neurons, causing active expiration and hypertension.
- Suppression of pFL neurons demonstrates therapeutic potential for hypertension treatment.
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