Component Of Exercise Pressor Reflex Research Articles

Mineralocorticoid receptor antagonists attenuate exaggerated exercise pressor reflex responses in hypertensive rats.

Exaggerated heart rate (HR) and blood pressure responses to exercise in hypertension are mediated, in part, by overactivity of the exercise pressor reflex (EPR). The mechanisms underlying this EPR dysfunction have not been fully elucidated. Previous studies have shown that stimulation of mineralocorticoid receptors (MRs) with exogenous administration of aldosterone in normal, healthy rats reproduces the EPR overactivity characteristic of hypertensive animals. Conversely, the purpose of this study was to examine whether antagonizing MR with spironolactone (SPIR) or eplerenone (EPL) in decerebrated hypertensive rats ameliorates abnormal EPR function. Changes in mean arterial pressure (MAP) and HR induced by EPR or muscle mechanoreflex (a component of EPR) activation were assessed in normotensive Wistar-Kyoto rats and spontaneously hypertensive rats (SHRs) fed normal chow (NC) or a customized diet containing either SPIR or EPL for 3 wk. SHRs treated with SPIR or EPL had significantly attenuated MAP responses to EPR (NC: 45 ± 7 mmHg, SPIR: 26 ± 4 mmHg, and EPL: 24 ± 5 mmHg, P = 0.02) and mechanoreflex (NC: 34 ± 9 mmHg, SPIR: 17 ± 3 mmHg, and EPL: 15 ± 3 mmHg, P = 0.03) activation. SHRs treated with SPIR or EPL also showed significantly attenuated HR responses to EPR (NC: 17 ± 3 beats/min, SPIR: 9 ± 1 beats/min, and EPL: 9 ± 2 beats/min, P = 0.01) and mechanoreflex (NC: 15 ± 3 beats/min, SPIR: 6 ± 1 beats/min, and EPL: 7 ± 1 beats/min, P = 0.01) activation. Wistar-Kyoto rats treated with SPIR did not demonstrate significant differences in MAP or HR responses to EPR or mechanoreflex activation. The data suggest that antagonizing MRs may be an effective strategy for the treatment of EPR overactivity in hypertension.NEW & NOTEWORTHY Exaggerated cardiovascular responses to exercise in hypertensive patients are linked with overactive exercise pressor reflexes (EPRs). Administration of low-dose mineralocorticoid receptor antagonists (spironolactone or eplerenone) effectively ameliorates abnormal EPR function in hypertension. Effective treatment of EPR overactivity may reduce the cardiovascular risks associated with physical activity in hypertension.

Neural control of circulation and exercise: a translational approach disclosing interactions between central command, arterial baroreflex, and muscle metaboreflex.

The last 100 years witnessed a rapid and progressive development of the body of knowledge concerning the neural control of the cardiovascular system in health and disease. The understanding of the complexity and the relevance of the neuroregulatory system continues to evolve and as a result raises new questions. The purpose of this review is to articulate results from studies involving experimental models in animals as well as in humans concerning the interaction between the neural mechanisms mediating the hemodynamic responses during exercise. The review describes the arterial baroreflex, the pivotal mechanism controlling mean arterial blood pressure and its fluctuations along with the two main activation mechanisms to exercise: central command (parallel activation of central somatomotor and autonomic descending pathways) and the muscle metaboreflex, the metabolic component of exercise pressor reflex (feedback from ergoreceptors within contracting skeletal muscles). In addition, the role of the cardiopulmonary baroreceptors in modulating the resetting of arterial baroreflex is identified, and the mechanisms in the central nervous system involved with the resetting of baroreflex function during dynamic exercise are also described. Approaching a very relevant clinical condition, the review also presents the concept that the impaired arterial baroreflex function is an integral component of the metaboreflex-mediated exaggerated sympathetic tone in subjects with heart failure. This increased sympathetic activity has a major role in causing the depressed ventricular function observed during submaximal dynamic exercise in these patients. The potential contribution of a metaboreflex arising from respiratory muscles is also considered.

고혈압 전단계자들에 대한 골격근 Group III 자극 시 시간에 따른 심혈관 반응

본 연구는 고혈압전단계자들에 대한 지속적인 건 스트레치시 시간에 따른 생리학적 반응을 분석하여 정상혈압자와 고혈압전단계자에 대한 EPR의 한 요소인 기계적 수용기가 혈압 및 혈역학 반응에 어떠한 영향을 주는지를 검토하였다. 그 결과, 안정 시와 시간에 따른 혈압 반응은 고혈압전단계자에 있어 SBP, MAP가 평균 20sec에서 통계적으로 가장 높은 경향을 보였으며(p<0.05), 정상혈압자에서는 SBP, DBP, MAP가 평균 45sec에서 가장 높은 경향을 보였다(p<0.05). 이는 고혈압 전단계자의 지속적인 수동적 건 스트레치 시 정상혈압자에 비해 Group III mechanoreceptors의 역기능에 따른 상승된 혈압 반응이 초기에 나타내었다고 사료된다. 또한 혈역학 반응에서 안정 시와 비교하여 지속적인 수동적건 스트레치 시 고혈압전단계자에서의 HR, SV, CO, TPR 모두 유의한 차이를 보이지 않았으나 정상혈압자에서 SV, CO가 통계적으로 유의한 차이를 보였다(p<0.05). 이는 CO, SV, HR, TPR이 정상혈압자에 비해 고혈압전단계자에 있어 높은 경향을 나타내었지만, 혈역학 반응은 본 연구를 통해 차이를 보이지 않아 앞으로 연구가 필요할 것으로 사료된다. The purpose of this study was to investigate whether group III muscle afferents play an important role eliciting abnormal blood pressure response mediated during passive muscle stretch in prehypertensive individuals. Eleven middle-aged prehypertensive men (average BP 133/80 mmHg) and nine middle-aged normotensive men (average BP 119/74 mmHg) participated in this study. After 1 min rest baseline data collection, the subject's foot was flexed (dorsiflexion) by an automated cybex for one minute. Systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial blood pressure (MAP), heart rate, stroke volume, cardiac output, and total peripheral resistance were continuously measured on a beat-by-beat basis from a finger via a Finapres device for 1 minute. To evaluate the role of mechanoreflex, a component of exercise pressor reflex, SBP, DBP, and MAP responses over the course of time were examined. The results showed that the pressor response mediated by the muscle mechanoreflex was faster in prehypertensive individuals compared to the normotensive individuals. The substantial pressor response was observed within mean 20 sec of the onset of passive stretch in prehypertension, while mean 45 sec in normotension (p<0.05). It is concluded that excessive pressor response produced during exercise in prehypertension may be due to the dysfunction of the mechano-receptors.

Mechanoreceptors In Skeletal Muscles Lead To A Greater Blood Pressure Increase During Exercise In Prehypertension

Previous studies strongly indicate that the exercise pressor reflex (EPR) plays an important role in the cardiovascular responses to dynamic exercise. Exercise elicits excessive pressor response in hypertension. However, it is not clear that the exaggerated cardiovascular response to exercise is mediated by EPR overactivity in hypertensive people. PURPOSE: To investigate the effects of mechanoreceptors (a component of EPR) on the cardiovascular responses during brief passive dorsiflexion of the foot in prehypertensive individuals. METHODS: Twenty healthy volunteers (12 prehypertension and 8 normotension) with a mean age of 46.7±1.0 years were recruited for this study. All subjects were instrumented to measure cardiac output (CO), mean arterial pressure (MAP) and heart rate (HR) and the responses before and after passive muscle stretch were observed in the same subjects. RESULTS: MAP increased with passive muscle stretch in both normotensive and prehypertensive conditions, however, MAP was significantly higher in prehypertensive individuals. The higher MAP in prehypertensive individuals was due to higher levels of total peripheral resistance.CONCLUSIONS: This study suggests that the enhanced cardiovascular response to exercise in hypertension may be mediated by excessive EPR. The EPR enhances vasoconstrictor tone during exercise in prehypertension causing larger increases in MAP despite depressed CO. Supported by Korea Research Foundation Grant funded by the Korean Government (KRF-2007-314-G00008