Nonuniform regional sympathetic nerve responses to hyperinsulinemia in rats

1993 ◽  
Vol 264 (2) ◽  
pp. R423-R427 ◽  
Author(s):  
D. A. Morgan ◽  
T. W. Balon ◽  
B. H. Ginsberg ◽  
A. L. Mark
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Plasma Insulin ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Wistar Kyoto ◽  
Alpha Chloralose

The insulin hypothesis of hypertension proposes that hyperinsulinemia increases sympathetic nerve activity (SNA) and raises arterial pressure. The goals of this study were 1) to determine if hyperinsulinemia produces regionally uniform or nonuniform increases in SNA and 2) to test the hypothesis that spontaneously hypertensive rats (SHR) have exaggerated sympathoadrenal responses to hyperinsulinemia. We measured plasma insulin, blood glucose, mean arterial pressure, and adrenal, renal, and lumbar SNA in alpha-chloralose-anesthetized SHR and normotensive Wistar-Kyoto (WKY) rats before and during infusion of two doses of insulin for 60 min each while maintaining euglycemia. In WKY rats, graded increases in plasma insulin from 27 +/- 5 (SE) to 200 +/- 29 microU/ml increased lumbar SNA from 100% to 285 +/- 26% but failed to significantly increase adrenal or renal SNA. In SHR rats, similar increases in plasma insulin from 27 +/- 4 to 213 +/- 33 microU/ml caused significant increases in adrenal (100% to 174 +/- 16%) and lumbar (100% to 307 +/- 26%) SNA but not in renal SNA. Despite increases in SNA, mean arterial pressure did not increase significantly in either group of rats. We conclude that 1) hyperinsulinemic euglycemic clamp produces regionally nonuniform increases in sympathetic nerve activity, and 2) there is a potentiated increase in adrenal SNA in SHR compared with WKY rats during hyperinsulinemia, whereas lumbar SNA responses were similar in the two strains, and renal SNA did not increase in either strain.

Nonuniform sympathetic nerve responses after sustained elevation in arterial pressure

1996 ◽  
Vol 271 (5) ◽  
pp. R1264-R1269 ◽  
Author(s):  
D. E. Claassen ◽  
D. A. Morgan ◽  
T. Hirai ◽  
M. J. Kenney
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Nerve Activity ◽  
Spontaneously Hypertensive ◽  
Aortic Depressor Nerve ◽  
Alpha Chloralose

We tested the hypothesis that sustained increases in mean arterial pressure (MAP) produce nonuniform changes in regional sympathetic nerve discharges (SND) after the return of MAP to control levels. Renal, adrenal, splanchnic, and lumbar SND were recorded before, during, and after a 30-min elevation in MAP produced by phenylephrine (PE) infusion in alpha-chloralose-anesthetized spontaneously hypertensive (SH) rats. SND remained reduced from control values after PE infusion, despite the return of MAP to control levels. Importantly, the duration of poststimulus sympathoinhibition was significantly less in adrenal and splanchnic SND compared with renal and lumbar SND. In sinoaortic-denervated SH rats, SND remained at control levels during and after PE infusion. Simultaneous recordings of aortic depressor nerve (ADN) activity and SND demonstrated that prolonged renal and lumbar sympathoinhibition occurred even when ADN activity fell below control levels after PE infusion. We conclude that poststimulus responses of efferent SND in SH rats are regionally nonuniform and that renal and lumbar sympathoinhibitory responses are not mediated solely by prolonged increases in afferent baroreceptor nerve activity.

scholarly journals Postexercise hypotension is mediated by reductions in sympathetic nerve activity

1999 ◽  
Vol 276 (1) ◽  
pp. H27-H32 ◽  
Author(s):  
Jennifer M. Kulics ◽  
Heidi L. Collins ◽  
Stephen E. DiCarlo
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Peripheral Resistance ◽  
Dynamic Exercise ◽  
Nerve Activity ◽  
Spontaneously Hypertensive ◽  
Before And After ◽  
Postexercise Hypotension ◽  
Carotid Arterial

Mean arterial pressure (MAP), the product of cardiac output (CO) and total peripheral resistance (TPR), is reduced below preexercise levels after a single bout of mild to moderate dynamic exercise. Thus acute, dynamic exercise may be used as a safe, therapeutic approach to reduce MAP. However, the mechanisms responsible for the postexercise hypotension (PEH) are unknown. We tested the hypothesis that PEH is associated with reductions in TPR and sympathetic nerve activity (SNA). Two experimental protocols were designed to test this hypothesis in male spontaneously hypertensive rats (SHR). In protocol 1( n = 9), CO and TPR were determined before, during, and after exercise. In protocol 2 ( n = 7), lumbar SNA (LSNA) was recorded before and after exercise. Rats in protocol 1 were chronically instrumented with left carotid arterial catheters and ascending aortic Doppler ultrasonic flow probes. Rats in protocol 2 were chronically instrumented with left carotid arterial catheters and electrodes around the lumbar sympathetic trunk. Dynamic treadmill exercise (9–12 m/min, 10% grade for 40 min) resulted in a postexercise reduction in MAP (from 143 ± 5 to 128 ± 4 mmHg, P < 0.05). Associated with the PEH was a reduction in TPR (from 28 ± 3 to 19 ± 2 mmHg/kHz; P < 0.05) and an elevation in CO (from 5.7 ± 0.4 to 7.2 ± 0.5 kHz; P < 0.05). The reductions in arterial pressure and TPR were associated with a decrease in LSNA (from 98 ± 3 to 49 ± 6%; P < 0.05). These results suggest that PEH is mediated by reductions in TPR and SNA.

Cardiovascular and neurohormonal effects of intravenous adrenomedullin in conscious rabbits

1995 ◽  
Vol 269 (5) ◽  
pp. R1289-R1293 ◽  
Author(s):  
M. Fukuhara ◽  
T. Tsuchihashi ◽  
I. Abe ◽  
M. Fujishima
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Conscious Rabbits ◽  
Renal Sympathetic

Adrenomedullin is a vasodilative peptide and shows slight homology with calcitonin gene-related peptide. In the present study, we investigated the effects of adrenomedullin on cardiovascular and neurohormonal responses in 13 conscious rabbits. The animals were chronically instrumented with bipolar electrodes on the left renal sympathetic nerve. Intravenous administration of human adrenomedullin (10, 100, 1,000, and 3,000 pmol/kg, n = 6) caused a dose-dependent reduction in mean arterial pressure (0 +/- 2, -1 +/- 2, -19 +/- 2, and -29 +/- 4 mmHg, respectively) concomitant with increases in heart rate, renal sympathetic nerve activity, plasma renin activity, and plasma norepinephrine. The significant reduction in mean arterial pressure induced by 1,000 pmol/kg of adrenomedullin occurred within 1 min after injection and lasted for 15 min (n = 7). In contrast, the significant increases in heart rate and renal sympathetic nerve activity lasted for more than 50 min. When mean arterial pressure was decreased by 15 mmHg by adrenomedullin, the increases in heart rate and renal sympathetic nerve activity were 53 +/- 8 beats/min and 78 +/- 13%, respectively, which were significantly smaller than those induced by intravenous injection of sodium nitroprusside (102 +/- 14 beats/min and 155 +/- 34%, respectively). These results suggest that intravenous adrenomedullin exerts a hypotensive action that is associated with the attenuated reflex-mediated sympathetic activation.

Effects of intravenous infusions of angiotensin II on muscle sympathetic nerve activity in humans

1991 ◽  
Vol 261 (3) ◽  
pp. R690-R696 ◽  
Author(s):  
T. Matsukawa ◽  
E. Gotoh ◽  
K. Minamisawa ◽  
M. Kihara ◽  
S. Ueda ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Sympathetic Outflow ◽  
Ang Ii ◽  
Nerve Activity ◽  
Intravenous Infusions

The effect of angiotensin II (ANG II) on the sympathetic outflow was examined in normal humans. The mean arterial pressure and muscle sympathetic nerve activity (MSNA) were measured before and during intravenous infusions of phenylephrine (0.5 and 1.0 micrograms.kg-1.min-1) or ANG II (5, 10, and 20 ng.kg-1.min-1) for 15 min at 30-min intervals. The baroreflex slope for the relationship between the increases in mean arterial pressure and the reductions in MSNA was significantly less acute during the infusions of ANG II than during the infusions of phenylephrine. When nitroprusside was infused simultaneously to maintain central venous pressure at the basal level, MSNA significantly increased during the infusions of ANG II (5 ng.kg-1.min-1 for 15 min) but not during the infusions of phenylephrine (1.0 micrograms.kg-1.min-1 for 15 min), with accompanying attenuation of the elevation in arterial pressure induced by these pressor agents. These findings suggest that ANG II stimulates the sympathetic outflow without mediating baroreceptor reflexes in humans.

Neurocirculatory Responses to Sevoflurane in Humans

1995 ◽  
Vol 83 (1) ◽  
pp. 88-95. ◽  
Author(s):  
Thomas J. Ebert ◽  
Michael Muzi ◽  
Craig W. Lopatka
Keyword(s):  
Heart Rate ◽  
Steady State ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Central Venous Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Venous Pressure ◽  
Central Venous ◽  
Nerve Activity

Background Sevoflurane and desflurane are new volatile anesthetics with low blood solubilities that confer properties of rapid anesthetic induction and emergence. Desflurane has been associated with neurocirculatory excitation after the rapid increase in inspired concentrations. The current study evaluated and compared the sympathetic and hemodynamic responses associated with the administration of sevoflurane to those associated with administration of desflurane in humans. Methods After Institutional Review Board approval, 21 healthy, young (19-32 yr) volunteers were randomly selected for participation. Arterial and central venous pressures were measured directly, and heart rate, forearm blood flow, and plasma norepinephrine concentrations were determined indirectly. Efferent muscle sympathetic nerve activity was recorded by microneurography. After neurocirculatory recordings at conscious baseline, measurements were repeated beginning 2 min after 2 mg/kg propofol while the anesthetic was increased incrementally by mask over a 10-min period at 1%, 2%, and 3% sevoflurane (n = 12) or 3%, 6%, and 9% desflurane (n = 9). Responses to intubation were recorded and, 20 min later, recordings were evaluated during steady-state periods of 0.41, 0.83, and 1.24 MAC. Data also were obtained after steady-state 0.83 MAC measurements when the inspired gas concentration was rapidly increased to either 3% sevoflurane or 9% desflurane ("transition" to 1.24 MAC). Results Neurocirculatory variables did not differ between the two groups at conscious baseline. During the period of administration via mask and during the "transition" period, the significant increases in sympathetic nerve activity, heart rate, mean arterial pressure, and central venous pressure associated with desflurane were not observed with sevoflurane. Ten minutes after induction, mean arterial pressure and heart rate responses to intubation did not differ between groups. With increasing anesthetic concentration, there were progressive and similar decreases in mean arterial pressure in both groups and no changes in heart rate. Central venous pressure, sympathetic nerve activity, and plasma norepinephrine increased with the greater minimum alveolar concentration multiple of desflurane but not with that of sevoflurane. Conclusions The neurocirculatory excitation seen with rapid increases in desflurane did not occur with sevoflurane. At steady-state, increasing the concentration of sevoflurane was associated with lower sympathetic nerve activity and central venous pressure and similar mean arterial pressure and heart rate with that of desflurane.

Dose-dependent Increases in the Renal Sympathetic Nerve Activity during Rapid Increase in Isoflurane Concentration in Intact, Lower Airway-deafferented, and Baroreceptor-deafferented Rabbits

1996 ◽  
Vol 84 (5) ◽  
pp. 1196-1204 ◽  
Author(s):  
Hirotsugu Okamoto ◽  
Sumio Hoka ◽  
Toshihiro Kawasaki ◽  
Tomoko Okuyama ◽  
Shosuke Takahashi
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Lower Airway ◽  
Direct Stimulation ◽  
Nerve Activity ◽  
Group 3 ◽  
Stimulation Of ◽  
Group 1

Background The inhalation of high concentrations of isoflurane has been reported to increase the heart rate and the concentration of serum catecholamines. Although the precise mechanisms for the sympathetic activation of isoflurane have yet to be clearly elucidated, they are considered to possibly originate from the stimulation of airway sensory afferents, the baroreceptor reflex, or the direct stimulation of the central nervous system. To determine how these three mechanisms contribute to sympathetic augmentation, the effects of lower airway deafferentation and baroreceptor deafferentation on the isoflurane-induced changes in the renal sympathetic nerve activity (RSNA) in tracheally intubated rabbits were examined. Methods Twenty rabbits were given basal anesthesia. After tracheotomy and during mechanical ventilation, the changes in the heart rate, mean arterial pressure, and RSNA in response to random exposures to 1%, 2%, 3%, and 4% isoflurane were examined. The animals were assigned to one of three groups; 1, the intact group (n = 6); 2, the baroreceptor-deafferented group (n = 9), in which the sinoaortic plus vagal nerves were cut; and 3, the lower airway-deafferented group (n = 5), which underwent a bilateral vagotomy. The exposure to isoflurane was for 10 min in group 1 and 5 min in groups 2 and 3. At least 1 h was allowed for the recovery interval between exposures to isoflurane. Results The inhalation of isoflurane caused dose-dependent increases in RSNA in all three groups. RSNA during high concentrations of isoflurane began to increase at 1 min, reaching the maximum at 4 or 5 min in group 1 (2.8- and 3.8-fold at 3% and 4% isoflurane, respectively) and group 3 (2.8- and 4.5-fold at 3% and 4% isoflurane, respectively), but it reached the peak at 2 or 3 min in group 2 (1.7- and 2.4-fold at 3% and 4% isoflurane, respectively) after the initiation of inhalation, in association with early slight increases followed by decreases of mean arterial pressure in groups 1 and 2 but only gradual decreases of mean arterial pressure in group 3. The increases in RSNA in group 3 were similar to group 1, however, those in group 2 were significantly attenuated compared with group 1. Conclusions The inhalation of isoflurane caused an increase of RSNA in intact, baroreceptor-deafferented, and lower airway-deafferented rabbits. The extent of the increases in RSNA was greater in intact and lower airway-deafferented rabbits than in baroreceptor-deafferented rabbits. Therefore, it is suggested that isoflurane may increase the efferent sympathetic nerve activity via the direct stimulation of the central nervous system and via the arterial baroreceptor reflex reflecting the reduction in arterial blood pressure. The stimulation of the vagally innervated airway may not contribute to the increase in the sympathetic nerve activity by isoflurane.

scholarly journals Muscle sympathetic nerve activity and hemodynamic responses to venous distension: does sex play a role?

2019 ◽  
Vol 316 (3) ◽  
pp. H734-H742 ◽  
Author(s):  
Daniel E. Mansur ◽  
Monique O. Campos ◽  
João D. Mattos ◽  
Adrielle C. S. Paiva ◽  
Marcos P. Rocha ◽  
...  
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Young Women ◽  
Femoral Artery ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Pressor Response ◽  
Muscle Sympathetic Nerve Activity ◽  
Venous Compliance ◽  
Nerve Activity

Peripheral venous distension mechanically stimulates type III/IV sensory fibers in veins and evokes pressor and sympathoexcitatory reflex responses in humans. As young women have reduced venous compliance and impaired sympathetic transduction, we tested the hypothesis that pressor and sympathoexcitatory responses to venous distension may be attenuated in women compared with men. Mean arterial pressure (photoplethysmography), heart rate (HR), stroke volume (SV; Modelflow), cardiac output (CO = HR × SV), muscle sympathetic nerve activity (MSNA), femoral artery blood flow, and femoral artery conductance (Doppler ultrasound) were quantified in eight men (27 ± 4 yr) and nine women (28 ± 4 yr) before [control (CON)], during (INF), and immediately after (post-INF) a local infusion of saline [5% of the total forearm volume (30 ml/min); the infusion time was 2 ± 1 and 1 ± 1 min ( P = 0.0001) for men and women, respectively] through a retrograde catheter inserted into an antecubital vein, to which venous drainage and arterial supply had been occluded. Mean arterial pressure increased during and after infusion in both groups (vs. the CON group, P < 0.05), but women showed a smaller pressor response in the post-INF period (Δ+7.2 ± 2.0 vs. Δ+18.3 ± 3.9 mmHg in men, P = 0.019). MSNA increased and femoral artery conductance decreased similarly in both groups (vs. the CON group, P < 0.05) at post-INF. Although HR changes were similar, increases in SV (Δ+20.4 ± 8.6 vs. Δ+2.6 ± 2.7 ml, P = 0.05) and CO (Δ+0.84 ± 0.17 vs. Δ+0.34 ± 0.10 l/min, P = 0.024) were greater in men compared with women. Therefore, venous distension evokes a smaller pressor response in young women due to attenuated cardiac adjustments rather than reduced venous compliance or sympathetic transduction. NEW & NOTEWORTHY We found that the pressor response to venous distension was attenuated in young women compared with age-matched men. This was due to attenuated cardiac adjustments rather than reduced venous compliance, sympathetic activation, or impaired transduction and vascular control. Collectively, these findings suggest that an attenuated venous distension reflex could be involved in orthostatic intolerance in young women.

Renal nerve activity and renal function during environmental stress in DOCA-NaCl rats

1986 ◽  
Vol 251 (2) ◽  
pp. R289-R294 ◽  
Author(s):  
J. P. Koepke ◽  
S. Jones ◽  
G. F. DiBona
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Renal Denervation ◽  
Sympathetic Nerve Activity ◽  
Hypertensive Rats ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Renal Sympathetic

The effects of a stressful environmental stimulus (air stress) on mean arterial pressure, heart rate, renal sympathetic nerve activity, and renal function were studied in conscious deoxycorticosterone acetate-sodium chloride (DOCA-NaCl) hypertensive rats, sham DOCA-NaCl normotensive rats, and DOCA-NaCl rats with renal denervation. In conscious DOCA-NaCl hypertensive rats, air stress decreased urine flow rate [36% from 17.9 +/- 3.0 microliter X min-1 X 100 g body wt-1 (BW)], urinary sodium excretion (39% from 3.1 +/- 0.5 microeq X min-1 X 100 g BW-1), fractional water excretion (24% from 4.72 +/- 1.00%), and fractional sodium excretion (28% from 5.72 +/- 1.08%) and increased renal sympathetic nerve activity (94% from 8.3 +/- 0.6 integrator resets/min), but no changes occurred in glomerular filtration rate (-15% from 0.40 +/- 0.06 ml X min-1 X 100 g BW-1) or effective renal plasma flow (-7% from 2.50 +/- 0.53 ml X min-1 X 100 g BW-1). Air stress had no effect on these measures in conscious sham DOCA-NaCl normotensive rats or DOCA-NaCl rats with renal denervation. Mean arterial pressure and heart rate were unaffected by air stress in these three groups. Renal denervation lowered base-line mean arterial pressure in DOCA-NaCl rats. Thus DOCA-NaCl hypertensive rats respond to environmental stress with increased renal sympathetic nerve activity and, consequently, antidiuresis and antinatriuresis.

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