Regulation of catecholamine-synthesizing enzymes in adrenals of Wistar rats under chronic stress

1993 ◽  
Vol 264 (5) ◽  
pp. R957-R962 ◽  
Author(s):  
V. Lemaire ◽  
M. Le Moal ◽  
P. Mormede
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Social Stress ◽  
Specific Activity ◽  
Sympathetic Innervation ◽  
Male Rats ◽  
Adrenal Weight ◽  
Inhibitory Influence ◽  
Chronic Social Stress ◽  
Sympathetic Nervous

We have shown previously that chronic social stress has differential effects on adrenal weight and on tyrosine hydroxylase (TH) and phenylethanolamine N-methyltransferase (PNMT) specific activity, depending on the experimental design. To determine the role of the sympathetic nervous system and of the hypothalamo-pituitary-adrenocortical axis (HPAA) in these modifications, we studied the mechanisms of regulation of these parameters in basal conditions as well as in response to reserpine treatment and chronic social stress in the Wistar strain of rats. We found that the adrenal weight is mostly dependent on the activity of the HPAA, which is increased in male rats living in mixed-sex colonies. PNMT specific activity is regulated by splanchnic innervation, confirming that its induction by social instability is a consequence of sympathetic nervous system hyperactivity. The increase of TH specific activity, as seen in unstable, mixed-sex colonies, is not under sympathetic control. However, we show that the pituitary may exert a tonic inhibitory influence, dependent on the sympathetic innervation. These data confirm that the HPAA and the sympathetic nervous system may be independently triggered in chronic social stress conditions.

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.

scholarly journals The adipokine chemerin amplifies electrical field-stimulated contraction in the isolated rat superior mesenteric artery

2016 ◽  
Vol 311 (2) ◽  
pp. H498-H507 ◽  
Author(s):  
Emma S. Darios ◽  
Brittany M. Winner ◽  
Trevor Charvat ◽  
Antoni Krasinksi ◽  
Sreenivas Punna ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Superior Mesenteric Artery ◽  
Sympathetic Nerve ◽  
Mesenteric Artery ◽  
Sympathetic Innervation ◽  
Electrical Field ◽  
Perivascular Adipose Tissue ◽  
Sympathetic Nervous

The adipokine chemerin causes arterial contraction and is implicated in blood pressure regulation, especially in obese subjects with elevated levels of circulating chemerin. Because chemerin is expressed in the perivascular adipose tissue (PVAT) that surrounds the sympathetic innervation of the blood vessel, we tested the hypothesis that chemerin (endogenous and exogenous) amplifies the sympathetic nervous system in mediating electrical field-stimulated (EFS) contraction. The superior mesenteric artery, with or without PVAT and with endothelium and sympathetic nerve intact, was mounted into isolated tissue baths and used for isometric contraction and stimulation. Immunohistochemistry validated a robust expression of chemerin in the PVAT surrounding the superior mesenteric artery. EFS (0.3–20 Hz) caused a frequency-dependent contraction in isolated arteries that was reduced by the chemerin receptor ChemR23 antagonist CCX832 alone (100 nM; with, but not without, PVAT), but not by the inactive congener CCX826 (100 nM). Exogenous chemerin-9 (1 μM)-amplified EFS-induced contraction in arteries (with and without PVAT) was blocked by CCX832 and the α-adrenergic receptor antagonist prazosin. CCX832 did not directly inhibit, nor did chemerin directly amplify, norepinephrine-induced contraction. Whole mount immunohistochemical experiments support colocalization of ChemR23 with the sympathetic nerve marker tyrosine hydroxylase in superior mesenteric PVAT and, to a lesser extent, in arteries and veins. These studies support the idea that exogenous chemerin modifies sympathetic nerve-mediated contraction through ChemR23 and that ChemR23 may be endogenously activated. This is significant because of the well-appreciated role of the sympathetic nervous system in blood pressure control.

Neonatal hyperthyroidism: effects on sympathetic responses to stress in adult rats

1983 ◽  
Vol 245 (1) ◽  
pp. R95-R99
Author(s):  
R. McCarty ◽  
R. F. Kirby ◽  
P. C. Brunjes
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Plasma Levels ◽  
Acute Stress ◽  
Male Rats ◽  
Adult Rats ◽  
Basal Plasma ◽  
Repeated Sampling ◽  
Neonatal Hyperthyroidism ◽  
Sympathetic Nervous

Treatment of developing rats with thyroid hormone results in accelerated maturation of sympathetic and adrenal medullary responses to reflex activation of central sympathetic outflow. In this study, we examined the effects of neonatal hyperthyroidism on the responsiveness of the sympathetic nervous system of adult rats to acute stress. Hyperthyroidism was produced in Long-Evans hooded rats by injections of thyroxine (neo-T4, 1 mg/kg body wt) on postnatal days 1-4. Littermate controls received injections of vehicle only. In adulthood, male rats of the two groups were prepared with chronic tail artery catheters to allow repeated sampling of blood and direct measurements of mean arterial pressure (MAP, mmHg) and heart rate (HR, beats/min). Two days after surgery, rats were stressed by exposure to 1 min of inescapable foot shock (2.0 mA, 0.6-s duration, every 6 s). The activity of the sympathetic nervous system was assessed by measuring plasma levels of norepinephrine (NE) and epinephrine (E). Basal plasma levels of NE and E and resting MAP did not differ between neo-T4 and control rats. However, basal HR was elevated in neo-T4 rats. Footshock-induced increments in plasma levels of both catecholamines were greater in neo-T4 compared with control rats even though behavioral responses to footshock were similar across groups. However, neo-T4 rats were more active when tested in an open field on each of 3 consecutive days. These findings indicate that neonatal treatment with T4 results in hyperresponsiveness of the sympathoadrenal medullary system to acute stress that persists into adulthood.

scholarly journals Transient Overexpression of VEGF-A in Adipose Tissue Promotes Energy Expenditure via Activation of the Sympathetic Nervous System

2018 ◽  
Author(s):  
Yueshui Zhao ◽  
Xin Li ◽  
Li Yanga ◽  
Kristin Eckel-Mahan ◽  
Qingchun Tong ◽  
...  
Keyword(s):  
Nervous System ◽  
Adipose Tissue ◽  
Energy Expenditure ◽  
Sympathetic Nervous System ◽  
Sympathetic Innervation ◽  
Hormone Sensitive Lipase ◽  
Immunofluorescent Staining ◽  
Short Period ◽  
Sympathetic Nervous ◽  
Transient Overexpression

AbstractAdipose-derived VEGF-A stimulates functional blood vessel formation in obese fat pads which in turn facilitates healthy expansion of the adipose tissue. However, the detailed mechanism(s) governing the process remains largely unknown. Here, we investigated the role of sympathetic nervous system activation in the process. To this end, we induced overexpression of VEGF-A in an adipose-specific doxycycline (Dox)-inducible transgenic mouse model for a short period of time during high fat-diet (HFD) feeding. We found that local overexpression of VEGF-A in adipose tissue stimulated lipolysis and browning rapidly after Dox induction. Immunofluorescent staining against tyrosine hydroxylase (TH) indicated higher levels of sympathetic innervation in adipose tissue of transgenic mice. In response to the increased norepinephrine (NE) level, expression of β3-andrenoceptor was significantly upregulated and the downstream protein kinase A (PKA) pathway was activated, as indicated by the enhanced phosphorylation of the whole PKA substrates, in particular the hormone sensitive lipase (HSL) in adipocytes. As the result, the adipose tissue exhibited increased lipolysis, browning, and energy expenditure. Importantly, all these effects were abolished upon the treatment with β3-adrenoceptor antagonist SR59230A. Collectively, these results demonstrate that transient overexpressed VEGF-A activates sympathetic nervous system which hence promotes lipolysis and browning in adipose tissue.

scholarly journals HIF-1α is required for development of the sympathetic nervous system

2019 ◽  
Vol 116 (27) ◽  
pp. 13414-13423 ◽  
Author(s):  
Romana Bohuslavova ◽  
Radka Cerychova ◽  
Frantisek Papousek ◽  
Veronika Olejnickova ◽  
Martin Bartos ◽  
...  
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Molecular Mechanisms ◽  
Cardiac Development ◽  
Sympathetic Innervation ◽  
Cardiac Contractility ◽  
Hypoxia Inducible Factor ◽  
Left Ventricular ◽  
Conditional Knockout ◽  
Sympathetic Nervous

The molecular mechanisms regulating sympathetic innervation of the heart during embryogenesis and its importance for cardiac development and function remain to be fully elucidated. We generated mice in which conditional knockout (CKO) of the Hif1a gene encoding the transcription factor hypoxia-inducible factor 1α (HIF-1α) is mediated by an Islet1-Cre transgene expressed in the cardiac outflow tract, right ventricle and atrium, pharyngeal mesoderm, peripheral neurons, and hindlimbs. These Hif1aCKO mice demonstrate significantly decreased perinatal survival and impaired left ventricular function. The absence of HIF-1α impaired the survival and proliferation of preganglionic and postganglionic neurons of the sympathetic system, respectively. These defects resulted in hypoplasia of the sympathetic ganglion chain and decreased sympathetic innervation of the Hif1aCKO heart, which was associated with decreased cardiac contractility. The number of chromaffin cells in the adrenal medulla was also decreased, indicating a broad dependence on HIF-1α for development of the sympathetic nervous system.

Influences of exogenous insulin on arterial blood pressure measurements of the rat

1989 ◽  
Vol 67 (6) ◽  
pp. 2335-2342 ◽  
Author(s):  
J. G. Edwards ◽  
C. M. Tipton
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Smooth Muscle ◽  
Sympathetic Nervous System ◽  
Arterial Blood Pressure ◽  
Insulin Infusion ◽  
Control Period ◽  
Male Rats ◽  
Arterial Blood ◽  
Sympathetic Nervous

Studies were undertaken with adult male rats to test the hypothesis that euglycemic hyperinsulinemia would alter mean arterial blood pressure (MAP) and heart rate (HR) relationships by activation of the sympathetic nervous system. Conscious rats were infused either with insulin or control vehicle (0, 0.47, 1.5, 4.7, 15.0 mU.kg-1.min-1) for 75 min before injection of hexamethonium. Compared with the control period, insulin infusion significantly increased MAP by 7.1 +/- 0.1, 12.7 +/- 2.0, and 19.7 +/- 0.3 (SE) mmHg and HR by 44 +/- 8.4, 66 +/- 10.3, and 95 +/- 6.3 beats/min, respectively, during the three highest rates of infusion. The dose-dependent increases in MAP and HR were due to increases in the activity of hexamethonium-sensitive pathways. In chemically sympathectomized rats, insulin infusion did not produce a significant increase in either MAP or HR. The influence of exogenous norepinephrine on MAP and HR was also studied after insulin infusion. Compared with the insulin-vehicle infusion, insulin infusion significantly depressed (P less than 0.05) the norepinephrine dose-response increase in MAP. In addition, isolated smooth muscle strips were studied to determine the influence of insulin on their in vitro responses to increasing doses of norepinephrine. Although insulin did not alter contractility, it significantly (P less than 0.05) decreased the sensitivity of the vascular strips to norepinephrine. Collectively, the data from these euglycemic experiments indicated that infusions of insulin caused increases in HR and MAP because of activation of the sympathetic nervous system, even though the responsiveness of the vascular smooth muscle was depressed.

Role of the sympathetic nervous system in cold-induced hypertension in rats

1991 ◽  
Vol 71 (1) ◽  
pp. 300-306 ◽  
Author(s):  
P. E. Papanek ◽  
C. E. Wood ◽  
M. J. Fregly
Keyword(s):  
Nervous System ◽  
Mean Arterial Pressure ◽  
Sympathetic Nervous System ◽  
Arterial Pressure ◽  
Male Rats ◽  
Indwelling Catheters ◽  
Arterial Blood ◽  
Exposure To Cold ◽  
Induced Hypertension ◽  
Sympathetic Nervous

Hypertension develops in rats exposed chronically to cold [6 +/- 2 degrees C (SE)] and includes both an elevation of mean arterial pressure and cardiac hypertrophy. Previous studies suggest that cold-exposed animals, at least initially, have a large sustained increase in the activity of their sympathetic nervous system, suggesting a failure of the baroreceptor system to provide sufficient negative feedback to the central nervous system. The present study was designed to investigate whether alterations in the activity of the sympathetic nervous system, including the baroreceptor reflex, occur during exposure to cold and whether they contribute to cold-induced hypertension. Twenty male rats were prepared with indwelling catheters in the femoral artery and vein. Ten of the rats were exposed to cold (6 +/- 2 degrees C) chronically, while the remaining 10 were kept at 26 +/- 2 degrees C. Withdrawal of arterial blood samples (less than 5 ml/kg), measurement of direct arterial pressures, and measurement of baroreflex function were carried out at 0800 h at intervals throughout the experiment. Norepinephrine and epinephrine concentrations in plasma were also determined at intervals throughout the experiment. Systolic, diastolic, and mean blood pressures of cold-exposed rats were increased to levels significantly above those of controls. The sensitivity of the baroreflex (delta heart period/delta mean arterial pressure) was decreased in the cold-treated group. The concentration of norepinephrine in plasma increased after 24 h of exposure to cold and remained elevated throughout the experiment, whereas the concentration of epinephrine in plasma increased initially but returned to control levels after 19 days of exposure to cold.(ABSTRACT TRUNCATED AT 250 WORDS)

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