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(Hypertension. 1996;27:276-280.)
© 1996 American Heart Association, Inc.

Articles

Sympathetic Nerve Activity and Insulin in Obese Normotensive and Hypertensive Men

Soffia Gudbjörnsdóttir; Peter Lönnroth; Yrsa Bergmann Sverrisdóttir; B. Gunnar Wallin; Mikael Elam

From The Lundberg Laboratory for Diabetes Research, Department of Internal Medicine (S.G., P.L.) and Institute of Clinical Neurosciences (Department of Neurophysiology) (Y.B.S., B.G.W., M.E.), Sahlgrenska University Hospital, Göteborg, Sweden.

Correspondence to Soffia Gudbjörnsdóttir, The Lundberg Laboratory for Diabetes Research, Department of Internal Medicine, Sahlgrenska University Hospital, S-41345 Göteborg, Sweden.

	Abstract

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Abstract The relationship between resting levels of muscle sympathetic nerve activity (MSA) and blood pressure is a matter of controversy. Body weight has recently been identified as an independent determinant of muscle sympathetic discharge, which may have influenced previous studies focused on MSA and mechanisms of hypertension. In the present study, we measured resting MSA and plasma insulin levels in 18 obese (body mass index, 32±4 kg/m²) (mean±SD), middle-aged (52±6 years), hypertensive (155±11/97±8 mm Hg) subjects and 16 age- and body mass index–matched normotensive control subjects. In the postabsorptive state, resting MSA was similar in the hypertensive and normotensive groups (43±4 versus 39±3 bursts per minute, 69±5 versus 64±5 bursts per 100 heart beats, P=NS) (mean±SEM) and did not correlate with either systolic or diastolic blood pressure. Weak but significant positive correlations were found between resting MSA and both fasting insulin levels (P<.05) and body mass index (P=.05) in hypertensive but not normotensive subjects. There was a strong positive correlation between fasting insulin and body mass index in both normotensive subjects and the entire study group (P<.005). Fasting insulin and body mass index correlated with diastolic blood pressure (P<.05) in the entire study group. In conclusion, a relationship between fasting insulin, body mass index, and blood pressure was confirmed, whereas only a weak correlation was found between MSA and fasting insulin in hypertensive but not normotensive subjects. The fact that MSA was similar in the two groups argues strongly against augmented MSA being important for the maintenance of hypertension, at least in middle-aged, obese men.

Key Words: microneurography • sympathetic nerve activity • hypertension • insulin • obesity

	Introduction

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Epidemiological studies have demonstrated an association between obesity, insulin resistance, and hypertension.¹ Even lean individuals with hypertension are insulin resistant and hyperinsulinemic,² and hypertension has been suggested to be an insulin-resistant state.³ An acute rise in plasma insulin levels is known to increase intraneurally recorded MSA,^{4 5} and sympathetic activation has been suggested to constitute a pathophysiological link between insulin resistance/hyperinsulinemia and primary hypertension.^{6 7} In agreement with this hypothesis, correlations were found between augmented MSA and both obesity⁸ and hypertension (see below), and weight reduction led to a decrease in both resting MSA and BP.⁹ On the other hand, studies of the relationship between resting MSA and BP level have yielded conflicting results.

Early studies showed no significant difference in resting MSA between patients with primary hypertension and normotensive control subjects.^{10 11} In contrast, Yamada and coworkers¹² found an increased MSA in a large group of hypertensive patients. Some subsequent studies have demonstrated increased MSA in young, mildly hypertensive subjects,^{13 14} whereas others have found no significant difference compared with control subjects.^{15 16} One reason for the varying results may be that hypertension covaries with other factors (such as obesity, altered glucose metabolism, and sleep disturbances), which per se may affect MSA.¹⁷ Thus, Scherrer et al⁸ recently found positive correlations between MSA, BMI, and plasma insulin and concluded that BMI and plasma insulin are independent determinants of MSA. These factors were not controlled in the majority of previous reports on the relationship between levels of MSA and BP. Therefore, the aim of the present study was to quantitate resting levels of MSA and fasting plasma insulin in middle-aged, obese men with established hypertension and in BMI- and age-matched control subjects to further investigate the relationship between resting MSA and BP level.

	Methods

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Subjects
Eighteen obese, white hypertensive men with no other disease and with no antihypertensive therapy or monotherapy only (8 with angiotensin-converting enzyme inhibitors, 4 with ß-blocking agents, 2 with calcium channel blocking agents, and 4 with no medication) were recruited by advertisement in a local newspaper. After an initial physical examination and biochemical characterization, the antihypertensive medication was discontinued 3 weeks before the study, with no adverse effects. Hypertension was defined as DBP higher than 90 mm Hg on three occasions during the 3 weeks after cessation of treatment. Sixteen BMI- and age-matched normotensive control subjects were recruited from the Obesity Outpatients Clinic of the Department of Internal Medicine. Clinical characteristics of the subjects are shown in Table 1. Informed written consent was obtained from each subject, and the study was approved by the local ethics committee.

View this table: [in this window] [in a new window]   Table 1. Clinical Characteristics of Study Subjects

Study Design
Left arm supine BP was measured weekly throughout the study period with a sphygmomanometer after 10 minutes of rest. DBP was defined as Korotkoff phase V. Three weeks after antihypertensive medication was discontinued, resting MSA was recorded and blood samples for analysis of plasma levels of insulin and glucose were taken, the experimental procedures starting at 8 AM after an overnight fast. The control subjects underwent the same protocol.

Microneurography
Multiunit efferent postganglionic sympathetic activity was recorded with a tungsten microelectrode with a tip diameter of a few microns inserted in a muscle fascicle of the peroneal nerve at the fibular head. A reference electrode was inserted subcutaneously 1 to 2 cm away from the recording electrode. When a muscle nerve fascicle had been identified, small electrode adjustments were made until a site was found in which sympathetic impulses with adequate signal-to-noise ratio could be recorded. Criteria for MSA and details regarding the recording technique have been described previously.¹⁸ The original nerve signal was fed through a band-pass filter with a bandwidth of 700 to 2000 Hz. A mean voltage neurogram was obtained by passage of the filtered neurogram through a resistance-capacitance integrating network with a time constant of 0.1 second. The integrated neurogram was displayed on an ink-jet recorder (Mingograph 800, Siemens-Elema Ltd) at a paper speed of 5 mm/s, together with an electrocardiogram derived with standard chest leads. Respiratory movements were monitored by a strain gauge attached to a rubber strap around the chest. All registered signals were stored on a VHS tape recorder (Racal Recorders Ltd). Sympathetic neural bursts were identified by inspection of the mean voltage neurogram. The number of sympathetic bursts was counted during the last 5 minutes of a 15- to 20-minute rest period. MSA is expressed as burst frequency (bursts per minute) and burst incidence (bursts per 100 heart beats).

Chemical Analyses
Blood glucose levels were determined with a glucose 6-phosphate dehydrogenase method (Beckman Instruments) (coefficient of variation, 3%). Plasma insulin was assayed with a radioimmunoassay (Pharmacia) (coefficient of variation, 6%).

Data Analysis
All data are presented as mean±SEM, except the values in Table 1, which are mean±SD. Two-tailed Student's t test for unpaired data was used to compare resting MSA levels in hypertensive and normotensive subjects. The relationships between MSA, BMI, plasma insulin levels, and BP were assessed with multiple regression analysis; a value of P<.05 was considered significant.

	Results

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Table 1 shows the clinical characteristics of all subjects. Mean BP values were 155±11/97±8 and 126±12/79±7 mm Hg in hypertensive (registered 3 weeks after withdrawal of medication) and normotensive subjects, respectively. Fasting blood glucose was similar in the two groups, but the hypertensive group tended to have a higher plasma insulin level (P=.1). Resting MSA was similar in normotensive and hypertensive subjects, when expressed as both burst frequency (39±3 versus 43±4 bursts per minute, P=NS) and burst incidence (64±5 versus 69±5 bursts per 100 heart beats, P=NS) (Fig 1). A correlation matrix for MSA burst incidence, BMI, plasma insulin, and DBP is shown in Table 2 for the entire study group and separately for hypertensive and normotensive subjects. MSA burst incidence was weakly correlated with plasma insulin levels and BMI in the hypertensive (r=.49, P<.05 and r=.47, P<.05, respectively) (Fig 2) but not in the normotensive subjects nor in the entire study group. MSA did not correlate with SBP (data not shown) or DBP.

View larger version (43K): [in this window] [in a new window]   Figure 1. Bar graphs show average resting MSA in hypertensive (hatched columns) and normotensive (open columns) subjects expressed as MSA burst frequency (bursts per minute) and burst incidence (bursts per 100 heart beats).

View this table: [in this window] [in a new window]   Table 2. Correlation Matrix Showing Pairwise Associations of Relevant Variables for Entire Study Group and Separately for Normotensive and Hypertensive Subjects

View larger version (17K): [in this window] [in a new window]   Figure 2. Scatterplots show relationship between resting MSA (bursts per 100 heart beats) and BMI and fasting plasma insulin concentrations in hypertensive subjects and age- and BMI-matched normotensive control subjects. The regression lines represent hypertensive subjects.

BMI correlated with plasma insulin levels in the entire study group (r=.65, P<.001) and normotensive subjects (r=.84, P<.001), whereas the relationship did not reach significance in the hypertensive group (r=.43, P=.07) (Table 2). BMI correlated with SBP (data not shown) and DBP in the entire study group and with SBP in the normotensive subjects (data not shown).

Plasma insulin correlated with SBP (r=.45, P<.05) (data not shown) and DBP (r=.39, P<.05) (Table 2) in the entire study group and with SBP in the normotensive group (r=.53, P<.05) (data not shown).

Multiple linear regression analysis with MSA as the dependent variable showed that BMI, plasma insulin, age, and DBP determined 5% and 6% of the variability of MSA expressed as burst incidence and burst frequency, respectively.

	Discussion

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The main result of the present study is that no difference in MSA was found between hypertensive and normotensive middle-aged obese men matched for BMI and age. Thus, the role of MSA in the development or maintenance of hypertension must be questioned.

MSA and BP Level
Previous studies on the relationship between resting levels of MSA and BP have yielded conflicting results (see above). Since there are large interindividual differences in resting MSA levels in healthy subjects,¹⁹ random differences related to too small subject groups may contribute to the varying results.²⁰ However, given the recent demonstration of a significant positive correlation between BMI/percent body fat and resting MSA,⁸ differences in body weight may also be a confounding factor. For example, in one study of established hypertensive patients with¹² and two studies of patients without^{10 11} evidence of increased MSA, body weight was not controlled for. Furthermore, in young borderline hypertensive subjects, both unaltered¹⁵ and augmented¹³ MSA have been reported, but in the latter study the hypertensive subjects were significantly heavier than the normotensive control subjects. In addition, the MSA increase in hypertensive subjects could not be confirmed in a later study from the same laboratory.¹⁶ A recent study of eight borderline hypertensive patients and eight weight- and age-matched normotensive control subjects showed a higher average MSA in the hypertensive group, but the difference was primarily due to two patients with markedly higher MSA levels than the rest of the study group.¹⁴ Another reason for variability among studies may be sex differences. Recently, women were found to have lower resting MSA levels than men²¹ ; therefore, differences in the proportions of men and women may also confound comparisons among groups. In the present study of 34 men, hypertensive and normotensive subjects matched for BMI and age did not differ in resting MSA. This finding argues against established hypertension being associated with augmented MSA.

MSA and Obesity
Body weight reduction in obese borderline hypertensive women has been shown to decrease MSA and DBP,⁹ which is compatible with a relationship between obesity and MSA. Recent studies have found a positive correlation between obesity and resting MSA.^{22 23} Spraul et al²² found this correlation in whites but not in age- and weight-matched Pima Indians, suggesting that a relationship between obesity and MSA may depend on genetic factors. As mentioned above, Scherrer and coworkers⁸ recently demonstrated a correlation between MSA, BMI, and body fat in a group of healthy men and women covering a broad spectrum of percent body fat and suggested body fat to be a major determinant of resting MSA in healthy subjects. In contrast, we found only a weak correlation between MSA and BMI in the hypertensive group and no correlation in the normotensive one. The reason for this discrepancy is unclear, but the fact that all our subjects were male and had a less wide span of both BMI and age may contribute. In fact, if subjects in the study group of Scherrer et al who fall within our BMI range (24 to 43 kg/m²) are considered, the correlation between BMI and MSA appears to be weak also in their study. Together with our present findings, this argues against the view that BMI is a major determinant of MSA. Regarding the fat distribution, it is worth noting that the two study groups showed no difference in waist-hip ratios and that there was no correlation between MSA and waist-hip ratios.

MSA and Plasma Insulin
An acute increase in plasma insulin level is known to augment MSA in normotensive^{4 5} and borderline hypertensive²⁴ subjects. In obese normotensive subjects, Vollenweider et al²³ found impaired muscle sympathetic responses to physiological hyperinsulinemia, whereas a normal increase in MSA has been reported in obese hypertensive subjects.²⁵ In the latter patient category, renal and total body norepinephrine spillovers remained unaffected during insulin clamp.²⁵

A correlation between fasting insulin level and MSA was recently demonstrated,⁸ indicating a relationship also between habitual insulin levels and MSA. In our study, no such correlation was found between MSA expressed as bursts per minute and fasting plasma insulin levels. MSA burst incidence (bursts per 100 heart beats) correlated weakly with plasma insulin in the hypertensive group but not in the normotensive or entire study group (Fig 2). Insulin has been assumed to stimulate sympathetic activity at a central level,²⁶ and the present finding may indicate a difference in central sympathetic response to insulin between the two groups. However, the relationship between MSA and insulin was weak also in hypertensive subjects, casting doubt on the functional importance of this relationship in established hypertension.

Obesity, Plasma Insulin, and Hypertension
The majority of newly diagnosed hypertensive individuals are obese.²⁷ Obesity, particularly of the abdominal type, is associated not only with hypertension but also with insulin resistance and secondary hyperinsulinemia,²⁸ which has been considered important for the development of high BP (see above). Arguing against this notion, several studies have demonstrated that the fasting insulin levels are elevated to a similar degree in obese normotensive and obese hypertensive individuals.^{3 29 30} In the present study, fasting insulin levels correlated weakly with DBP in the entire study group but did not differ significantly between normotensive and hypertensive subjects. Thus, fasting insulin level does not appear to be the factor mediating a coupling between obesity and hypertension. On the other hand, insulin levels attained during an oral glucose tolerance test are generally higher in obese hypertensive than obese normotensive subjects,³¹ leaving the possibility that stimulated insulin levels or the insulin resistance as such may play a role. However, fasting insulin levels correlate strongly with standard measurements of insulin resistance obtained during euglycemic hyperinsulinemic clamp³² (r=.7 in our laboratory, unpublished observations, 1995). Given the lack of difference in MSA in the present study, one possibility is that the difference between hypertensive and normotensive subjects lies in different modulating actions of insulin/insulin resistance on neuroeffector transfer at the vascular level.³³ In this context, it is of interest that insulin resistance in obese subjects has recently been shown to be associated with augmented norepinephrine sensitivity and decreased norepinephrine clearance,³⁴ which potentially could contribute to hypertension.

In conclusion, the present data confirm that BMI and plasma insulin levels are closely related and both of these factors correlate weakly with BP. On the other hand, the relationship between MSA and each of these factors remains unclear, and in our present study group BMI, plasma insulin, DBP, and age only determined 5% of the variability in MSA when analyzed with multiple linear regression. Furthermore, MSA did not differ significantly between normotensive and hypertensive subjects. Taken together, these findings cast doubt on the notion that altered MSA is an underlying mechanism for hypertension in obese, middle-aged men.

	Selected Abbreviations and Acronyms

 

BMI = body mass index BP = blood pressure DBP = diastolic blood pressure MSA = muscle sympathetic nerve activity SBP = systolic blood pressure

	Acknowledgments

 
This study was supported by grants from the Swedish Medical Research Council (3546, 10864) and Inga-Britt and Arne Lundberg Foundation. Y.B.S. was supported by the Nordic Academy for Advanced Study (NorFA 94.30.065/00). We thank Margareta Landén and Tomas Karlsson for laboratory assistance.

Received June 13, 1995; first decision August 10, 1995; accepted October 23, 1995.

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This Article Abstract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Gudbjörnsdóttir, S. Articles by Elam, M. Search for Related Content PubMed PubMed Citation Articles by Gudbjörnsdóttir, S. Articles by Elam, M. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Medline Plus Health Information High Blood Pressure Nutrition Obesity