Hypertension and insulin resistance: role of sympathetic nervous system activity

1992 ◽  
Vol 263 (5) ◽  
pp. E935-E942 ◽  
Author(s):  
M. A. Supiano ◽  
R. V. Hogikyan ◽  
L. A. Morrow ◽  
F. J. Ortiz-Alonso ◽  
W. H. Herman ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Multiple Regression Model ◽  
Metabolic Effects ◽  
Plasma Norepinephrine ◽  
Intravenous Glucose ◽  
Arterial Blood ◽  
Sympathetic Nervous ◽  
Intravenous Glucose Tolerance Tests

he purpose of this study was to test the hypothesis that heightened sympathetic nervous system (SNS) activity contributes to the mechanism by which hypertension is associated with insulin resistance in humans. We performed frequently sampled intravenous glucose tolerance tests to determine tissue sensitivity to metabolic effects of insulin (SI) and measured plasma norepinephrine (NE) levels in 21 normotensive and 14 hypertensive Caucasian subjects. Compared with the normotensive subjects, hypertensive subjects had decreased SI (5.4 +/- 0.5 vs. 4.0 +/- 0.7 x 10(-5) x min-1 x pM-1; P = 0.03) but similar plasma NE levels (normotensive: 1.82 +/- 0.12 vs. hypertensive: 1.73 +/- 0.16 nM; P = 0.23). In a multiple regression model, only body mass index (BMI) and mean arterial blood pressure (MABP) were significant independent predictors of SI [SI = (-0.513)(BMI) + (-0.058)(MABP) + 23.6; r = 0.748; P = 0.0001]; age, plasma glucose, epinephrine, and NE level did not enter this model. As an additional test of this hypothesis, seven hypertensive subjects were restudied after 10 days of guanadrel therapy to determine whether SI would increase during suppression of SNS activity by guanadrel. Despite a significant reduction in plasma NE levels with guanadrel (baseline: 1.63 +/- 0.18 vs. guanadrel: 0.99 +/- 0.14 nM; P = 0.01), there was no significant change in SI (baseline: 2.97 +/- 0.78 vs. guanadrel: 2.41 +/- 0.54 x 10(-5).min-1 x pM-1; analysis of variance P = 0.57). We conclude that, in the Caucasian population we studied, heightened SNS activity is not essential for the insulin resistance observed in hypertensive humans.

Effects of chronic NO synthase inhibition in rats on renin-angiotensin system and sympathetic nervous system

1995 ◽  
Vol 268 (6) ◽  
pp. H2267-H2273 ◽  
Author(s):  
A. Zanchi ◽  
N. C. Schaad ◽  
M. C. Osterheld ◽  
E. Grouzmann ◽  
J. Nussberger ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Plasma Norepinephrine ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Arterial Blood ◽  
Sympathetic Nervous

This study was designed to assess the role of renin and of the sympathoadrenal system in the maintenance of the hypertension induced by chronic nitric oxide synthase (NOS) inhibition in rats kept on a normal (RS) or a low-sodium (LS) diet. With the administration of NG-nitro-L-arginine methyl ester (L-NAME) in drinking water (0.4 milligrams) for 6 wk, mean intra-arterial blood pressure rose to a similar extent to 201 mmHg in the RS and 184 mmHg in the LS animals. Simultaneously, plasma norepinephrine was increased to 838 and 527 pg/ml and epinephrine to 2,041 and 1,341 pg/ml in RS and LS, respectively. Plasma neuropeptide Y levels did not change. Plasma renin activity rose to 21 ng.ml-1.h-1 in RS but remained at 44 ng.ml-1.h-1 in the LS. Both losartan (10 mg/kg) and phentolamine (0.1 mg/kg) intravenous bolus injections reduced blood pressure considerably in the L-NAME hypertensive animals. Whole brain NOS activity was reduced by 84%. Hypertension induced by chronic NOS inhibition in LS as well as in RS fed rats seems to be sustained by an interaction of several mechanisms, including the activation of the sympathetic nervous system and the renin-angiotensin system.

Glucose increases rat plasma norepinephrine levels by direct action on the brain

1991 ◽  
Vol 261 (6) ◽  
pp. R1351-R1357 ◽  
Author(s):  
B. E. Levin
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Plasma Glucose ◽  
Direct Action ◽  
Rat Plasma ◽  
Plasma Norepinephrine ◽  
Intravenous Bolus ◽  
Intravenous Glucose ◽  
Sympathetic Nervous ◽  
The Brain

The hypothesis that glucose can selectively activate the sympathetic nervous system (SNS) by direct action on the brain was tested using plasma norepinephrine (NE) and epinephrine (Epi) responses to intracarotid and intravenous glucose injections as indexes of SNS and adrenal medullary responses, respectively. Intracarotid glucose bolus injections (0.1 g/kg) transiently raised plasma glucose (22%) and insulin (98%) levels at 2 min and increased plasma NE, but not Epi, levels from 2 to 60 min. Areas under the NE curve were 700% higher than equiosmolar doses of mannitol. An intravenous glucose bolus (1 g/kg) gave quantitatively similar but delayed (30 min) NE responses to the 0.1 g/kg intracarotid dose but raised plasma glucose 500% and insulin 1,700% above baseline at 2 min postinjection. Slow intracarotid glucose infusions for 60 min at 4 mg.kg-1.min-1 raised plasma NE levels from 30 to 60 min with 250% higher areas under the NE curve than the intracarotid and intravenous bolus doses but without a change in plasma glucose, insulin, or Epi levels. Infusions at 6 mg.kg-1.min-1 transiently raised plasma NE levels at 30 min without altering glucose, insulin, or Epi levels. These results suggest that glucose alone can produce a selective, delayed SNS activation by a direct action on the brain.

Effect of acute sympathetic nervous system activation on flow-mediated dilation of brachial artery

2006 ◽  
Vol 290 (4) ◽  
pp. H1446-H1453 ◽  
Author(s):  
Kenneth S. Dyson ◽  
J. Kevin Shoemaker ◽  
Richard L. Hughson
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Brachial Artery ◽  
Cold Pressor Test ◽  
Plasma Norepinephrine ◽  
Flow Mediated Dilation ◽  
Brachial Artery Diameter ◽  
Peak Shear Stress ◽  
Sympathetic Nervous ◽  
General Response

We tested the hypothesis that flow-mediated dilation (FMD) of the brachial artery would be impaired by acute increases in sympathetic nervous system activity (SNA) in models where similar peak shear stress stimulus was achieved by varying the duration of forearm muscle ischemia. Eleven healthy young men were studied under four different conditions, each with its own control: lower body suction (LBS), cold pressor test (CPT), mental arithmetic task (MAT), and activation of muscle chemoreflex (MCR). The duration of ischemia before observation of FMD by ultrasound imaging was 5 min each for control, LBS, and CPT; 3 min for MAT; and 2-min for MCR. Peak shear rate was not different between control and any of the SNA conditions, although total shear in the first minute was reduced in MAT. MCR was the only condition in which brachial artery vasoconstriction was observed before forearm occlusion [4.38 (SD 0.53) vs. control 4.60 (SD 0.53) mm, P < 0.05]; however, diameter increased to the same absolute value as that of the control, so the percent FMD was greater for MCR [9.85 (SD 2.33) vs. control 5.29 (SD 1.50)%]. Blunting of the FMD response occurred only in the CPT model [1.51 (SD 1.20)%]. During SNA, the increase in plasma cortisol from baseline was significant only for MCR; the increase in plasma norepinephrine was significant for MCR, LBS, and CPT; and the increase in epinephrine was significant only for MCR. These results showed that the four models employed to achieve increases in SNA had different effects on baseline brachial artery diameter and that blunted FMD is not a general response to increased SNA.

Interactions between ANG II, sympathetic nervous system, and baroreceptor reflexes in regulation of blood pressure

1992 ◽  
Vol 262 (6) ◽  
pp. E763-E778 ◽  
Author(s):  
I. A. Reid
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Blood Pressure Control ◽  
Cardiovascular Responses ◽  
Pressure Control ◽  
Ang Ii ◽  
Arterial Blood ◽  
Baroreceptor Reflexes ◽  
Sympathetic Nervous

The renin-angiotensin system plays an important role in the regulation of arterial blood pressure and in the development of some forms of clinical and experimental hypertension. It is an important blood pressure control system in its own right but also interacts extensively with other blood pressure control systems, including the sympathetic nervous system and the baroreceptor reflexes. Angiotensin (ANG) II exerts several actions on the sympathetic nervous system. These include a central action to increase sympathetic outflow, stimulatory effects on sympathetic ganglia and the adrenal medulla, and actions at sympathetic nerve endings that serve to facilitate sympathetic neurotransmission. ANG II also interacts with baroreceptor reflexes. For example, it acts centrally to modulate the baroreflex control of heart rate, and this accounts for its ability to increase blood pressure without causing a reflex bradycardia. The physiological significance of these actions of ANG II is not fully understood. Most evidence indicates that the actions of ANG to enhance sympathetic activity do not contribute significantly to the pressor response to exogenous ANG II. On the other hand, there is considerable evidence that the actions of endogenous ANG II on the sympathetic nervous system enhance the cardiovascular responses elicited by activation of the sympathetic nervous system.

The sympathetic muscle metaboreflex is not different in the third trimester in normotensive pregnant women.

2020 ◽  
Author(s):  
Rachel J. Skow ◽  
Andrew R. Steele ◽  
Graham M. Fraser ◽  
Margie H. Davenport ◽  
Craig D. Steinback
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Pregnant Women ◽  
Isometric Handgrip ◽  
Third Trimester ◽  
Muscle Metaboreflex ◽  
The Third ◽  
Arterial Blood ◽  
Sympathetic Nervous

Isometric handgrip (IHG) is used to assess sympathetic nervous system responses to exercise and may be useful at predicting hypertension in both pregnant and non-pregnant populations. We have previously observed altered sympathetic nervous system control of blood pressure in late pregnancy. Therefore, we measured muscle sympathetic nerve activity (MSNA) and blood pressure during muscle metaboreflex activation (IHG) in normotensive pregnant women in the third trimester compared to healthy non-pregnant women. Nineteen pregnant (32±3wks gestation) and fourteen non-pregnant women were matched for age, non/pre-pregnant BMI, and parity. MSNA (microneurography), heart rate (ECG), and arterial blood pressure (Finometer) were continuously recorded during ten minutes of rest, and then during two-minutes of IHG at 30% of maximal voluntary contraction, and two-minutes of post-exercise circulatory occlusion (PECO). Baseline SNA was elevated in pregnant (41±11 bursts/min) compared to non-pregnant women (27 ± 9 bursts/minute; p=0.005); however, the sympathetic baroreflex gain and neurovascular transduction were not different between groups (p=0.62 and p=0.32, respectively). During IHG and PECO there was no significant differences in the pressor response (∆MAP) during IHG and PECO was not different between groups (p=0.25, main effect of group) nor the sympathetic response (interaction effect: p=0.16, 0.25, and 0.27 for burst frequency, burst incidence, and total SNA respectively). These data suggest that pregnant women who have maintained sympathetic baroreflex and neurovascular transduction also have similar sympathetic and pressor responses during exercise.

Antecedent short-term central nervous system administration of estrogen and progesterone alters counterregulatory responses to hypoglycemia in conscious male rats

2007 ◽  
Vol 293 (6) ◽  
pp. E1511-E1516 ◽  
Author(s):  
Darleen A. Sandoval ◽  
Bin Gong ◽  
Stephen N. Davis
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Reproductive Hormones ◽  
Male Rats ◽  
Plasma Norepinephrine ◽  
Central Administration ◽  
Short Term ◽  
Counterregulatory Hormones ◽  
Sympathetic Nervous

The aim of this study was to test the hypothesis that antecedent short-term administration of estradiol or progesterone into the central nervous system (CNS) reduces levels of neuroendocrine counterregulatory hormones during subsequent hypoglycemia. Conscious unrestrained male Sprague-Dawley rats were studied during randomized 2-day experiments. Day 1 consisted of an 8-h lateral ventricle infusion of estradiol (1 μg/μl; n = 9), progesterone (1 μg/μl; n = 9), or saline (0.2 μl/min; n = 10). On day 2, a 2-h hyperinsulinemic (30 pmol·kg−1·min−1) hypoglycemic (2.9 ± 0.2 mM) clamp was performed on all rats. Central administration of estradiol on day 1 resulted in significantly lower plasma epinephrine levels during hypoglycemia compared with saline, whereas central administration of progesterone resulted in increased levels of plasma norepinephrine and decreased levels of corticosterone both at baseline and during hypoglycemia. Glucagon responses during hypoglycemia were unaffected by prior administration of estradiol or progesterone. Endogenous glucose production following day 1 estradiol was significantly lower during day 2 hypoglycemia, and consequently, the glucose infusion rate to maintain the glycemia was significantly greater after estradiol administration compared with saline. These data suggest that 1) CNS administration of both female reproductive hormones can have rapid effects in modulating levels of counterregulatory hormones during subsequent hypoglycemia in conscious male rats, 2) forebrain administration of reproductive hormones can significantly reduce pituitary adrenal and sympathetic nervous system drive during hypoglycemia, 3) reproductive steroid hormones produce differential effects on sympathetic nervous system activity during hypoglycemia, and 4) reduction of epinephrine resulted in significantly blunted metabolic counterregulatory responses during hypoglycemia.

Frequency response characteristic of sympathetic-mediated vasomotor waves in conscious rats

1996 ◽  
Vol 271 (4) ◽  
pp. H1416-H1422 ◽  
Author(s):  
H. M. Stauss ◽  
K. C. Kregel
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Frequency Response ◽  
Arterial Blood Pressure ◽  
Nerve Stimulation ◽  
Splanchnic Nerve ◽  
Conscious Rats ◽  
Arterial Blood ◽  
Sympathetic Nervous

Power spectrum analysis of arterial blood pressure (BP) and heart rate (HR) has been used to investigate autonomic nervous system activity. Sympathetic-mediated vasomotor tone has been attributed to the BP power at frequencies between 0.05 and 0.15 Hz in humans and dogs and between 0.2 and 0.8 Hz in rats. In contrast, it has been suggested that the sympathetic nervous system is too sluggish to transmit frequencies higher than 0.017 Hz in dogs. Thus we investigated the frequency-response characteristics of the transmission of peripheral sympathetic nerve discharge to peripheral vascular resistance and arterial blood pressure in conscious rats. Eleven rats were instrumented with arterial catheters, nerve electrodes on the sympathetic splanchnic nerve, and flow probes on the superior mesenteric artery. The splanchnic nerve was cut proximal to the electrode to avoid afferent nerve stimulation. The next day the nerve was stimulated at frequencies of 0.05, 0.1, 0.2, 0.5, 1.0, and 2.0 Hz while mesenteric blood flow, BP, and HR were recorded in conscious rats. Mesenteric resistance (MR) was calculated off-line. Nerve stimulation at 0.05, 0.1, 0.2, 0.5, and 1.0 Hz significantly increased the power in MR at these respective frequencies. The greatest response was found between 0.2 and 0.5 Hz. These oscillations in MR were translated to oscillations in BP, but not in HR. Nerve stimulation on the second day, when the nerve was degenerated, did not elicit oscillations in MR or BP. We conclude that the peripheral sympathetic nervous system in rats can transmit signals at frequencies higher than those traditionally assigned to sympathetic vasomotor activity in several species, including humans, and may even overlap with the respiration-related high-frequency range.

scholarly journals Bacillus anthracis lethal toxin alters regulation of visceral sympathetic nerve discharge

2012 ◽  
Vol 112 (6) ◽  
pp. 1033-1040 ◽  
Author(s):  
A. A. Garcia ◽  
R. J. Fels ◽  
L. J. Mosher ◽  
M. J. Kenney
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Bacillus Anthracis ◽  
Sympathetic Nerve ◽  
Critical Role ◽  
Lethal Factor ◽  
Lethal Toxin ◽  
Arterial Blood ◽  
Sympathetic Nervous ◽  
Nerve Discharge

Bacillus anthracis infection is a pathophysiological condition that is complicated by progressive decreases in mean arterial pressure (MAP). Lethal toxin (LeTx) is central to the pathogenesis of B. anthracis infection, and the sympathetic nervous system plays a critical role in physiological regulation of acute stressors. However, the effect of LeTx on sympathetic nerve discharge (SND), a critical link between central sympathetic neural circuits and MAP regulation, remains unknown. We determined visceral (renal, splenic, and adrenal) SND responses to continuous infusion of LeTx [lethal factor (100 μg/kg) + protective antigen (200 μg/kg) infused at 0.5 ml/h for ≤6 h] and vehicle (infused at 0.5 ml/h) in anesthetized, baroreceptor-intact and baroreceptor (sinoaortic)-denervated (SAD) Sprague-Dawley rats. LeTx infusions produced an initial state of cardiovascular and sympathetic nervous system activation in intact and SAD rats. Subsequent to peak LeTx-induced increases in arterial blood pressure, intact rats demonstrated a marked hypotension that was accompanied by significant reductions in SND (renal and splenic) and heart rate (HR) from peak levels. After peak LeTx-induced pressor and sympathoexcitatory responses in SAD rats, MAP, SND (renal, splenic, and adrenal), and HR were progressively and significantly reduced, supporting the hypothesis that LeTx alters the central regulation of sympathetic nerve outflow. These findings demonstrate that the regulation of visceral SND is altered in a complex manner during continuous anthrax LeTx infusions and suggest that sympathetic nervous system dysregulation may contribute to the marked hypotension accompanying B. anthracis infection.

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