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(Hypertension. 1995;26:348-354.)
© 1995 American Heart Association, Inc.

Articles

Sympathetic Modulation of Radial Artery Compliance in Congestive Heart Failure

Guido Grassi; Cristina Giannattasio; Monica Failla; Antonio Pesenti; Giovanni Peretti; Edoardo Marinoni; Nicoletta Fraschini; Sabrina Vailati; Giuseppe Mancia

From Cattedra di Medicina Interna I, Università di Milano and Ospedale S. Gerardo dei Tintori, Monza, and Istituto di Clinica Medica Generale and Centro di Fisiologia Clinica e Ipertensione, Ospedale Maggiore and Università di Milano, Milano, Italy.

Correspondence to Prof Giuseppe Mancia, Medicina Interna I, Ospedale S. Gerardo dei Tintori, Via Donizetti 106, 20052, Monza (MI), Italy.

	Abstract

Top Abstract Introduction Effect of Adrenergic Stimulation... Sympathetic Activation and... Arterial Compliance and... References

 
Abstract Animal studies have suggested that arterial compliance can be modulated by adrenergic influences. Whether this adrenergic modulation also occurs in humans is still a matter of debate. In the present article we address this issue by examining the relationships between sympathetic tone and arterial compliance in a variety of physiological and pathophysiological conditions. We have found that cigarette smoking, ie, an action that produces a marked sympathetic activation, causes a significant reduction in radial artery compliance, as measured by an echotracking device capable of providing continuous beat-to-beat evaluation of this hemodynamic variable. When expressed as compliance index, ie, as the ratio between the area under the compliance-pressure curve and pulse pressure, the reduction amounted to 35.7±4.8% (mean±SEM) and was independent of the smoking-related blood pressure increase. Furthermore, pharmacological stimulation of adrenergic receptors located in the arterial wall was also shown to affect arterial compliance because the radial artery compliance index was markedly reduced (-29.5±3.9%) during phenylephrine infusion in the brachial artery at doses devoid of any systemic blood pressure effect. Evidence was also obtained that the relationship between sympathetic activation and arterial compliance has pathophysiological relevance, because in 17 patients with congestive heart failure (New York Heart Association classes II through IV) there was a significant inverse correlation (r=.62, P<.01) between muscle sympathetic nerve activity (directly measured by microneurography in the peroneal nerve) and radial artery compliance. Finally, we have recently observed that anesthesia of the brachial plexus, a maneuver that induces a transient blockade of nerve conduction to the upper limb, markedly increases radial artery compliance (change in compliance index, +30.0±5.0%). Thus, at least at the radial artery level arterial compliance is under a pronounced tonic restraint by sympathetic influences and can be modulated in either direction by reflex or central alterations in sympathetic drive. This modulation has pathophysiological implications.

Key Words: arteries • radial artery • compliance • sympathetic nervous system • heart failure, congestive • pressoreceptors

	Introduction

Top Abstract Introduction Effect of Adrenergic Stimulation... Sympathetic Activation and... Arterial Compliance and... References

 
Several studies performed in the last few years have shown that the alterations in arterial compliance that occur in physiological conditions and a number of cardiovascular diseases are accounted for by structural and/or functional factors.^{1 2} In vitro studies and in vivo observations in experimental animals have suggested that among the functional factors, alterations in vascular smooth muscle tone induced by adrenergic influences are often involved.^{3 4 5 6}

However, information on the role of adrenergic influences in modulating arterial compliance in humans is limited. The present article will address this issue by describing three sets of human data: first, the effect on radial artery compliance of pharmacological or neural stimulation of adrenoceptors anatomically located in the conduit arteries; second, the role of sympathetic factors in the modifications of radial artery compliance occurring in congestive heart failure; and third, the effect on radial artery compliance of anesthesia of the brachial plexus, ie, a maneuver that transiently abolishes sympathetic tone to the upper limb.

	Effect of Adrenergic Stimulation on Radial Artery Compliance

Top Abstract Introduction Effect of Adrenergic Stimulation... Sympathetic Activation and... Arterial Compliance and... References

 
Our group⁷ and others⁸ have shown that radial artery compliance can be markedly reduced by adrenergic stimulation. In eight healthy habitual smokers (age, 36.1±3.6 years; mean±SEM) a marked sympathetic stimulation was obtained by smoking of a cigarette, ie, a condition in which nicotine absorption affects central sympathetic mechanisms and increases norepinephrine release from sympathetic nerve terminals.^{9 10 11} Smoking lasted 5 minutes, and before, during, and after smoking blood pressure was continuously measured in a finger by a photoplethysmographic device (Finapres 2300, Ohmeda)¹² while ipsilateral radial artery diameter was continuously assessed by a Doppler echocardiographic device capable of accurately tracking systolic-diastolic movements of the radial artery walls (NIUS 02, Asulab).^{13 14} Radial artery compliance was evaluated by the arctangent model of Langewouters et al¹⁵ and expressed in three different fashions: (1) Compliance values at each blood pressure from diastole to systole to obtain compliance-pressure curves over the existing blood pressure range; (2) the area under the curve relating compliance to arterial blood pressure normalized for pulse pressure, termed compliance index; and (3) the area under the curve relating compliance to arterial blood pressure for the blood pressure range common to the no smoking and smoking conditions, termed compliance index under isobaric conditions. As shown in Fig 1 (top), over the first 5 minutes of cigarette smoking blood pressure and heart rate increased markedly. These hemodynamic changes were accompanied by a marked reduction in radial artery diameter and compliance throughout the existing systolic-diastolic pressure range (Fig 1, middle). The compliance index was reduced by 35.7±4.8% (P<.05), and the compliance index in isobaric conditions was reduced by 22.5±4.2% (P<.01), indicating that the smoking-induced increase in blood pressure was not responsible for this phenomenon (Fig 1, bottom). The changes in blood pressure, heart rate, radial artery diameter, and compliance index were still fully manifest after 10 minutes from the beginning of smoking (Fig 2) and were always statistically significant compared with the presmoking values.

View larger version (18K): [in this window] [in a new window]   Figure 1. Top, Bar graphs show mean arterial pressure (MAP) and heart rate (HR) before smoking (open bars) and during smoking (black bars). Middle and bottom, Line graphs show radial artery diameter-pressure curves and radial artery compliance-pressure curves (, nonsmoking; , smoking), and bar graphs show radial artery compliance index and isobaric radial artery compliance index (open bars, nonsmoking; black bars, smoking) in the same conditions. Data were averaged for the period before smoking and 5 minutes of smoking; mean±SEM from eight subjects. Statistical significance of difference in mean values before and during smoking was assessed by two-way ANOVA using Student's t test for paired observations to determine the difference between the two conditions. *P<.05, **P<.01 before smoking vs during smoking. In the same eight subjects but in a different experimental session, smoking for 5 minutes increased plasma norepinephrine from 238.0±51 to 321.1±56 pg/mL and plasma epinephrine from 24.1±8.2 to 46.0±12 pg/mL (mean±SEM). Differences were statistically significant (P<.05). Plasma catecholamines were assessed from venous blood samples with high-performance liquid chromatography.16

View larger version (16K): [in this window] [in a new window]   Figure 2. Line graphs show time course of changes in systolic pressure (S), diastolic pressure (D), heart rate, radial artery diameter, and radial artery compliance index during the presmoking period (open circles), smoking period (small closed circles), and 5 minutes after the end of smoking (large closed circles). Data were calculated as averages of 1-minute values before and during smoking and as averages of 5-minute values after smoking. Mean±SEM from the eight subjects of Fig 1 (from Giannattasio et al7 by permission).

Further evidence that adrenergic influences can markedly affect radial artery compliance has been obtained through a different experimental approach. In nine untreated subjects with mild essential hypertension (age, 46.8±4.8 years; mean±SEM) we measured radial artery diameter and compliance as described above. Radial artery diameter was measured at the diastolic pressure value, and radial artery compliance was expressed as described above, ie, as compliance-pressure curve, compliance index, and isobaric compliance index. Measurements were performed in control conditions and during a 15-minute infusion of phenylephrine in the brachial artery, the dose used (0.08 µg/kg per minute) being just below that required to induce an arterial blood pressure increase. The rationale of this study was to determine, via a massive stimulation of adrenergic receptors, the potential ability of the adrenergic system to modulate arterial compliance under circumstances in which possible confounding effects of an alteration of systemic hemodynamics were avoided. During the phenylephrine infusion radial artery diameter and compliance fell markedly throughout the systolic-diastolic pressure range. As shown in Table 1 the compliance index decreased by 29.5±3.9% compared with the value measured before phenylephrine infusion. A similar reduction (-32.1±4.0%) was seen for the isobaric compliance index given the lack of blood pressure increase during the intra-arterial infusion of the drug. Conversely, radial artery diameter and compliance increased throughout the systolic-diastolic pressure range when papaverine was infused for 15 minutes into the brachial artery, the dose used (0.8 µg/kg per minute) being just below that causing a blood pressure reduction. Under this condition the increases in compliance index and isobaric compliance index were 32.1±3.1% and 34.7±2.9%, respectively.

View this table: [in this window] [in a new window]   Table 1. Percent Changes in Radial Artery Diameter and Arterial Compliance Induced by Intra-arterial Infusion of Phenylephrine and Papaverine in Nine Mildly Essential Hypertensive Patients

Thus, the compliance of middle-sized arteries can be reduced by short-term increases in sympathetic drive. If a massive adrenergic stimulation is obtained by pharmacological means, the reduction in arterial compliance can be a marked one. It is likely that this is due to an increase in the contractile state of vascular smooth muscle causing a reduction in the arterial elastic modulus.⁴ Arterial compliance can also be increased much above the baseline value, indicating the existence of a marked "compliance reserve" with respect to baseline conditions. This can be obtained by vascular smooth muscle relaxation independent of changes in adrenergic drive.

	Sympathetic Activation and Radial Artery Compliance in Congestive Heart Failure

Top Abstract Introduction Effect of Adrenergic Stimulation... Sympathetic Activation and... Arterial Compliance and... References

 
Plasma norepinephrine measurements, calculation of plasma norepinephrine spillover, and direct recording of efferent postganglionic muscle sympathetic nerve activity have provided evidence that congestive heart failure is characterized by sympathetic activation.^{17 18 19 20 21} It has also been shown that congestive heart failure is accompanied by a reduction in arterial compliance.^{22 23 24} To clarify whether these two phenomena are related, we studied 17 hospitalized patients (age, 59.7±2.5 years; mean±SEM) with congestive heart failure (New York Heart Association classes II through IV). Heart failure was due to either idiopathic dilated cardiomyopathy (n=9) or coronary heart disease (n=8). Patients were included in the study if there was (1) no history or evidence of arterial hypertension, diabetes mellitus, or renal insufficiency; (2) no history of myocardial infarction in the 6 months preceding the study; (3) no clinical or laboratory evidence of major atherosclerotic lesions at carotid and femoral arteries; and (4) no major arrhythmias. Any cardiovascular drug treatment was withdrawn 5 days before the study, with the exception of diuretics and digitalis, which were maintained in 4 patients because of the severity of the congestive heart failure condition. Measurements consisted of beat-to-beat arterial blood pressure (Finapres technique),¹² heart rate (electrocardiogram), left ventricular end-diastolic diameter, and ejection fraction (echocardiography).²⁵ Plasma renin activity and plasma norepinephrine were also measured by radioimmunoassay²⁶ and high-performance liquid chromatography,¹⁶ respectively, of blood samples taken from an antecubital vein. Finally, efferent postganglionic muscle sympathetic nerve activity (MSNA) was measured in the left peroneal nerve by microneurography, as described previously,^{11 27} and radial artery diameter and compliance were measured by the method mentioned above and described in detail elsewhere.^{7 13 14} As mentioned above, radial artery compliance was expressed as compliance values over the systolic-diastolic pressure range, compliance index, and compliance index in isobaric conditions. All measurements were performed in the morning with the patient supine.

In the group as a whole, baseline systolic pressure was 124.7±4.6 mm Hg (mean±SEM), diastolic pressure was 75.3±3.2 mm Hg, heart rate was 80.5±2.6 beats per minute, left ventricular end-diastolic diameter was 64.8±3.0 mm, left ventricular ejection fraction was 41.1±3.5%, plasma renin activity was 8.8±2.1 ng/mL per hour, and plasma norepinephrine was 488.0±41 pg/mL. MSNA was 62.1±4.5 when assessed as bursts per minute and 76.3±4.4 when assessed as bursts per 100 heartbeats to correct for between-subject differences in heart rate.^{11 27} Radial artery diameter was 3.30±0.11 mm, and radial artery compliance index was 4.04±0.65 mm²/mm Hg · 10^-3. Left ventricular end-diastolic diameter and left ventricular ejection fraction were clearly below and plasma renin activity and plasma norepinephrine concentrations clearly above normal ranges.^{16 26 28 29} Even compliance index and microneurographic values were below and above, respectively, the reported normal values.^{7 14 21 24 29}

As shown in Fig 3 there was a significant inverse relationship between radial artery compliance index and MSNA, when the latter was expressed as both bursts per minute and bursts per 100 heartbeats. The relationship was significant also when the 4 patients in whom diuretics and digitalis were not withdrawn were excluded and calculations were made on 13 patients only (r=.58 and r=.51, respectively; P<.05). In contrast, no relationship was found between radial artery compliance index and mean arterial pressure, plasma norepinephrine, or plasma renin activity (r=.25, r=.08, and r=.19, respectively; P=NS). Radial artery diameter also showed no correlation with MSNA, plasma norepinephrine, or plasma renin activity. Thus, in congestive heart failure the greater the MSNA the lower the radial artery compliance, suggesting that the impairment of arterial compliance characterizing this condition may depend on sympathetic activation. This activation seems to be more precisely quantified by direct sympathetic nerve recording than by plasma norepinephrine measurements, probably because in congestive heart failure a plasma norepinephrine increase depends also on a reduced tissue clearance of this substance.^{18 30} This does not deny the possibility that other factors known to be activated in congestive heart failure may constrict arterial smooth muscle, thereby contributing to the reduction in compliance. In our patients, however, the renin-angiotensin system seemed to be of little importance in causing arterial compliance alterations because no correlation was seen between the elevated plasma renin values and the arterial compliance reduction.

View larger version (10K): [in this window] [in a new window]   Figure 3. Scatterplots show inverse relationship between radial artery compliance and muscle sympathetic nerve activity (MSNA) expressed as bursts (bs) per minute (left) and bursts per 100 heartbeats (hb, right). Compliance is expressed as compliance index (see text).

Do alterations of radial artery compliance (ie, a muscle artery) occurring in congestive heart failure reflect compliance alterations in larger elastic arteries? This question cannot be answered by our data. However, although the techniques used did not permit estimation of compliance-pressure curves, thereby accounting for possible changes in compliance caused by blood pressure changes, several studies have reported a reduction of large artery compliance in congestive heart failure.^{2 22 31 32} Furthermore, in our congestive heart failure patients we measured arterial baroreflex sensitivity by the vasoactive drug infusion technique,³³ ie, by stepwise intravenous infusion of phenylephrine at doses of 0.3, 0.6, and 0.9 µg/kg per minute, each step being maintained for 5 minutes, and by stepwise intravenous infusion of nitroprusside at doses of 0.4, 0.8, and 1.2 µg/kg per minute, each step also being maintained for 5 minutes. The first drug to be infused was selected randomly, and a 45-minute recovery period was observed between the end of the first vasoactive drug infusion and the beginning of the second. Data were collected in the same experimental session in which radial artery data were collected. Baroreflex sensitivity was estimated by averaging the ratio between the percent changes in MSNA induced by mean arterial pressure (diastolic pressure plus one third pulse pressure) changes separately for baroreceptor stimulation (phenylephrine) and unloading (nitroprusside).

As indicated above, radial artery compliance was expressed as a single figure by calculating the area under the curve relating compliance to the existing systolic-diastolic pressure range corrected for pulse pressure (compliance index). It can be seen from Fig 4 that when assessed for both baroreceptor stimulation and baroreceptor unloading, the sensitivity of the baroreceptor-MSNA reflex was directly related to radial artery compliance. Because baroreceptors are stretch receptors located in the carotid arteries, the subclavian artery, and the aorta,^{34 35} which respond to the arterial distension caused by pressure stimuli,^{33 36} this allows us to suggest that at least in congestive heart failure the reduction in compliance seen in middle-sized muscle arteries reflects a reduction in large arteries as well. It also implies (albeit the evidence has only a correlative nature) that the reduction of arterial compliance occurring in congestive heart failure probably leads to an impairment of reflex restraint of sympathetic tone, namely, that the reduction in arterial compliance may represent a causative factor for the sympathetic activation characterizing congestive heart failure.

View larger version (15K): [in this window] [in a new window]   Figure 4. Scatterplots show direct relationship between radial artery compliance and sensitivity of arterial baroreflex control of muscle sympathetic nerve activity (MSNA) assessed for baroreceptor stimulation (phenylephrine, left) and baroreceptor deactivation (nitroprusside, right). Compliance is expressed as compliance index.

	Arterial Compliance and Sympathetic Tone

Top Abstract Introduction Effect of Adrenergic Stimulation... Sympathetic Activation and... Arterial Compliance and... References

 
Evidence that sympathetic activation is accompanied by a reduction of arterial compliance does not answer the question of whether in resting conditions (ie, without any laboratory or pharmacological interventions capable of modifying sympathetic activity) arterial compliance is under sympathetic influences. We addressed this issue in six patients (age, 60.6±2.9 years; mean±SEM) in whom the brachial plexus had to be acutely anesthetized (via local injections of 3 mg/kg mepivacaine 0.1% and bupivacaine 0.5%) to surgically correct Dupuytren's disease. Radial artery diameter, radial artery compliance, and finger blood pressure were continuously measured by the techniques used in the studies mentioned above, and the measurements were obtained before and 20 minutes after the brachial plexus anesthesia. The measurements were completed over 15 minutes, and blockade of nerve conduction was verified by the occurrence of sensorimotor paralysis of the ipsilateral limb. Radial artery compliance was expressed as values obtained over the systolic-diastolic wave range and as compliance indexes as mentioned above. As shown in the example of Fig 5 and in the average data of Table 2, pharmacological blockade of the brachial plexus did not alter blood pressure, heart rate, and radial artery diameter. In contrast, a marked increase in radial artery compliance was observed. On average, the increase in radial artery compliance index amounted to 30.0±5.0%. Thus, radial artery compliance cannot only be markedly reduced when the sympathetic nervous system is phasically activated but it can also be markedly increased when sympathetic activity is suddenly blocked. At least at the radial artery level, arterial compliance is therefore under a pronounced tonic sympathetic restraint that allows both sympathetic-related reductions and sympathetic-related increases in arterial wall distensibility after central reflex alterations in sympathetic drive.

View larger version (17K): [in this window] [in a new window]   Figure 5. Tracings show original recordings of beat-to-beat radial artery diameter (top) and arterial compliance (bottom) changes from one subject who underwent brachial plexus anesthesia. Blood pressure (BP) and heart rate (HR) were not affected by the maneuver, which markedly increased arterial compliance and to a lesser extent arterial diameter.

View this table: [in this window] [in a new window]   Table 2. Hemodynamic Effects of Brachial Plexus Anesthesia in Six Patients

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