Physiological studies have long documented the key role played by the autonomic nervous system in modulating cardiovascular functions and in controlling blood pressure values, both at rest and in response to environmental stimuli. Experimental and clinical investigations have tested the hypothesis that the origin, progression, and outcome of human hypertension are related to dysfunctional autonomic cardiovascular control and especially to abnormal activation of the sympathetic division. Here, we review the recent literature on the adrenergic and vagal abnormalities that have been reported in essential hypertension, with emphasis on their role as promoters and as amplifiers of the high blood pressure state. We also discuss the possible mechanisms underlying these abnormalities and their importance in the development and progression of the structural and functional cardiovascular damage that characterizes hypertension. Finally, we examine the modifications of sympathetic and vagal cardiovascular influences induced by current nonpharmacological and pharmacological interventions aimed at correcting elevations in blood pressure and restoring the normotensive state.

The Autonomic Nervous System and Hypertension

BackgroundPrevious studies have shown that obesity is characterized by a sympathetic overactivity coupled with an insulin resistance state and a baroreflex impairment. The present study was set out to compare the effects of peripheral versus central obesity on sympathetic, metabolic and reflex funct

Effect of central and peripheral body fat distribution on sympathetic and baroreflex function in obese normotensives.

The sections in this article are:


1
Techniques
1.1
Carotid Sinus Massage

1.2
Electrical Stimulation of Carotid Sinus Nerves

1.3
Section or Anesthesia of Carotid Sinus Nerves and Vagi

1.4
Occlusion of Common Carotid Arteries

1.5
Neck Chamber

1.6
Vasoactive Drugs

1.7
Nonselective Techniques




2
Arterial Baroreceptor Control of Heart Rate
2.1
Autonomic Mediation

2.2
Other Properties

2.3
Relationship to Base-Line R-R Interval

2.4
Relationship to Respiratory Cycle




3
Arterial Baroreceptor Control of Atrioventricular Conduction and Ventricles

4
Carotid Baroreceptor Control of Blood Pressure

5
Carotid Baroreceptor Influence on Cardiac Output and Total Peripheral Resistance

6
Arterial Baroreceptor Control of Regional Circulations

7
Arterial Baroreceptor Control of Veins

8
Set Point of Carotid Baroreflex

9
Aortic Baroreflexes

10
Factors That Modify Arterial Baroreceptor Control of Circulation
10.1
Age

10.2
Exercise

10.3
Mental Stress

10.4
Sleep

10.5
Anesthesia

10.6
Central Blood Volume and Posture




11
Pathological States
11.1
Hypertension

11.2
Heart Disease

11.3
Carotid Sinus Syndrome

11.4
Other Pathological Conditions




12
Modification of Arterial Baroreflexes by Drugs
12.1
β-Adrenergic Antagonists

12.2
Cardiac Glycosides

12.3
Antihypertensive Drugs

Arterial Baroreflexes in Humans

The various structures in the heart are regulated by both divisions of the autonomic nervous system. The sympathetic division exerts facilitatory effects, whereas the parasympathetic has an inhibitory influence. The central nervous system controls the relative levels of sympathetic and vagal activity, usually in a reciprocal fashion; that is, as sympathetic activity is increased, parasympathetic activity is usually diminished, and vice versa. In certain regions of the heart, such as the nodal tissues, parasympathetic effects tend to predominate over sympathetic influences. In other regions, however, such as the ventricular myocardium, the effects of the sympathetic division are usually much greater than those of the parasympathetic division. When both divisions are active simultaneously, the sympathetic and vagal effects are usually not additive in a simple, algebraic fashion, but the sympathetic—parasympathetic interactions tend to be highly nonlinear.

Neural Control of the Heart

Autonomic cardiovascular control in pregnancy.

Although human baroreflexes are known to exert a powerful physiological control on heart rate, little information exists on the physiological control they exert on the atrioventricular conduction system. In 11 normotensive subjects with normal atrioventricular conduction, we altered baroreceptor activity by injection of pressor and depressor drugs (phenylephrine and trinitroglycerin) and recorded mean arterial pressure (MAP, catheter measurements), R-R interval, and pre-His and post-His intervals (A-H and H-V, His bundle recording). With the subjects in sinus rhythm, increasing MAP by 21+/- 1 mm Hg caused a marked lengthening (250 +/- 28 msec), and decreasing MAP by 17 +/- 2 mm Hg a marked shortening (142 +/- 16 msec) of the R-R interval. There was little change in the A-H interval and no change at all in the H-V interval. However, when the R-R interval was kept constant in these subjects by atrial pacing, a similar increase and decrease in MAP caused, respectively, a marked lengthening (49 +/- 6 msec) and shortening (19 +/- 3 msec) of the A-H interval, although the H-V interval remained unaffected. Thus physiological ranges of baroreceptor activation have a marked influence on the atrioventricular node but apparently not on the ventricular portion of the atrioventricular conduction system. This influence is unmasked when pacing prevents the baroreceptor influence on the sinoatrial node.

Baroreceptor control of atrioventricular conduction in man.

In humans, arterial baroreceptow depress atrioventricular (AV) conduction through vagal influences on the AV node but not on the His-Purkinje fibers. We investigated the influence on AV conduction of an excitatory neural influence, i.e., isometric exercise (handgrip). In subjects with normal AV conduction, blood pressure was measured by an intra-arterial catheter, R-R interval by an electrocardiogram, and A-H and H-V intervals (representing conduction, respectively, through the AV node and the His-Purkinje fibers) by His bundle recording. Handgrip raised blood pressure markedly, it shortened R-R interval, and caused no change in A-H and H-V intervals. Because prior studies had demonstrated that autonomic influences over AV conduction can be quantified accurately only when heart rate is constant, the subjects also were studied during atrial pacing. Under this condition, handgrip again caused a marked pressor response but also induced a marked shortening in the A-H interval (30%) whereas the H-V interval still wax unaffected. The handgrip-induced shortening in the A-H Interval was less pronounced after atropine but it was also Impaired by propranolol. Thus AV conduction normally is modulated by inhibitory influences but also by powerful excitatory stimuli. Like the inhibitory influences, the excitatory ones are seen mainly at constant heart rate and are limited to the AV node with no effect on the His-Purkinje fibers. Unlike the Inhibitory Influences, however, the excitatory modulation is substantially mediated via the cardiac sympathetic nerves.

R Perondi

Papers

Baroreceptor control of atrioventricular conduction in man.

Modulation of atrioventricular conduction by isometric exercise in human subjects.