Effects of chronic lard feeding on sympathetic nervous system activity in the rat

1994 ◽  
Vol 267 (5) ◽  
pp. R1320-R1328 ◽  
Author(s):  
J. B. Young ◽  
P. A. Daly ◽  
K. Uemura ◽  
F. Chaouloff
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Sympathetic Nerves ◽  
Plasma Norepinephrine ◽  
Interscapular Brown Adipose Tissue ◽  
Brown Adipose ◽  
Chronic Ingestion ◽  
Sympathetic Nervous ◽  
Specific Stimulation ◽  
Kidney Liver

The level of sympathetic nervous system (SNS) activity in obesity is controversial, with reports claiming either increased or decreased SNS activity. The following studies examined SNS activity in a dietary form of obesity, ingestion of a lard-enriched diet for 4 wk. Plasma norepinephrine (NE) levels were 61% higher in rats fed the lard-enriched diet than in chow-fed controls at 20 degrees C (200 +/- 24 pg/ml vs. 124 +/- 6, P < 0.005) and remained elevated after 1 h of cold exposure (4 degrees C). [3H]NE turnover was markedly increased in heart, but not in interscapular brown adipose tissue (IBAT), kidney, liver, skeletal muscle, or spleen of rats fed the high-fat diet. By contrast, ingestion of a diet similarly enriched with sucrose raised rates of [3H]NE turnover in IBAT as well as in heart. Thus chronic ingestion of a lard-enriched diet induces region-specific stimulation of SNS activity that is greater in heart than in IBAT. Whereas the absence of an SNS response to lard in IBAT may contribute to weight gain in these animals, activation of cardiac sympathetic nerves may promote development of hypertension in this model of obesity.

Tissue-specific increase in norepinephrine turnover by central interleukin-1, but not by interleukin-6, in rats

1994 ◽  
Vol 266 (2) ◽  
pp. R400-R404 ◽  
Author(s):  
A. Terao ◽  
M. Oikawa ◽  
M. Saito
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Interleukin 1 ◽  
Corticosterone Level ◽  
Plasma Corticosterone ◽  
Interscapular Brown Adipose Tissue ◽  
Norepinephrine Turnover ◽  
Brown Adipose ◽  
Intracerebroventricular Injections ◽  
Sympathetic Nervous

To examine the effects of brain cytokines on the sympathetic nervous system, norepinephrine (NE) turnover in peripheral organs (spleen, lung, diaphragm, pancreas, heart, liver, kidney, and interscapular brown adipose tissue) was assessed after intraperitoneal or intracerbroventricular administrations of human recombinant interleukin (IL)-1 beta and IL-6 in rats. An intraperitoneal injection of IL-1 (1 microgram/rat) accelerated NE turnover in the spleen, lung, diaphragm, and pancreas without appreciable effects in other organs examined. When IL-1 was injected intracerebroventricularly at much lower doses (1-100 ng/rat), a dose-dependent increase in NE turnover was observed in the spleen, lung, diaphragm, and pancreas. IL-6 did not affect NE turnover in every organ examined, even when it was given at much higher doses, 100 micrograms/rat and 100 ng/rat for intraperitoneal and intracerebroventricular injections, respectively. In contrast to tissue NE turnover, plasma corticosterone level was increased after the administration of IL-6 as well as IL-1, regardless of the site of administration. These results suggest that central IL-1, but not IL-6, increases sympathetic nerve activity in some specific organs, whereas both cytokines are effective for adrenocortical activation. A possible role of the sympathetic nervous system in physiological and immune responses to central IL-1 was discussed.

Diminished sympathetic nervous system activity in genetically obese (ob/ob) mouse

1983 ◽  
Vol 245 (2) ◽  
pp. E148-E154 ◽  
Author(s):  
J. B. Young ◽  
L. Landsberg
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Cold Exposure ◽  
Feedback Regulation ◽  
Turnover Rates ◽  
Interscapular Brown Adipose Tissue ◽  
Peripheral Tissues ◽  
Brown Adipose ◽  
Sympathetic Nervous ◽  
Long Acting

The genetically obese (ob/ob) mouse exhibits defective thermoregulatory responses to cold exposure. Pathophysiological explanations for this phenomenon have focused on abnormalities in intracellular metabolism or insensitivity of peripheral tissues to the thermogenic effects of catecholamines. Because the sympathetic nervous system (SNS) is subject to feedback regulation, a peripheral impairment in thermogenesis should be associated with a compensatory increase in SNS activity. To examine SNS activity in the ob/ob mouse, norepinephrine (NE) turnover was measured in heart and interscapular brown adipose tissue (IBAT) of ob/ob and lean mice. The results from studies utilizing radiolabeled NE or inhibition of NE biosynthesis with alpha-methyl-p-tyrosine to measure NE turnover demonstrated reductions in SNS activity of 33-56% in heart and of 45-73% in IBAT in ob/ob mice at ambient temperature (22 degrees C) compared with measurements in lean controls. During cold exposure (4 degrees C) NE turnover increased in heart and IBAT to a similar extent in both ob/ob and lean mice, but NE turnover rates in heart, and probably in IBAT as well, remained lower in the obese mice than in the lean despite the gradual development of hypothermia in the ob/ob mice during this period. Administration of naltrexone, a long-acting opiate antagonist, failed to reverse the suppression of SNS activity observed in the ob/ob mice. These data indicate that diminished SNS activity in ob/ob mice may be an additional factor contributing to the defective thermogenesis characteristic of these animals.

Norepinephrine turnover in iron deficiency at three environmental temperatures

1988 ◽  
Vol 255 (1) ◽  
pp. R90-R96 ◽  
Author(s):  
J. Beard ◽  
B. Tobin ◽  
S. M. Smith
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Sympathetic Nervous System Activity ◽  
Interscapular Brown Adipose Tissue ◽  
System Activity ◽  
Nervous System Activity ◽  
Brown Adipose ◽  
Iron Deficient ◽  
Sympathetic Nervous ◽  
Environmental Temperatures

Iron-deficient anemic rats had a significant elevation in urinary norepinephrine (NE) after 7 days at 30 and 24 degrees C, but not at 10 degrees C, compared with control animals. NE turnover studies were performed to examine sympathetic nervous system activity in a tissue-specific fashion. NE content in myocardium decreased by nearly 50% in hypertrophied iron-deficient hearts at all three temperatures, whereas fractional turnover rates were compensatorily increased. In contrast, interscapular brown adipose tissue NE turnover was significantly reduced to 30% of normal in iron-deficient animals at both 30 and 10 degrees C. Serum triiodothyronine concentrations were similar to controls at 30 degrees C but were decreased at lower temperatures. Serum tetraiodothyronine concentrations were lower in iron-deficient animals at all three environmental temperatures. We conclude that increased sympathetic nervous system activity compensatory to temperatures below thermoneutrality is less well controlled in iron-deficient animals than in controls, and at a low environmental temperature this may possibly explain the poor thermoregulatory capacity of iron-deficient animals. A generalized hypernoradrenergic state is not supported by our NE turnover study and does not explain the elevated urine NE concentrations.

Increased sympathetic nervous system activity in rats fed a low-protein diet

1985 ◽  
Vol 248 (5) ◽  
pp. R627-R637 ◽  
Author(s):  
J. B. Young ◽  
L. N. Kaufman ◽  
M. E. Saville ◽  
L. Landsberg
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Deficient Diet ◽  
Interscapular Brown Adipose Tissue ◽  
Caloric Density ◽  
Low Protein ◽  
Brown Adipose ◽  
Sympathetic Nervous

To examine the state of sympathetic nervous system (SNS) function in animals fed a protein-restricted diet, [3H] norepinephrine ([3H]-NE) turnover was measured in heart and interscapular brown adipose tissue (IBAT) of rats fed synthetic diets of equal caloric density containing 22% protein (as casein) or 7% protein (the difference being made up by sucrose). Because dietary availability of tyrosine is a potential mediator of SNS responses to protein ingestion, a third diet (7% protein supplemented with tyrosine) was also tested. After 12 days dietary preparation [3H]-NE turnover was increased 35-70% in heart by 7% protein feeding and 93-103% in IBAT. When smaller animals were fed the synthetic diets for 4-5 wk, sympathetic stimulation in those given the protein-restricted formula was also apparent, although demonstration of this response was complicated by comparative problems due to the marked differences in body size between normal and protein-restricted groups. Addition of tyrosine (sufficient to normalize plasma and brain tyrosine levels) was without effect on the stimulation of NE turnover induced by the protein-deficient diet. Similarly, augmented urinary NE excretion observed in animals consuming the 7% protein diet was unaffected by supplemental tyrosine. Urinary dopamine excretion, however, was uniquely and strikingly elevated with restoration of dietary tyrosine to animals fed the low-protein diet. Thus isocaloric substitution of sucrose for casein in the diet activates the SNS in heart and IBAT, a response unrelated to limitation of dietary tyrosine.

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.

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.

CNS origins of the sympathetic nervous system outflow to brown adipose tissue

1999 ◽  
Vol 276 (6) ◽  
pp. R1569-R1578 ◽  
Author(s):  
Maryam Bamshad ◽  
C. Kay Song ◽  
Timothy J. Bartness
Keyword(s):  
Nervous System ◽  
Adipose Tissue ◽  
Sympathetic Nervous System ◽  
Brown Adipose Tissue ◽  
Pseudorabies Virus ◽  
Critical Role ◽  
Hypothalamic Nucleus ◽  
Brown Adipose ◽  
Sympathetic Nervous ◽  
Diet Induced Thermogenesis

Brown adipose tissue (BAT) plays a critical role in cold- and diet-induced thermogenesis. Although BAT is densely innervated by the sympathetic nervous system (SNS), little is known about the central nervous system (CNS) origins of this innervation. The purpose of the present experiment was to determine the neuroanatomic chain of functionally connected neurons from the CNS to BAT. A transneuronal viral tract tracer, Bartha’s K strain of the pseudorabies virus (PRV), was injected into the interscapular BAT of Siberian hamsters. The animals were killed 4 and 6 days postinjection, and the infected neurons were visualized by immunocytochemistry. PRV-infected neurons were found in the spinal cord, brain stem, midbrain, and forebrain. The intensity of labeled neurons in the forebrain varied from heavy infections in the medial preoptic area and paraventricular hypothalamic nucleus to few infections in the ventromedial hypothalamic nucleus, with moderate infections in the suprachiasmatic and lateral hypothalamic nuclei. These results define the SNS outflow from the brain to BAT for the first time in any species.

Abstract 291: Antihypertensive Effect Of Bia 5-1058 a New Selective Peripheral Dopamine β-hydroxylase Inhibitor

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Bruno Igreja ◽  
Nuno M Pires ◽  
Lyndon C Wright ◽  
Patrío Soares-da-Silva
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Receptor Antagonist ◽  
Antihypertensive Effect ◽  
Antihypertensive Drugs ◽  
Radio Telemetry ◽  
Sympathetic Nerves ◽  
Maximum Reduction ◽  
Sympathetic Nervous

The sympathetic nervous system can alter blood pressure by modulation of cardiac output, peripheral vascular resistance and renal function. One strategy for controlling sympathetic nerve function is to reduce the biosynthesis of norepinephrine (NE) via inhibition of dopamine β-hydroxylase (DβH; EC 1.14.17.1 ), the enzyme that catalyses the conversion of dopamine (DA) to NE in sympathetic nerves. BIA 5-1058 is a reversible DβH inhibitor that decreases NE levels in peripheral sympathetically innervated tissues slowing down sympathetic nervous system drive, without effect in brain tissues. In freely moving SHR implanted with radio-telemetry transmitters single administration of BIA 5-1058 showed a dose (3, 30 and 100 mg/Kg) and time dependent effect on blood pressure with no significant effect on heart rate (HR) and total activity monitored over a 96-hour period. The maximum reduction on systolic blood pressure (SBP) was -10.8, -21.1 and -35.2 mmHg for 3, 30 and 100 mg/Kg, respectively and the maximum reduction on diastolic blood pressure (DBP) was -9.9, -18.4 and -24.8 mmHg for 3, 30 and 100 mg/Kg, respectively. The antihypertensive effect of BIA 5-1058 (30 mg/Kg) was further evaluated in combination with efficacious doses of well-known antihypertensive drugs, like the ACE inhibitor captopril, the AT1 receptor antagonist losartan, the diuretic hydrochlorothiazide, beta-blocker metoprolol, the alpha-1 receptor antagonist prazosin, and the calcium channel blocker diltiazem. All drugs were administered orally (single dose) in a cross-over design and the effect was monitored for 72 hours. The combination of BIA 5-1058 with any of the tested antihypertensive drugs caused a stronger and prolonged blood pressure decrease than any of the compounds alone.In conclusion, peripheral DβH inhibitors can be used, alone or in combination with others antihypertensive drugs, to reduce blood pressure.

Sympathetic regulation of cerebral blood flow during seizures in newborn lambs

1988 ◽  
Vol 255 (3) ◽  
pp. H563-H568
Author(s):  
C. D. Kurth ◽  
L. C. Wagerle ◽  
M. Delivoria-Papadopoulos
Keyword(s):  
Blood Flow ◽  
Nervous System ◽  
Cerebral Blood Flow ◽  
Sympathetic Nervous System ◽  
Sympathetic Nerves ◽  
The Other ◽  
Cerebral White Matter ◽  
Blood Flows ◽  
Sympathetic Regulation ◽  
Sympathetic Nervous

We examined cerebral blood flow (CBF) regulation by the sympathetic nerves in 12 newborn lambs (3–11 days old) during seizures, a potent reflex stimulator of the sympathetic nervous system. CBF was measured with microspheres, and seizures were induced with bicuculline. In six of these lambs, one hemibrain was denervated (D) chronically by interrupting the ipsilateral cervical sympathetic trunk; the other hemibrain remained innervated (I). Before and after 10, 35, and 70 min of seizures, cerebral gray matter blood flow (mean +/- SE ml.min-1.100 g-1) was, respectively, 12 +/- 3 (9%), 71 +/- 12 (21%), 120 +/- 15 (38%), and 54 +/- 5 (14%) greater (P less than 0.05) in the D than in the I hemibrain. In the cerebral white matter, hippocampus, caudate, and thalamus blood flows to the D and I hemibrains were similar before seizures but during seizures they were 10–39% greater (P less than 0.05) in the D than in the I hemibrain. Midbrain, brainstem, and cerebellum D and I blood flows were always similar. In the other six lambs, acute denervation during seizures increased ipsilateral cerebral gray and hippocampus blood flow by 10–31%, but unilateral electrical stimulation decreased ipsilateral cerebral gray, cerebral white, hippocampus, thalamus, and caudate blood flow by 17–27%. The data demonstrate that, during seizures, sympathetic nerve activity modifies regional CBF and the effect is sustained, suggesting a role for the sympathetic nervous system in newborn CBF regulation.

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