The Effect of Propranolol on Vascular Responses to Sympathetic Nerve Stimulation

Dawes, P. M.; Faulkner, Dale

doi:10.1111/j.1476-5381.1975.tb07389.x

Cited by 15 publications

(5 citation statements)

References 19 publications

(20 reference statements)

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“…Despite the clear-cut b-dilatation in the small vessels, a reinforcement of the sympathetically evoked net increase of total vascular resistance was, however, not revealed when the dilator response was blocked by propranolol. This is in contrast t o the findings of Viveros, Garlick and Renkin (1968) and of Dawes and Faulkner (1975), who reported that @-blockade potentiated sympathetic vasoconstriction. This conclusion, however, was reached using constant flow perfusion.…”

Section: Discussioncontrasting

confidence: 90%

Beta Adrenergic Dilator Component of the Sympathetic Vascular Response in Skeletal Muscle Influence on the micro‐circulation and on transcapillary exchange

Lundvall

Järhult

1976

Acta Physiologica Scandinavica

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A neurogenic beta-adrenergic vasodilatation in skeletal muscle has been indicated by some recent investigations. The present study describes the extent to which this neurogenic beta-dilator mechanism contributes to the integrated vascular response in consecutive sections of the muscle vascular bed during sympathetic nerve activation. This was done by studying the vascular reactions to graded sympathetic stimulation (1-16 Hz) before and after beta-adrenoceptor blockade. Beta-blockade did not influence significantly the sympathetically induced changes of total muscle vascular resistance or capacitance. Vascular tone in the "micro-vessels" during stimulation was, however, clearly more pronounced in the beta-blocked than in the non-blocked region, as revealed by segmental resistance analysis and by determination of precapillary sphincter tone (CFC). In addition, beta-blockade markedly reduced the net transcapillary absorption of extravascular fluid evoked by nerve activation. This effect could be ascribed to the mentioned influence on the precapillary sphincters, leading to a decrease of the number of capillaries available for transcapillary exchange, and to a limitation of the nerve induced fall of capillary hydrostatic pressure. The described effects of alpha-blockade were observed at all rates of sympathetic stimulation.--The conclusion was reached that the beta-adrenergic dilator component of the sympathetic vascular response in skeletal muscle significantly modifies the alpha-adrenergic constriction in the micro-vessels. It is suggested that, in the intact organism, this neurogenic beta-dilator mechanism is primarily aimed at improving the transcapillary exchange.

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Section: Discussioncontrasting

confidence: 90%

Beta Adrenergic Dilator Component of the Sympathetic Vascular Response in Skeletal Muscle Influence on the micro‐circulation and on transcapillary exchange

Lundvall

Järhult

1976

Acta Physiologica Scandinavica

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“…Several investigators have reported dilator responses to sympathetic nerve stimulation Jarhult, 1974, 1976;Tuttle and Moe, 1973;Viveros et al, 1968), whereas others have found none in animals that had received both an a-adrenoceptor antagonist and atropine (Belfrage and Rosell, 1976;Dawes and Faulkner, 1975;Glick et al, 1967;Folkow and Uvnas, 1950;Rosell and Belfrage, 1975;Youmans et al, 1955;Vatner and McRitchie, 1976). Viveros et al, (1968) observed vasodilation in the perfused gracilis muscle of the dog in response to sympathetic nerve stimulation after administration of dibozane and atropine, vasodilation that was then blocked by propranolol.…”

Section: Discussionmentioning

confidence: 99%

“…One of the more widely quoted papers is that of Viveros et al (1968) in which sympathetic nerve stimulation or norepinephrine given ia causes vasodilation in the perfused gracilis muscle in dogs treated with dibozane and atropine. However, other investigators have failed to identify such responses (Youmans et al, 1955;Glick et al, 1967;Rosell and Belfrage, 1975;Belfrage and Rosell, 1976;Folkow and Uvnas, 1950;Dawes and Faulkner, 1975;Vatner and McRitchie, 1976). Youmans et al (1955) suggested that the adrenoceptors that subserve vasodilation in dog skeletal muscle (/S-2 by modern terminology) are under only hormonal (epinephrine) control and do not respond to sympathetic nerve stimulation.…”

Section: Evidence For Lack Of Innervation Of /?-2 Adrenoceptors In Thmentioning

confidence: 99%

Evidence for lack of innervation of beta-2 adrenoceptors in the blood vessels of the gracilis muscle of the dog.

Russell¹,

Moran²

1980

Circulation Research

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Cardiac /S-l adrenoceptors respond to sympathetic nerve stimulation (SNS), but it is not clear that SNS evokes fi-2 adrenoceptor-mediated vasodilation. Sensitivity of B adrenoceptors to catecholamines and to SNS was evaluated in dogs. Norepinephrine (NE) and epinephrine (E) were equipotent vasoconstrictors (femoral artery blood flow or gracilis autoperfusion pressure) before aadrenoceptor blockade with dibozane (DIB). After DIB, NE was 1/100 as potent a vasodilator as E, which was equipotent with isoproterenol (ISO). SNS evoked gracilis muscle vasoconstriction before DIB and vasodilation after. Dilation induced by SNS or acetylcholine (ACH) after DIB was blocked by atropine (AT), but that caused by NE was not. Dilation evoked by NE, E, or I after DIB and AT was blocked by propranolol (PROP). Vasoconstrictor responses to NE, E, or SNS in dogs without DIB were not augmented by PROP at a dose that blocked the dilator effect of ISO. NE and E were equipotent and both 1/10 as potent as ISO as positive inotropic and chronotropic agents. Cardiac responses to NE, E, ISO, and SNS were antagonized by PROP. Subclassification of adrenoceptors that subserve cardiac stimulation as fi-1 and that subserve vasodilation as fi-2 was substantiated. Cardiac fi-1 adrenoceptors responded to SNS and to circulating E and NE. Vascular fi-2 adrenoceptors responded to circulating E, to ISO, and to high doses of NE, but not to SNS. fi-2 Adrenoceptors in blood vessels appear not to be innervated and may function as hormone receptors sensitive primarily to E released from the adrenal medulla, rather than to NE released from adrenergic nerves.

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“…7 This action has also been suggested as contributing to the hypotensive effect of propranolol, although Dawes and Faulkner could not find evidence of such effect in the circulatory response to lumbar sympathetic nerve stimulation in the hind limb of the dog. 5 The likelihood of testing these possibilities in man is limited. One might examine the effect of stimuli capable of eliciting a neurally mediated cardiovascular reaction, and evaluate in qualitative and quantitative terms the variations in response induced by long-term beta adrenergic…”

mentioning

confidence: 99%

Antihypertensive action of propranolol in man: Lack of evidence for a neural depressive effect

Guazzi

Fiorentini

Polese

et al. 1976

Clin Pharma and Therapeutics

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The hypothesis that a neural depressive action is related to the antihypertensive effects of beta blockers has been evaluated in 14 essential hypertensive male patients through the circulatory response to noxious stimuli. The pressor reaction to mental arithmetic was primarily mediated by cardiac stimulation (beta receptors activation), that to cold by vasoconstriction (alpha receptors activation). Arithmetic and cold were tested to separate the effects of peripheral beta blackade from possible neural and other influences. After propanolol (320 mg per day for 3 wk): (1) The baseline pressure was reduced; (2) appearance, peak, and disappearance time of the circulatory reaction to either stimulus was not altered; (3) the pressor effect of arithmetic was decreased in an extent proportional to the reduced rise of cardiac output; and (4) pressure during cold reached the pretreatment levels through an augmented increase of vascular resistance. Our findings indicate that propranolol depresses only the circulatory reactions mediated through beta receptors activation and provide no evidence of effects other than beta blockade.

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The Effect of Propranolol on Vascular Responses to Sympathetic Nerve Stimulation

Cited by 15 publications

References 19 publications

Beta Adrenergic Dilator Component of the Sympathetic Vascular Response in Skeletal Muscle Influence on the micro‐circulation and on transcapillary exchange

Beta Adrenergic Dilator Component of the Sympathetic Vascular Response in Skeletal Muscle Influence on the micro‐circulation and on transcapillary exchange

Evidence for lack of innervation of beta-2 adrenoceptors in the blood vessels of the gracilis muscle of the dog.

Antihypertensive action of propranolol in man: Lack of evidence for a neural depressive effect

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