Baroreceptor control of atrioventricular conduction in man.

Mancia, Giuseppe; Bonazzi, O; Pozzoni, L; Ferrari, Alberto; Gardumi, M; Gregorini, L; Perondi, R

doi:10.1161/01.res.44.6.752

Cited by 48 publications

(23 citation statements)

References 33 publications

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“…12 2) If the above modification of the baroreceptor reflex includes its powerful control of the atrioventricular node, 13 ANF might help depress arteriovenous conduction and terminate an episode of paroxysmal tachycardia.…”

Section: Discussionmentioning

confidence: 99%

Atrial natriuretic factor and arterial baroreceptor reflexes in unanesthetized rats.

et al. 1990

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The modulation exerted by atrial natriuretic factor (ANF) on the cardiac and vascular influences of arterial baroreceptors was investigated in two groups of unanesthetized, chronically instrumented normotensive rats. In group 1, the reflex control of heart rate was assessed by graded baroreceptor stimulations and deactivations obtained by intravenous boluses of phenylephrine and nitroprusside. Under either circumstance, baroreceptor reflex sensitivity was expressed as the linear regression slope relating the chronotropic responses to the drug-induced mean arterial pressure changes. In group 2, right common carotid occlusion was performed in rats with their aortic and left carotid sinus baroreceptors denervated to assess the baroreceptor control of blood pressure; the reflex response was quantitated as the peak blood pressure rise observed during the maneuver. The reflex studies were performed before and during atriopeptin III infusion (0.15-0.20 jtg/kg/min for 60 minutes). ANF augmented the bradycardic response to phenylephrine by 102.5±29% (p<0.01), reduced the tachycardic response to nitroprusside by 67.7 ±6.4% (/?<0.01), and failed to modify the pressor response to carotid occlusion (-6.8±2.1%, /?=NS). In a separate group of rats infused with low dose nitroprusside, no change in the baroreceptor-heart rate reflex was observed. ANF infusion (0.20 /tg/kg/min) performed in further separate groups of conscious rats raised plasma ANF to 480±58 fmol/ml. Values in control vehicle-infused rats were 50±8 fmol/ml. Vascular reactivity (pressor response to intravenous phenylephrine boluses in anesthetized, sinoaorticdenervated rats) was only minimally reduced by ANF. It is concluded that ANF at doses within the pathophysiological range exerts a complex modulatory effect on arterial baroreceptor reflexes, consisting of potentiation of the cardioinhibitory, no change of the vascular, and depression of the cardioexcitatory reflex influences. These data may have pathophysiological implications in high ANF release states. (Hypertension 1990*,15:162-167)

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Section: Discussionmentioning

confidence: 99%

Atrial natriuretic factor and arterial baroreceptor reflexes in unanesthetized rats.

et al. 1990

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“…This can be inferred from the finding that from normotension to mild and more severe degrees of blood pressure elevation, there is a gradual reduction of the bradycardic and tachycardic responses to baroreceptor stimulation and deactivation, respectively (Figure 4, left), 41 a major mechanism of heart rate control. Because these responses are largely reduced, or even abolished, by the administration of atropine, 64 the mechanism is likely to be a progressive impairment of cardiac vagal modulation.…”

Section: Sympathetic Activation and Hypertension Severitymentioning

confidence: 99%

The Autonomic Nervous System and Hypertension

Mancia

Grassı

2014

Circulation Research

494

373

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T hat hypertension is due to a derangement of sympathetic and parasympathetic cardiovascular regulation is one of the most widely accredited and tested hypotheses in cardiovascular research. Its proposal followed from the demonstration that autonomic cardiovascular influences play a fundamental role in homeostatic control of the cardiovascular system. In animal models of hypertension, both an increased sympathetic nerve activity and a reduction of vagal cardiac tone are associated with and responsible for the appearance and maintenance of high blood pressure, with their role expanding to include hypertension-related sequelae.1-3 Albeit through a longer and more difficult journey, evidence is now available that similar autonomic alterations may have a causative or cocausative role also in the generation and maintenance of human hypertension. [4][5][6][7] We begin this review by describing the alterations in autonomic cardiovascular control that characterize human hypertension. We then discuss the possible mechanisms underlying these alterations and the evidence that they contribute to the functional and structural changes of the heart and systemic circulation that accompany a chronic hypertensive state and lead to its clinical complications. Finally, we consider the effects of nonpharmacological and pharmacological treatment of hypertension on autonomic cardiovascular control. Our focus is limited to the condition defined as essential or primary hypertension, with no reference to the secondary forms of high blood pressure because secondary hypertension accounts for only a small fraction of the overall prevalence of hypertension 8 and its causes do not include alterations of central or reflex autonomic drive. In addition, the concomitant alterations of sympathetic and parasympathetic cardiovascular control that develop in secondary hypertension have been less extensively documented and remain somewhat controversial. 1,4,6 Autonomic Dysfunction in PrehypertensionAbnormal increases in circulating plasma levels of the adrenergic neurotransmitters norepinephrine and epinephrine The Autonomic Nervous System and Hypertension Giuseppe Mancia, Guido GrassiThis Review is in a thematic series on The Autonomic Nervous System and the Cardiovascular System, which includes the following articles:

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“…We previously have addressed this problem in humans by inducing physiological alterations in arterial baroreceptor activity while recording His bundle potentials and have concluded that a powerful vagal influence on atrioventricular conduction does operate normally. We have also observed, however, that this influence is complex, because it is exerted on some but not all portions of the atrioventricular conduction system and is modified to a large extent by concomitant alterations in cardiac cycle length (Mancia et al, 1979).…”

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confidence: 88%