Effects of Autonomic Blockade on the Baroreflex in Man at Rest and During Exercise

Pickering, Thomas G.; Gribbin, B.; Petersen, E. Strange; Cunningham, D. J.; Sleight, Peter

doi:10.1161/01.res.30.2.177

Cited by 210 publications

(111 citation statements)

References 18 publications

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“…The increase in heart rate produced by exercise in man is due to a progressive increase in sympathetic activity as the level of exercise increases, accompanied by a gradual withdrawal of vagal parasympathetic tone (Robinson et al, 1966;Pickering et al, 1972). The tachycardia observed after vasodilator therapy is mainly due to increased sympathetic activity (Glick & Braunwald, 1965;O'Malley et al, 1976;Davies et al, 1979), although a reduction in vagal tone may contribute to the response (Mroczec et al, 1976;Man in 'T Veld et al, 1980).…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular effects of alinidine and propranolol alone and in combination with hydralazine in normal man.

Nicholls¹,

Harron²,

Shanks³

1983

Brit J Clinical Pharma

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1 The effect of single oral doses of alinidine 80 mg, propranolol 40 mg, hydralazine 50 mg, alinidine 80 mg combined with hydralazine 50 mg, propranolol 40 mg combined with hydralazine 50 mg, and placebo on arterial pressure and heart rate was studied in five normal volunteers in the supine and standing positions and during exercise. Observations were made before and at 1, 2, 3, 4 and 6 h after drug administration. 2 Alinidine 80 mg and propranolol 40 mg significantly reduced heart rate in the supine position, and on exercise. The reductions in supine heart rate produced by alinidine and propranolol were not significantly different, but the maximum effect of alinidine on exercise heart rate was observed later than that of propranolol. Propranolol reduced heart rate in the standing position at all time intervals after drug administration, but alinidine reduced standing heart rate only at 6 h (P < 0.01 when compared to placebo). 3 Hydralazine 50 mg increased supine heart rate by 8-10 beats min-' when compared to the pre-treatment value. These increases were significant (P < 0.05) when compared to the pre-treatment value, but not when compared to placebo. Hydralazine increased standing heart rate from 71.4 + 6.5 to 90.0 + 7.0 beats min-' (P < 0.05 when compared to placebo), but had no effect on exercise heart rate. The small increase in supine heart rate following hydralazine therapy was reduced by alinidine and propranolol, but only propranolol reduced the significant increase in standing heart rate produced by hydralazine. 4 Hydralazine reduced diastolic arterial pressure in the supine position at 2 and 4 h after drug administration (P < 0.05 when compared to placebo), but had no effect on systolic or diastolic arterial pressure in the standing position or on exercise. 5 Propranolol produced small reductions in systolic arterial pressure in the standing position, which were not significant when compared to placebo; diastolic pressure was unchanged. Propranolol reduced systolic pressure during exercise at 2, 4 and 6 h after drug administration (P < 0.05 when compared to placebo); diastolic pressure was unchanged. The effects of hydralazine and propranolol combined on arterial pressure in the standing position were similar to those observed after propranolol alone, but combined therapy produced a greater reduction in exercise systolic pressure, although these differences were not significant. 6 Alinidine reduced systolic arterial pressure in the supine position at 3, 4 and 6 h after drug administration (P < 0.01) and diastolic pressure at 2 and 4 h (P < 0.05 when compared to placebo). Alinidine reduced systolic arterial pressure in the standing position at 3, 4 and 6 h after drug administration (P < 0.05) and diastolic pressure at 2 h (P < 0.01) and 6 h (P < 0.05 when compared to placebo). During exercise, alinidine produced a small reduction in systolic arterial pressure which was not significant, and a reduction in diastolic pressure at 1 h (P < 0.05 when compared to placebo). The effects of hydralazine and alini...

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Section: Discussionmentioning

confidence: 99%

Cardiovascular effects of alinidine and propranolol alone and in combination with hydralazine in normal man.

Nicholls¹,

Harron²,

Shanks³

1983

Brit J Clinical Pharma

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“…Highpressure (carotid sinus and aortic arch baroreceptor) baroreflex sensitivity was evaluated by recording cardiac slowing in response to acute phenylephrineinduced hypertension. 48 The subject inhaled three times from a gasfilled ampule of amyl nitrite broken under the nose.…”

Section: Assessment Of Baroreflex Sensitivitymentioning

confidence: 99%

Baroreflex sensitivity and heredity in essential hypertension.

1992

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BACKGROUND Abnormalities in baroreflex control of heart rate may be important in the pathogenesis of essential hypertension. METHODS AND RESULTS To investigate the influence of heredity on baroreflex function, we measured baroreflex sensitivity in 40 untreated patients with essential hypertension grouped by the presence (FH+) or absence (FH-) of a family history of hypertension and in 24 normotensive counterparts. Baroreflex sensitivity was assessed by both high-pressure (phenylephrine bolus) and low-pressure (amyl nitrite inhalation) stimuli. Subject groups were matched for age, blood pressure, body weight, and race. Baroreflex sensitivity (in milliseconds per millimeter of mercury) assessed by amyl nitrite inhalation was 24.3 +/- 2.8 in FH- normotensives, 12.3 +/- 1.7 in FH+ normotensives, 15.4 +/- 3.3 in FH- hypertensives, and 8.1 +/- 1.2 in FH+ hypertensives. Baroreflex sensitivity assessed by phenylephrine bolus was 28.8 +/- 5.6 in FH- normotensives, 19.3 +/- 2.8 in FH+ normotensives, 19.1 +/- 2.0 in FH- hypertensives, and 13.6 +/- 1.3 in FH+ hypertensives. Two-factor analysis of variance showed significant effects on baroreflex sensitivity for blood pressure status (normotensive versus hypertensive) and for family history of hypertension. After control line (controlling) for the effects of several variables, including age, mean arterial pressure, body weight, and race through multiple linear regression analysis, the effect of family history of hypertension on baroreflex sensitivity was still highly significant. Indeed, of all variables investigated, family history of hypertension was the strongest unique baroreflex sensitivity predictor. CONCLUSIONS These data suggest that the impairment in baroreflex sensitivity in hypertension is in part genetically determined and may be an important hereditary component in the pathogenesis of essential hypertension.

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“…All cardiac cycles during the pressure rise were included in these calculations since respiration does not alter this determination of BRS in subjects with slopes less than 15 msec/mm Hg. 17 For each phenylephrine injection, regression equations were calculated with shifts, or delays, of from 0 to + 3 cardiac cycles interposed between the systolic pressure and pulse interval regressed against it. 24 At heart rates below 75 beats/min the correlation between these two variables was usually best with a delay of 0 cycles.…”

Section: Calculation Of Baroreceptor Reflex Sensitivitymentioning

confidence: 99%

“…This technique examines primarily the parasympathetic efferent limb of this reflex. 17 Persons with more sensitive baroreceptor reflexes exhibit a greater reflex bradycardia for a similar absolute increase in blood pressure. Increasing age and mean arterial pressure (MAP) act independently to lower the slope of this response.…”

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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Effects of Autonomic Blockade on the Baroreflex in Man at Rest and During Exercise

Cited by 210 publications

References 18 publications

Cardiovascular effects of alinidine and propranolol alone and in combination with hydralazine in normal man.

Cardiovascular effects of alinidine and propranolol alone and in combination with hydralazine in normal man.

Baroreflex sensitivity and heredity in essential hypertension.

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

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