Biomedical subjects

B G Wallin

Publications and source records attributed to B G Wallin.

At least 19 recordsLinked to original sources

PubMed1997

Sympathetic nerve traffic correlates with the release of nitric oxide in humans: implications for blood pressure control.

1. Resting human sympathetic vasoconstrictor traffic displays large reproducible inter-individual differences which are similar in nerves to muscle, heart and kidney. In spite of this there is no correlation between levels of blood pressure and sympathetic traffic. To test the hypothesis that the pressor effect of the vasoconstrictor activity is counteracted by a circulating dilating factor we measured muscle nerve sympathetic activity (MSA) and an indicator of nitric oxide release (plasma nitrate) in healthy young males. 2. Sympathetic activity was recorded with the microneurographic technique in the peroneal nerve and a forearm venous plasma sample was obtained in twenty-one normotensive males aged 21-28 years. Plasma nitrate was analysed by gas chromatography and mass spectrometry. 3. There was a positive linear correlation between the plasma nitrate concentration and the strength of MSA both when the nerve activity was expressed as bursts per minute and bursts per 100 heart beats (r = 0.51, P = 0.02 and r = 0.46, P = 0.04, respectively). 4. The data suggest that the stronger the sympathetic activity the higher the release of the dilating substance, nitric oxide. This would be expected to counteract vasoconstrictor effects of the nerve traffic and thereby contribute to the lack of relationship between resting levels of MSA and blood pressure. We speculate that altered coupling between sympathetic traffic and nitric oxide release may cause abnormal peripheral resistance, e.g. in hypertension.

Adult↗

PubMed1996

The discharge behaviour of single sympathetic neurones supplying human sweat glands.

Firing properties of single sudomotor axons were studied via tungsten microelectrodes inserted percutaneously into cutaneous fascicles of the peroneal nerve in awake subjects. Sweating was induced by radiant heat and measured by changes in skin electrical resistance within the innervation territory on the dorsum of the foot. Eight units were classified as sudomotor neurones because spike-triggered averaging revealed a time-locked relationship between the unitary discharge and the subsequent decrease in skin resistance (1.12 +/- 0.05 s), but no relationship to skin blood flow (measured by a laser-doppler probe). Sudomotor units usually fired only one (maximum six) spike(s) in a sympathetic burst. The mean firing rate was 0.62 Hz, but instantaneous frequencies above 50 Hz could be generated. R-wave triggered histograms and coherence analysis revealed significant coupling between the firing of three sudomotor neurones and the ECG. Moreover, the firing of four sudomotor neurones showed a weak but significant correlation with the spontaneous fluctuations in cardiac interval, diastolic pressure, or the rate of fall in arterial pressure. We conclude that the discharge of human sudomotor neurones is modulated by baroreceptor input.

Adult↗

PubMed1996

Renal noradrenaline spillover correlates with muscle sympathetic activity in humans.

1. To study the relationship between indices of resting sympathetic traffic in nerves to skeletal muscles and the kidneys, simultaneous measurements were made of muscle sympathetic activity in the peroneal nerve and renal noradrenaline spillover in ten healthy normotensive males aged 18-69 years (mean 42 years). 2. Group mean levels (+/-S.D.) of muscle sympathetic activity and renal spillover were 22 +/- 17 bursts min-1 and 105 +/- 49 ng min-1, respectively. There were significant positive correlations between individual values of muscle sympathetic activity and renal noradrenaline spillover (r = 0.76, P < 0.01) and similarly between muscle sympathetic activity and renal venous plasma concentration of noradrenaline(r = 0.79, P < 0.007). 3. The results indicate that, although the sympathetic system has the capacity for selective activation of different subdivisions, in healthy human subjects resting traffic is similar or proportional in sympathetic nerves to skeletal muscles and the kidney.

Adult↗

PubMed1996

Lateralization of cutaneous inflammatory responses in patients with unilateral paresis after poliomyelitis.

Unilateral paresis remaining after poliomyelitis may affect the expression of inflammatory diseases by lateralization of the disease manifestations. The purpose of this study was to assess the impact of the unilateral paresis after poliomyelitis on lateralization of neurogenic inflammation and immune responsiveness. The delayed-type hypersensitivity (DTH) reaction to tuberculin was used as an in vivo measure of antigen-specific T lymphocyte reactivity. Assessment of axon reflex vasodilatation was simultaneously employed to test for neurogenic inflammation. Fourteen of the 16 polio patients displayed a positive DTH reaction to tuberculin. All but two showed weaker DTH reaction on the paretic- compared to the contralateral-side (P = 0.001). Magnitude of electrically evoked axon reflexes significantly correlated to asymmetries of DTH responses. We conclude that damage of lower motor neuron leads to ipsilateral down-regulation of T cell-mediated cutaneous inflammation. This lateralization of DTH responses is related to deficiencies in motor and sympathetic innervation of the paretic extremity.

Adult↗

PubMed1996

Sympathetic nerve activity and insulin in obese normotensive and hypertensive men.

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.

Adult↗

PubMed1996

Reduced heart rate variability after right-sided stroke.

BACKGROUND AND PURPOSE: Recently, asymmetries have been demonstrated in skin sudomotor and vasomotor function after unilateral cerebral lesions. The present study was performed to determine whether other bedside tests reflecting sympathetic and parasympathetic cardiovascular functions would reveal differences with respect to the side of cerebrovascular lesions. METHODS: Heart rate variability during deep breathing as well as blood pressure and heart rate changes during tilt and isometric handgrip was measured in a group of patients with a monofocal stroke and compared with similar data from age-matched patients with transient ischemic attack and healthy control subjects. RESULTS: Compared with left-sided stroke and with the control subjects, stroke location on the right side was associated with a reduced respiratory heart rate variability (P > .01), a reflex mainly under parasympathetic control. In contrast, reflexes mainly reflecting peripheral sympathetic function were equal for right- and left-sided lesions. CONCLUSIONS: Since an imbalance in cardiac autonomic innervation may be crucial for the generation of cardiac arrhythmias and since reduced heart rate variability has been associated with increased mortality, the findings suggest that the risk of sudden death may be correlated with lateralization and location of the brain infarct after stroke.

Analysis of Variance↗

PubMed1996

Depressed baroreflex sensitivity in patients with obstructive sleep apnea.

Muscle nerve sympathetic activity (MSA), the interval between two R-waves in the ECG, or the interbeat interval (RR-interval), and blood pressure (BP) were recorded in 10 awake patients with obstructive sleep apnea (OSA) and in nine sex- and age-matched controls. Changes in RR-interval and MSA, evoked by sodium nitroprusside-induced reduction of BP, were used to quantitate baroreflex sensitivity. Both the cardiac (expressed as the RR-interval versus mean arterial BP slope) and the muscle sympathetic (mean MSA area versus diastolic BP slope) baroreflex sensitivity were depressed in patients as compared with controls. Cardiac baroreflex slope sensitivity (expressed as a regression coefficient) was 5.5 +/- 1.2 (mean +/- SEM) in patients and 9.6 +/- 0.96 in controls (p < 0.05). The corresponding figures for the sympathetic slope sensitivity were -4.9 +/- 0.9 and -13.1 +/- 2.3, respectively (p < 0.05). Differences remained after stepwise correction for age, body mass index (BMI), and to some extent BP. Resting MSA correlated with cardiac (r = 0.67, p < 0.003) and sympathetic (r = 0.56, p < 0.025) baroreflex sensitivity in the entire study group. We conclude that OSA patients exhibit an impaired baroreflex sensitivity to a hypotensive stimulus, which may represent an adaptive response to changes in BP or hypoxemia occurring in association with nocturnal apneas. Baroreflex adaptation may also contribute to the augmentation of resting MSA observed in OSA patients in this as well as in a previous study.

Adult↗

PubMed1995

Modulation of muscle sympathetic activity during spontaneous and artificial ventilation and apnoea in humans.

Respiratory modulation of muscle sympathetic activity was compared in relaxed subjects breathing spontaneously and in anaesthetized and non-anaesthetized subjects ventilated artificially with intermittent positive pressure. Muscle sympathetic activity was recorded directly from the peroneal nerve using the microneurographic technique. Arterial pressure was monitored continuously either by finger-pulse photoplethysmography (Finapres) or intraarterially. Respiratory modulation of sympathetic activity, heart rate and arterial pressure was measured by averaging consecutive breaths to the ECG R-wave closest to the onset of inspiration. In relaxed subjects (n = 15) breathing quietly the averaged sympathetic activity was greatest during late expiration and the first half of inspiration and minimal after the peak of inspiration, after correcting for delays within the baroreflex loop. Systolic and diastolic pressures fell during inspiration. In anaesthetized or awake subjects ventilated artificially at normal tidal volumes the pattern of respiratory modulation of sympathetic activity was preserved but the changes in arterial pressure were reversed and respiratory sinus arrhythmia abolished. Ventilation with positive end-expiratory pressure (20 cmH2O) increased the overall level of sympathetic activity and enhanced the breath-to-breath modulation. We conclude that, although baroreceptors provide potent modulation of muscle sympathetic activity in humans, the inspiratory inhibition of sympathetic activity does not depend on an increase in arterial pressure and hence an increase in baroreceptor input.

Adult↗

PubMed1995

Effects of static lung inflation on sympathetic activity in human muscle nerves at rest and during asphyxia.

Muscle sympathetic activity is inhibited during the second half of phasic lung inflation associated with normal (negative pressure) breathing or artificial ventilation with intermittent positive-pressure, and this inspiratory inhibition appears unrelated to the associated changes in arterial pressure. In this present study we tested the hypothesis that a static inflation of the lungs would cause a sustained inhibition of muscle sympathetic activity. Microneurographic techniques were used to record muscle sympathetic activity from the peroneal nerve, and arterial pressure was monitored continuously by finger-pulse photoplethysmography (Finapres). In nine subjects static lung inflation, brought about either actively or passively, caused a pronounced and sustained increase in sympathetic activity (not the predicted decrease) that could not be explained by changes in arterial pressure. When delivered at the end of a voluntary end-expiratory apnoea, static lung inflation caused an initial inhibition of the large chemoreceptor-induced sympathetic bursts and a subsequent excitation that was sustained for the duration of the lung inflation. These observations indicate that respiration can affect muscle sympathetic activity in humans in two opposing ways: inhibition during phasic increases in lung volume, and excitation during large static increases in lung volume. Neither phenomenon depends on changes in arterial pressure, and hence influences of carotid arterial and aortic (high-pressure) baroreceptors can be excluded. We suggest that the initial inhibition is evoked from lung or chest-wall receptors and the static exitation from unloading of cardiopulmonary (low pressure) baroreceptors.

Adult↗

PubMed1995

Arteriovenous anastomoses and the thermoregulatory shift between cutaneous vasoconstrictor and vasodilator reflexes.

The reflex changes in skin blood flow which occur in response to various non-thermal stimuli (e.g., deep inspiratory gasps, arousing or painful stimuli, emotional stress) are profoundly influenced by the thermoregulatory state. The aim of the present study was to evaluate the involvement of arteriovenous anastomoses in the thermoregulatory modulation of skin vasomotor reflexes elicited by painful intraneural electrical stimulation and emotional stress (forced arithmetics), respectively. Vasomotor responses were recorded with laser Doppler flowmeters (LDF) placed on glabrous skin containing arteriovenous anastomoses (3rd finger and thenar eminence) and hairy skin which lack them (dorsal side of the first metacarpal bone). In some experiments, a laser Doppler flowmeter emitting laser light of two different wavelengths (infrared and green light) into the same skin site was used to record skin perfusion at different depths of glabrous skin on the thenar eminence. 40 subjects were investigated, both in the cold state (finger skin temperatures below 25 degrees C) and after subsequent warming (finger skin temperatures above 30 degrees C). Thermoregulatory modulation of electrical stimulation- or stress-induced vasomotor reflexes occurred both in glabrous and hairy skin, but hairy skin differed from glabrous skin by showing no significant vasoconstrictions. Relative perfusion changes were most marked in laser Doppler flowmeter recordings using the deeper penetrating infrared light. The results suggest that arteriovenous anastomoses are major contributors to the vasoconstrictor component of vasomotor reflexes in glabrous skin of warm subjects. The reflex increase in perfusion, on the other hand, which occurs in both glabrous and hairy skin of cold subjects may be mediated by resistance vessels.

Adult↗

PubMed1995

Axon-reflex-mediated vasodilatation in the psoriatic plaque?

Blood flow in the psoriatic plaque is increased, but the underlying mechanisms are not known. The aim of the present study was to examine whether neurogenic factors are important for blood flow regulation in the plaque. Local neurogenic mechanisms were inhibited by surface anesthesia and central nervous control by conduction anesthesia of nerves to the psoriatic plaque. The differences in skin perfusion before and after anesthesia were measured with a laser Doppler perfusion imager. The skin perfusion in psoriatic plaques located in hairy skin was unaffected by conduction anesthesia, but surface anesthesia of the plaque evoked a marked blood flow reduction. The perfusion in ultraviolet-B-irradiated skin, used as a control for nonspecific phenomena, was reduced after local application of indomethacin but was unaffected or increased after surface anesthesia. The results are compatible with the idea that a local neurogenic mechanism (axon-reflex) contributes to the high blood flow in the psoriatic plaque.

Adult↗

PubMed1995

Central blood volume influences sympathetic sudomotor nerve traffic in warm humans.

The objective of this study was to test whether changes in central blood volume can induce reflex effects on sweating. Multi-unit skin sympathetic nerve activity (SSA) was recorded from the posterior cutaneous nerve of the forearm or radial nerve branches in 11 healthy volunteers. Skin electrical resistance and skin blood flow were recorded in the area innervated by the impaled nerve fascicle. Sudomotor nerve traffic and sweating was induced by whole body heating. Lower body negative pressure (LBNP) and tilting (30 degrees head up) was used for blood volume displacement from the chest to the lower body. Low levels of LBNP (5 and 10 mmHg) had no effect on blood pressure, heart rate or skin blood flow but induced a prompt inhibition of SSA and a reduced number of transient skin resistance changes (n = 9), both rapidly returning to control levels after cessation of LBNP. Quantitatively, the effect was similar at both levels of LBNP. Head up tilting also reduced SSA (n = 3, 19 tilt manoeuvres). A capacity for mental stress-induced SSA increase remained during LBNP. Spontaneous fluctuations in blood pressure did not affect SSA, arguing against arterial (high-pressure) baroreceptors modulating SSA. Consequently, the present results indicate that unloading of cardiopulmonary (low-pressure) volume receptors reduces sympathetic sudomotor nerve traffic and sweating in warm subjects. It is suggested that the reflex contributes to counteracting hypovolaemia.

Adrenergic Fibers↗

PubMed1995

Lateralization of T-lymphocyte responses in patients with stroke. Effect of sympathetic dysfunction?

BACKGROUND AND PURPOSE: A number of clinical observations indicate that stroke affects the course of immune-mediated diseases by lateralization of the disease manifestations, such as arthritis. The purpose of this study was to assess the impact of early stroke on lateralization of immune responsiveness. METHODS: The delayed-type hypersensitivity (DTH) reaction to purified protein derivative was used as an in vivo measure of antigen-specific T-lymphocyte reactivity. Assessment of axon reflex vasodilation was simultaneously used to test for cutaneous sympathetic activity. RESULTS: There were no significant differences with regard to lateralization of DTH reactivity when all stroke patients were tested. However, patients with minor stroke displayed a significant (P < .001) decrease of DTH reaction on the paretic side compared with the contralateral side. In contrast, patients with major stroke showed a significant increase (P = .022) of DTH reaction on the paretic side. Patients with left hemiparesis had a significantly greater (P = .045) DTH response on the affected side than patients with a right hemiparesis. In addition, only the patients with motor deficit but not with sensory deficit or aphasia displayed side differences in DTH responses. When electrically evoked axon reflexes were studied in relation to DTH reactions, a significant correlation (r = .64; P < .001) was found between side asymmetries of DTH responses and side asymmetries of axon reflexes in an innervated skin area. No similar relation was present in skin areas where cutaneous sympathetic activity had been blocked by regional anesthesia. CONCLUSIONS: Early stroke lateralizes T-cell-mediated cutaneous inflammation. This effect depends on (1) the localization of the brain lesion, (2) the clinical course of the disease, and (3) the presence of motor deficit and may be mediated by (4) alteration of the cutaneous sympathetic nerve traffic.

Adolescent↗

PubMed1994

The discharge behaviour of single vasoconstrictor motoneurones in human muscle nerves.

1. The discharge behaviour of fourteen single sympathetic vasoconstrictor efferents was studied using a tungsten microelectrode inserted percutaneously into a motor fascicle of the radial or peroneal nerve in eight awake supine subjects. Units were classified as vasoconstrictor because their firing properties correlated appropriately to changes in cardiac interval and arterial pressure. 2. On average, individual vasoconstrictor units discharged in only 21% of heart beats, with an overall mean frequency of 0.47 Hz. Usually only one spike was generated per cardiac cycle. Calculated from cardiac cycles in which a unit fired from two to seven spikes, the mean within-burst firing rate was 18.8 +/- 2.5 Hz (mean +/- S.E.M.); but instantaneous frequencies above 50 Hz were occasionally observed. 3. Measured from a defined R-wave of the ECG, the spike onset latency varied over 358 +/- 33 ms, suggesting considerable variation of synaptic delays in the baroreflex arc. This latency had a relatively uniform temporal relationship with the burst onset or peak latency, compatible with a fixed recruitment order of individual sympathetic neurones. 4. In view of the low average firing rate of individual units we suggest that the variable instantaneous firing rates may optimize the contractile responses of vascular smooth muscle.

Adult↗

PubMed1994

Coupling between variations in strength and baroreflex latency of sympathetic discharges in human muscle nerves.

1. Pulse-synchronous multiunit muscle nerve sympathetic activity was recorded simultaneously from two nerves together with ECG in eleven healthy subjects; seven recordings were made from the two peroneal nerves during prolonged expiratory apnoeas and four from a radial and a peroneal nerve during lower body negative pressure of 10-40 mmHg. The neural records were displayed in mean voltage neurograms (time constant 0.1 s) and for each mean voltage burst the following measures were taken and related to each other: amplitude, duration, rise time, decay time and baroreflex latency (from the appropriate R-wave of the ECG to the peak of the burst). 2. Average baroreflex latencies were 1.3 s in the peroneal nerves and 0.9 s in the radial nerve. There were significant positive correlations between both the amplitudes and the baroreflex latencies of corresponding bursts in peroneal-peroneal recordings and in radial-peroneal recordings. 3. In all nerves baroreflex latency shortened significantly when burst amplitude increased. The correlation between burst amplitude and baroreflex latency was weaker in the radial than in the peroneal nerve. The average variation of baroreflex latency in peroneal-peroneal recordings was 0.20 +/- 0.02 s in both legs, and in radial-peroneal recordings the variation was 0.09 +/- 0.01 s in the radial nerve and 0.12 +/- 0.02 s in the peroneal nerve. 4. When peroneal burst amplitudes increased, burst duration increased. This was due to increases of both the rise time and the decay time of the burst, the latter being the greater.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1994

Sympathetic muscle nerve activity, peripheral blood flows, and baroreceptor reflexes in humans during propofol anesthesia and surgery.

BACKGROUND: With percutaneous recordings of muscle nerve sympathetic activity (MSA), it is possible to study interactions between the autonomic nervous system and anesthetics. This study describes the effects of propofol infusion both before and during microlaryngoscopy. METHODS: Nine patients participated. MSA was recorded, muscle and skin blood flows were measured. Sodium nitroprusside-induced decreases in blood pressure were used to quantitate baroreceptor reflex sensitivity. RESULTS: During steady state propofol anesthesia (0.1 mg.kg-1.min-1), "total MSA" (MSA burst area per minute) was 37% (P < 0.05) of awake control value; leg blood flow recorded by strain-gauge plethysmography was 227% (difference not significant); and skin blood flow recorded by laser Doppler flowmetry and finger pulse plethysmography was 300% (P < 0.05) and 376% (P < 0.05) of respective awake control values. During microlaryngoscopy, when mean arterial blood pressure was controlled as close as possible to mean arterial blood pressure in the awake state by individually adjusted propofol infusion rates (average 0.33 mg.kg-1.min-1) MSA was restored to 93% of the activity before anesthesia, and leg blood flow increased further. Both cardiac and muscle sympathetic baroreflex sensitivities were depressed by propofol. During surgery the cardiac baroreflex sensitivity decreased further, whereas the muscle sympathetic baroreflex sensitivity was unchanged. CONCLUSIONS: Propofol is a potent inhibitor of sympathetic neuronal activity and decreases the sensitivity of the baroreflex. When used to control the pressor response during surgery, the vasodilatating effect of propofol overrides the neural vasoconstriction induced by surgery, and a further inhibition of the cardiac baroreflex is observed.

Adult↗

PubMed1994

Skin sympathetic nerve activity and effector function during sleep in humans.

Multi-unit sympathetic skin nerve activity (SSA) in the peroneal nerve was recorded together with electrical skin resistance, skin blood flow and (in some subjects) finger blood pressure during sleep in 22 sleep-deprived healthy subjects. The average strength of sympathetic activity in different sleep stages was measured during 5-min periods as the area-under-curve of the integrated neurogram. Stage 2 sleep was reached by 15 subjects, stages 3-4 by nine and rapid eye movement (REM) sleep by six subjects. Non-REM sleep was always associated with an increased skin resistance, which was larger in glabrous than in hairy skin (293 +/- 48 vs. 175 +/- 4% of awake control level, n = 10, P < 0.05). Skin blood flow also increased during sleep, with a mean maximal increase of 397 +/- 79% of the awake control level (n = 11, P < 0.05). In spite of these changes of effector function no significant difference in mean SSA was found between the awake control period and periods of non-REM sleep, but during REM sleep SSA increased with 34% (P < 0.05) compared with the immediately preceding stage 2 period. In stage 2 sleep, K-complexes were associated with bursts of SSA followed by transient changes of skin resistance, blood flow and arterial blood pressure. When both skin resistance and blood flow were recorded within the innervation area of the impaled fascicle, single bursts or short periods of increased SSA could be succeeded by increased skin blood flow without concomitant skin resistance change. This indicates the existence of specific sympathetic vasodilator fibres in the skin. Therefore the unchanged strength of multiunit SSA during non-REM sleep in the face of increases of skin resistance and blood flow may be a consequence of an increased sympathetic vasodilator nerve activity combined with decreases of vasoconstrictor and sudomotor traffic.

Adult↗

PubMed1994

The effect of metformin and insulin on sympathetic nerve activity, norepinephrine spillover and blood pressure in obese, insulin resistant, normoglycemic, hypertensive men.

To evaluate the effect of metformin on insulin sensitivity and to further examine the relationship between insulin resistance, sympathetic nerve activity and blood pressure, 6 obese insulin resistant, normoglycemic hypertensive men were investigated (age 49 +/- 2 years, BMI 27.6 +/- 1.2, mean +/- SEM). The study had a placebo controlled, double blind, cross over design with 6 weeks' metformin treatment (850 mg b.i.d) vs placebo. Blood pressure was measured weekly. At the end of each treatment period, glucose infusion rate (GIR), muscle sympathetic nerve activity (MSA) and renal and total body norepinephrine (NE) kinetics (radioisotope dilution) were examined during euglycemic hyperinsulinemic clamp. Fasting insulin was 13 +/- 3 and 10 +/- 2 mU/l and fasting glucose 5.3 +/- 0.2 and 5.1 +/- 0.1 mmol/l after placebo and metformin treatment, respectively (ns). GIR during the last hour of the insulin clamp was 3.7 +/- 0.6 vs 3.6 +/- 0.6 mg/kg x min (ns). Resting MSA, total body and right renal NE spillover did not differ significantly after placebo and metformin treatment. Systolic and diastolic blood pressures were 151 +/- 10/95 +/- 5 mmHg after placebo and 146 +/- 5/94 +/- 5 mmHg after metformin treatment (ns). Thus metformin treatment did not have any significant effect on insulin sensitivity, blood pressure or sympathetic activity in this small group of patients. Renal plasma flow and MSA increased significantly during the insulin clamp, whereas renal NE and total body NE spillover remained unchanged, suggesting nonuniform regional sympathetic nerve responses to acute hyperinsulinemia.

Antihypertensive Agents↗