Nociceptive pulmonary‐cardiac reflexes are altered in the spontaneously hypertensive rat

Abstract

Key pointsr We investigated the cardiovascular and respiratory responses of the normotensive Wistar-Kyoto (WKY) rat and the spontaneously hypertensive (SH) rat to inhalation and intravenous injection of the noxious stimuli allyl isothiocyanate (AITC).r AITC inhalation evoked atropine-sensitive bradycardia in conscious WKY rats, and evoked atropine-sensitive bradycardia and atenolol-sensitive tachycardia with premature ventricular contractions (PVCs) in conscious SH rats.r Intravenous injection of AITC evoked bradycardia but no tachycardia/PVCs in conscious SHs, while inhalation and injection of AITC caused similar bradypnoea in conscious SH and WKY rats.r Anaesthesia (inhaled isoflurane) inhibited the cardiac reflexes evoked by inhaled AITC but not injected AITC.r Data indicate the presence of a de novo nociceptive pulmonary-cardiac reflex triggering sympathoexcitation in SH rats, and this reflex is dependent on vagal afferents but is not due to steady state blood pressure or due to remodelling of vagal efferent function.Abstract Inhalation of noxious irritants/pollutants activates airway nociceptive afferents resulting in reflex bradycardia in healthy animals. Nevertheless, noxious pollutants evoke sympathoexcitation (tachycardia, hypertension) in cardiovascular disease patients. We hypothesize that cardiovascular disease alters nociceptive pulmonary-cardiac reflexes. Here, we studied reflex responses to irritants in normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive (SH) rats. Inhaled allyl isothiocyanate (AITC) evoked atropine-sensitive bradycardia with atrial-ventricular (AV) block in conscious WKY rats, thus indicating a parasympathetic reflex. Conversely, inhaled AITC in conscious SH rats evoked complex brady-tachycardia J. Shane Hooper completed his BS in biology at the University of South Carolina and attaining a Professional Science Masters in biotechnology at the University of South Florida led him to realize that his scientific career would be in the field of research. He stayed at USF to complete his PhD studying arrhythmia evoked by airway nociceptive reflexes in healthy and cardiovascular diseased rats. He has learned that his true passion is in doing in vivo research and perfecting the required surgical procedures. His biggest challenge and future aspirations are to understand how cardiovascular disease alters neuronal interactions between the lungs and the heart. 3256 J. S. Hooper and others J Physiol 597.13with both AV block and premature ventricular contractions (PVCs). Atropine abolished the bradycardia and AV block, but the atropine-insensitive tachycardia and PVCs were abolished by the β 1 -adrenoceptor antagonist atenolol. The aberrant AITC-evoked reflex in SH rats was not reduced by acute blood pressure reduction by captopril. Surprisingly, intravenous AITC only evoked bradycardia in conscious SH and WKY rats. Furthermore, anaesthesia reduced the cardiac reflexes evoked by inhaled but not injected AITC. Nevertheless, anaesthesia had little effect on AITC-evoked respiratory ...

Nociceptive pulmonary‐cardiac reflexes: role of autonomic nervous system and hypertension

“…In SH rats, inhalation of AITC increased the time spent in bradypnoea but did not decrease breathing rate. Unlike the effects of AITC inhalation already mentioned, the injection of AITC did not induce tachyarrhythmia in Hooper et al (2019) carried out precollicular decerebration of the SH rats, during which they were atropinized, subjected to neuromuscular blockade and mechanically ventilated. Under these conditions, inhalation of AITC caused hypertension and decreased RRi.…”

“…Inhalation of pollutants results in cardiovascular system responses through a reflex, directly related to the respiratory system, in which nociceptive afferents of the lower airways trigger responses in cardiac function. This reflex called the nociceptive cardiopulmonary reflex is largely controlled by ANS (Hooper et al 2019). Although there is ample evidence regarding the impact of this reflex on healthy animals, the effects of pollution on the modulation of cardiac function in CVD remain unclear.…”

“…Although there is ample evidence regarding the impact of this reflex on healthy animals, the effects of pollution on the modulation of cardiac function in CVD remain unclear. In this sense, looking to fill this gap in the literature, Hooper et al (2019) investigated whether a pre-existing CVD -hypertension -modifies nociceptive pulmonary-cardiac reflexes. This study was recently published in The Journal of Physiology and has gained our interest.…”

“…Using spontaneously hypertensive (SH) and Wistar-Kyoto (WKY) rats, Hooper et al (2019) performed an elegant and meticulous experimental design to explore the mechanisms involved in the cardiopulmonary reflex against inhalation of noxious substances. For this, diaphragmatic electromyography (dEMG) and electrocardiogram radiotelemetry (ECG) were used.…”

“…The findings of this study elucidate mechanisms involved in the reflex regulation of heart rate evoked by cardiopulmonary irritants, complementing the literature data that emphasize the autonomic imbalance in hypertension. The data presented by Hooper et al (2019) are especially important when for the first time a study showed that inhalation of TRPA1 and TRPV1 agonists culminates in different cardiorespiratory responses in normotensive and hypertensive rats, and these effects are modulated by ANS. An article previously published by the same research group had shown that AITC caused substantial bradycardia with prolonged RRi, in Sprague-Dawley rats (Hooper et al 2016).…”