Effect of Bicycling on the Baroreflex Regulation of Pulse Interval

Bristow, James; Brown, E. B.; Cunningham, D. J.; Howson, M. G.; Petersen, E. Strange; Pickering, Thomas G.; Sleight, Peter

doi:10.1161/01.res.28.5.582

Cited by 156 publications

(80 citation statements)

References 12 publications

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“…The observation in the present study that the animals with hypertrophy but without overt heart failure had less reduction of sensitivity than the group with overt heart failure suggests that the severity of this dysfunction of the baroreceptor reflex arc may be a function of the severity of the cardiac abnormality. Apparently, the sensitivity of this reflex is altered under other circumstances as well, since it has been shown to be accentuated during natural sleep (11) and depressed in hypertension in experimental animals (20) and man (21) and during anesthesia (13) and exercise (22,23) . 1 Baroreceptor Reflex in Heart Failure in man; resetting of the threshold without a change in sensitivity of the reflex has been produced by hypercapnia in normal subjects (24).…”

Section: Discussionmentioning

confidence: 99%

Alterations in the Baroreceptor Reflex in Conscious Dogs with Heart Failure

Higgins¹,

Vatner²,

Eckberg³

et al. 1972

J. Clin. Invest.

220

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A B S T R A C T The effectiveness of the baroreceptor reflex in conscious dogs with experimental cardiac hypertrophy and heart failure was compared with that in a group of normal conscious dogs. Cardiac hypertrophy and heart failure were produced by tricuspid avulsion and progressive pulmonary stenosis. The sensitivity of the baroreceptor reflex to transient hypertension was assessed by determining the slope of the regression line relating the prolongation of the R-R interval to the rise in systolic arterial pressure during the transient elevation of arterial pressure induced by an intravenous injection of 1-phenylephrine. The mean slope averaged 22.4 +2.3 msec/mm Hg in 16 normal animals, 23.1 ±1.5 in five sham-operated animals, and was significantly reduced to 8.3 ±0.8 in 10 dogs with hypertrophy alone (P < 0.001), and to 3.3 ±0.5 in nine dogs with heart failure (P < 0.001). The response to baroreceptor hypotension was compared during bilateral carotid artery occlusion (BCO) in six normal and six heart failure dogs previously instrumented with Doppler flow transducers on the superior mesenteric and renal arteries. During BCO, in normal dogs arterial pressure increased 52 ±4 mm Hg, heart rate 33 ±2 beats/min, mesenteric resistance 0.17 ±0.03 mm Hg/ml per min, and renal resistance 0.37 ±0.10 mm Hg/ml per min. In the heart failure group all of these variables increased significantly less (P < 0.01 ); arterial pressure rose 25 ±3 mm Hg, heart rate 13 ±4 beats/min, mesenteric resistance 0.04 ±0.007 mm Hg/ ml per min, and renal resistance 0.18 ±0.09 mm Hg/ ml per min.

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Section: Discussionmentioning

confidence: 99%

Alterations in the Baroreceptor Reflex in Conscious Dogs with Heart Failure

Higgins¹,

Vatner²,

Eckberg³

et al. 1972

J. Clin. Invest.

220

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“…The effect of such factors on the baroreceptor reflex control of heart rate is well documented. Mental arithmetic, 43 handgrip, 44 ' 43 and dynamic exercise 46 attenuate (probably centrally) the baroreceptor reflex regulation of heart rate. The extent of this attenuation cannot be predicted from heart rate responses to pressor doses of phenylephrine given when subjects are resting quietly.…”

mentioning

confidence: 99%

Factors influencing blood pressure and heart rate variability in hypertensive humans.

et al. 1988

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SUMMARY We examined the influence of baroreceptor reflex sensitivity (the increase in pulse interval in response to a phenylephrine-induced increase in blood pressure), age, blood pressure, and /3-adrenergic receptor blockade on the variability of blood pressure and heart rate in essential hypertension. Fifty-six subjects were studied before treatment; intra-arterial blood pressure was recorded outside the hospital for 24 hours. Variability was defined (from all beats occurring while subjects were awake) as the standard deviation about the average waking value for mean arterial pressure (MAP) or pulse interval. The correlation (r) between baroreceptor reflex sensitivity and blood pressure variability was -0.47 (p<0.0002). Baroreceptor reflex sensitivity was the only independent determinant of blood pressure variability on multiple regression analysis. Thirty subjects were restudied after 5 months of /3-adrenergic receptor blockade. Ambulatory blood pressure was lower during treatment, whereas pulse interval, its variability, and baroreceptor reflex sensitivity were higher. Blood pressure variability was unchanged. The variability of MAP was inversely correlated with baroreceptor reflex sensitivity before (r = -0.42, p<0.02) and during ( r = -0.45, p < 0.02) treatment, but it was unrelated to the average ambulatory MAP or to the variability of pulse interval either before or during /3-blockade. Sixteen subjects whose average waking ambulatory blood pressure was 140/90 mm Hg or less were not treated. This group of borderline hypertensive subjects had less variable MAP than did the remaining 40 subjects (12.4 ± 2.3 [SD] vs 14.5 ± 2.5 mm Hg; p<0.01). We conclude that 1) the decline in baroreceptor reflex sensitivity is the principal determinant of increased blood pressure variability in hypertension, 2) MAP and its variability are regulated independently, 3) heart rate variability is not influenced by baroreceptor reflex sensitivity and is unrelated to blood pressure variability, and 4) the blood pressure of subjects with borderline hypertension is not excessively labile. in normal and hypertensive humans, 1 but factors that might influence and regulate this variability remain imperfectly understood. Considerable experimental evidence supports the concept that the arterial baroreceptor reflex is intimately involved in the short-term regulation of arterial blood pressure. Denervation of the sinoaortic baroreceptors in rats and dogs consistently increases the beat-to-beat variation of blood pressure but has less dramatic and disputed effects on its level.2 " 5 Central interruption of the baroreceptor reflex by lesioning nucleus tractus solitarii produces hypertension, tachycardia, and increased blood pressure variability in awake animals. 6 Selective removal of the noradrenergic innervation of this nucleus does not induce hypertension, but it does cause an increase in blood pressure variability that is inversely related to a decrease in the baroreceptor reflex control of heart rate.

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“…The most likely explancationi for the sutstaine(l excitatorv response is the reported inhibition of the arterial baroreceptor reflex during exercise (11,29). Althouglh the arterial baroreflex is suppressed durinig exercise, the input fromii the baroreceptors can modulate the siomatic reflex.…”

Section: Resultsmentioning

confidence: 99%

“…Conversely, activation of somatic receptors triggers excitatory reflex responses as a result of increased symipathetic adrenergic discharge (7)(8)(9)(10). Exercise is a potent stimulus to somatic receptors anid results in reflex increases in heart rate, meian arterial pressure, and systemic vascular resistance (8,11,12). The effects of exercise on cardioptlmiioniary receptors are less well-defined but the increase in ventricular contractility and stroke voltumiie wouil(d be expected to aiugment the discharge of' cardlioptl m)oniarv receptors with vagal afferents (13,14) anid, thuis, reflexlv inhibit sympathetic ouitflow to the resistaniee vessels (14).…”

Section: Introductionmentioning

confidence: 99%