Relative Roles of the Sympathetic and Parasympathetic Nervous Systems in the Reflex Control of Heart Rate

Glick, Gerald; Braunwald, Eugene; Hoff, Hebbel E.

doi:10.1097/00132586-196606000-00008

Cited by 34 publications

(40 citation statements)

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“…slight fall in rate to below the control level produced by noradrenaline and phenylephrine resulted from an inhibition of sympathetic activity as it did not occur after propranolol. These conclusions agree with those of Aviado & Wnuck (1957) but are at variance with the observations of Glick & Braunwald (1965), who showed that the slowing of heart rate in response to the elevation of arterial pressure by phenylephrine was completely abolished by atropine but not affected by pronethalol; they concluded that the slowing resulted entirely from increased parasympathetic activity.…”

Section: Discussionsupporting

confidence: 92%

The Effect of Propranolol on the Cardiovascular Responses to Isoprenaline, Adrenaline and Noradrenaline in the Anaesthetized Dog

Shanks¹

1966

British Journal of Pharmacology and Chemotherapy

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Section: Discussionsupporting

confidence: 92%

The Effect of Propranolol on the Cardiovascular Responses to Isoprenaline, Adrenaline and Noradrenaline in the Anaesthetized Dog

Shanks¹

1966

British Journal of Pharmacology and Chemotherapy

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“…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). The tachycardia observed after hydralazine therapy is reduced by 3-adrenoceptor blockade with propranolol (Brunner et al, 1967;Zacest et al, 1972;Velasco et al, 1978), oxprenolol (Davies et al, 1979) and alprenolol (Sannerstedt et al, 1971).…”

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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“…After 1 mg of propranolol, the effect of adrenaline on the heart was blocked and a bradycardia occurred. This can be attributed to a reflex increase in vagal activity (Glick & Braunwald, 1965) in response to the increase in arterial pressure which adrenaline produced as a result of propranolol blocking its peripheral vasodilator but not its vasoconstrictor action (Brick et al, 1966). I.C.I.…”

Section: Discussionmentioning

confidence: 99%

Comparison of the effects of I.C.I. 50172 and propranolol on the cardiovascular responses to adrenaline, isoprenaline and exercise

Brick

Hutchison

McDevitt

et al. 1968

British J Pharmacology

121

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The intravenous infusion of I.C.I. 50172 in doses up to 20 mg reduced, although not significantly, the increase in heart rate produced by the infusion of isoprenaline in healthy volunteers; the response to adrenaline was significantly reduced. The infusion of 1 mg propranolol abolished these responses After the pre‐treatment of subjects with atropine or hexamethonium, I.C.T. 50172 produced a significant reduction in an isoprenaline tachycardia. This reduction was not competitive and did not exceed 50%. The intravenous injection of 4 mg I.C.I. 50172 reduced an exercise tachycardia; its effect was less than that of 4 mg propranolol. This difference became greater as the doses of the two drugs were increased. The dextro isomer of propranolol had no effect on the exercise tachycardia; I.C.I. 45763 reduced it to the same extent as propranolol. The intravenous injection of I.C.I. 50172 reduced the increase in heart rate produced by tilting a normal subject from the supine to 80° head‐up position. After the administration of atropine, I.C.I. 50172 almost abolished the response. In the presence of atropine, I.C.I. 50172 was as active as propranolol in reducing the increase in heart rate on tilting. The reason for the differences in the effects of I.C.I. 50172 on the increases in heart rate brought about by the three procedures is not clear. The increase in forearm blood flow produced by the infusion of isoprenaline into the brachial artery was not reduced by the intra‐arterial administration of I.C.I. 50172.

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Relative Roles of the Sympathetic and Parasympathetic Nervous Systems in the Reflex Control of Heart Rate

Cited by 34 publications

References 0 publications

The Effect of Propranolol on the Cardiovascular Responses to Isoprenaline, Adrenaline and Noradrenaline in the Anaesthetized Dog

The Effect of Propranolol on the Cardiovascular Responses to Isoprenaline, Adrenaline and Noradrenaline in the Anaesthetized Dog

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

Comparison of the effects of I.C.I. 50172 and propranolol on the cardiovascular responses to adrenaline, isoprenaline and exercise

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