Effects of noradrenaline and nicotinic acid on plasma free fatty acids and oxygen consumption in cold-adapted rats.

A 3-h noradrenaline (NA) infusion (1.5 microgram kg-1 min-1) produced a sustained enhanced oxygen consumption (O2 cons.) in cold-adapted rats. Plasma free fatty acid (FFA) levels were elevated by NA in control and in cold-adapted rats, but to lesser extent in cold-adapted rats; the increase was maintained at a plateau in both groups during the entire period of NA infusion. A 1-h nicotinic acid (Nic A) infusion (1.5 mg kg-1 min-1) added to the NA infusion inhibited the calorigenic response to NA in cold-adapted rats and reduced the elevated plasma FFA concentration in control and in cold-adapted rats to values below basal levels. However, when the Nic A infusion was stopped, the O2 cons. was increased again in cold-adapted rats by the uninterrupted NA infusion, without the simultaneous increase of the plasma FFA concentration; the plasma FFA concentration was maintained in cold-adapted rats below basal values and merely brought back to basal levels in control rats. From these results, it is suggested that plasma FFA are not an essential substrate to the calorigenic response to NA observed in cold-adapted rats, as 85% of the response can occur when the plasma FFA concentration is very low.     

Lymphatic transport rate of noradrenaline during adrenergic thermogenesis

The lymphatic concentration of noradrenaline (NA) and lymph flow in the thoracic duct of cold-acclimated rats were measured under conditions of the quasi-stationary thermogenic response to i.v. infused NA. Both parameters increased linearly with increased rate of NA infusion. The lymphatic transport rate of NA is quadratically related to the infusion rate which indicates the same relation for the efflux of NA from blood into the extravascular space. This non-linear efflux of NA causes a non-linear thermogenic response to NA.     

Role of alpha adrenoceptors and nitric oxide on cardiovascular responses in acute and chronic hypertension

The contribution of α-adrenoceptors and nitric oxide (NO) on the alterations of sympathetically mediated cardiovascular responses after acute (AcH) and chronic (ChH) hypertension was evaluated in pithed aortic coarcted hypertensive rats. Pressor and tachycardia response produced by electrical stimulation of preganglionic sympathetic fibers or exogenous noradrenaline (NA) were recorded in the absence and presence of prazosin (α₁-antagonist), rauwolscine (α₂-antagonist), or N ^G-nitro-l-arginine methyl ester (l-NAME; an inhibitor of NO synthase). Compared with age-matched sham-operated rats (Nt), the pressor response produced by electrical stimulation or NA was smaller in AcH rats and larger in ChH rats. Prazosin caused a decrease of pressor response elicited by electrical stimulation or NA in all groups. However, this effect was higher in ChH. Rauwolscine produced a similar increase of sympathetically mediated pressor response in Nt and AcH rats. Nevertheless, this antagonist did not affect the sympathetically mediated pressor response in ChH rats. In addition, rauwolscine did not affect the NA-induced pressor response in all groups. The pressor response elicited by l-NAME was larger in all groups compared without l-NAME and in presence of l-arginine. Moreover, l-NAME in the presence of NA increased sympathetically mediated pressor response is in all groups, compared without it or in the presence of l-arginine. Compared with Nt, basally produced NO in aortic rings was increased in AcH but decreased in ChH. Collectively, our data suggest that decreased cardiovascular reactivity in AcH is due to an increase in basally produced NO. In ChH, enhanced cardiovascular response appears to be associated with a decrease in produced NO and an increase in released NA from sympathetic nerves.     

Two-way avoidance and acute shock stress induced alterations of regional noradrenergic, dopaminergic and serotonergic activity in Roman high- and low-avoidance rats

Various brain regions of male RHA/Verh and RLA/Verh rats were dissected out and deep-frozen immediately after 30 min in a shuttle box involving a) no shock (control), b) 40 inescapable shocks or c) 40 avoidable shocks. The RHA/Verh rats used in the "c" category exhibited about 80-85% learned avoidance. 5-HT, 5-HIAA, NA, MHPG-SO4, DA, DOPAC and HVA levels were subsequently measured in selected regions. NA levels were considerably reduced in the hypothalamus and pons/medulla of both selected lines of rats after acute shock stress, supporting the results of numerous studies which have indicated that NA turnover is nonspecifically increased by all types of stress, at least in those regions. An increase in cortical MHPG-SO4 and a reduction in hypothalamic 5-HT seen after avoidance learning also occurred after shock stress in RHA/Verh rats. Whereas RLA/Verh rats showed an increased metabolism of 5-HT in the hypothalamus and pons/medulla after shock stress, RHA/Verh rats showed the opposite response in the hypothalamus after the same treatment. A reduction in 5-HT metabolism was also evident in RHA/Verh rats, after avoidance learning, in the cortex, hippocampus and hypothalamus. These results indicated, pending further studies regarding, for example, possible genetic differences in tryptophan uptake and utilization, that 5-HT probably plays at least a modulatory role in the reaction to stress, and in avoidance behavior. That role may be either active or passive, depending upon the emotional status of the subjects. In regard to the DA responses measured in striatum and hypothalamus of the two rat lines, some divergent inter-treatment tendencies, as well as some similarities, were seen in DA metabolism in both regions, but almost none of the differences were significant.     

Incremental Changes in Extracellular Noradrenaline Availability in the Frontal Cortex Induced by Naturalistic Environmental Stimuli: A Microdialysis Study in the Freely Moving Rat

Abstract: Changes in levels of extracellular noradrenaline (NA), 3,4-dihydroxyphenylacetic acid (DOPAC), and 5-hydroxyindole-3-acetic acid (5-HIAA) in the frontal cortex, induced by exposure of unrestrained, conscious rats to novel environments, were compared using in vivo microdialysis. NA efflux increased when rats were transferred to a novel cage, but this was not significant when compared with either basal efflux or with changes after equivalent handling in their home cage. Increasing the intensity of illumination of the novel cage by fivefold significantly increased NA efflux with respect to basal efflux but not handled controls. However, a sustained and significant increase in NA efflux (cf. basal efflux or handled controls) was found when an unfamiliar conspecific was also present in the novel cage. In all cases, basal efflux was restored within 1 h of returning rats to their home cage. Neither handling nor environmental stimuli described above affected DOPAC efflux. 5-HIAA efflux was increased (cf. basal) in the presence of an unfamiliar conspecific, but this increase was no greater than that in handled rats. It is concluded that different naturalistic stimuli cause incremental changes in the levels of extracellular NA in the frontal cortex; these changes affect both phasic and tonic components of the response.     

Different alterations in the development of the noradrenergic innervation of the cerebellum and the brain stem produced by neonatal 6-hydroxydopa.

The administration of 6-hydroxydopa (6-OH-DOPA) to rats during their pre- or postnatal development, produced long-term modifications in the distribution of noradrenaline (NA) within the brain. In the cerebellum, the concentration of NA was increased in adult rats exposed to the drug between the day 16 of gestation and the day of birth. When injected 3 days after birth, the drug did not modify NA levels while treatment at 20 days produced a marked depletion of cerebellar NA. The concentration of NA in the brain stem showed a different pattern of response to 6-OH-DOPA. Prenatal administration elevated NA in this region and, in contrast to the response of the cerebellum, injections in the inmediate postnatal period also elevated the transmitter content. Treatment at 20 days after birth resulted in a marked depletion of NA levels in the adult brain stem. These results demonstrate the existence of temporal differences in the responses to neonatal 6-OH-DOPA in two structures innervated by noradrenergic pathways originated in neurons of the nucleus locus coeruleus.     

Alterations in Perivascular Sympathetic and Nitrergic Innervation Function Induced by Late Pregnancy in Rat Mesenteric Arteries

Background and Purpose

We investigated whether pregnancy was associated with changed function in components of perivascular mesenteric innervation and the mechanism/s involved.

Experimental Approach

We used superior mesenteric arteries from female Sprague-Dawley rats divided into two groups: control rats (in oestrous phase) and pregnant rats (20 days of pregnancy). Modifications in the vasoconstrictor response to electrical field stimulation (EFS) were analysed in the presence/absence of phentolamine (alpha-adrenoceptor antagonist) or L-NAME (nitric oxide synthase-NOS- non-specific inhibitor). Vasomotor responses to noradrenaline (NA), and to NO donor DEA-NO were studied, NA and NO release measured and neuronal NOS (nNOS) expression/activation analysed.

Key Results

EFS induced a lower frequency-dependent contraction in pregnant than in control rats. Phentolamine decreased EFS-induced vasoconstriction in segments from both experimental groups, but to a greater extent in control rats. EFS-induced vasoconstriction was increased by L-NAME in arteries from both experimental groups. This increase was greater in segments from pregnant rats. Pregnancy decreased NA release while increasing NO release. nNOS expression was not modified but nNOS activation was increased by pregnancy. Pregnancy decreased NA-induced vasoconstriction response and did not modify DEA-NO-induced vasodilation response.

Conclusions and Implications

Neural control of mesenteric vasomotor tone was altered by pregnancy. Diminished sympathetic and enhanced nitrergic components both contributed to the decreased vasoconstriction response to EFS during pregnancy. All these changes indicate the selective participation of sympathetic and nitrergic innervations in vascular adaptations produced during pregnancy.     

Nicotinamide improves glucose metabolism and affects the hepatic NAD-sirtuin pathway in a rodent model of obesity and type 2 diabetes

Nicotinic acid (NA) and nicotinamide (NAM) are major forms of niacin and exert their physiological functions as precursors of nicotinamide adenine dinucleotide (NAD). Sirtuins, which are NAD-dependent deacetylases, regulate glucose and lipid metabolism and are implicated in the pathophysiology of aging, diabetes, and hepatic steatosis. The aim of this study was to investigate the effects of two NAD donors, NA and NAM, on glucose metabolism and the hepatic NAD-sirtuin pathway. The effects were investigated in OLETF rats, a rodent model of obesity and type 2 diabetes. OLETF rats were divided into five groups: (1) high fat (HF) diet, (2) HF diet and 10 mg NA/kg body weight (BW)/day (NA 10), (3) HF diet and 100 mg NA/kg BW/day (NA 100), (4) HF diet and 10 mg NAM/kg BW/day (NAM 10), and (5) HF diet and 100 mg NAM/kg BW/day (NAM 100). NA and NAM were delivered via drinking water for four weeks. NAM 100 treatment affected glucose control significantly, as shown by lower levels of accumulative area under the curve during oral glucose tolerance test, serum fasting glucose, serum fasting insulin, and homeostasis model assessment of insulin resistance, and higher levels of serum adiponectin. With regard to NAD-sirtuin pathway, intracellular nicotinamide phosphoribosyltransferase, NAD, the NAD/NADH ratio, Sirt1, 2, 3, and 6 mRNA expressions, and Sirt1 activity all increased in livers of NAM 100-treated rats. These alterations were accompanied by the increased levels of proliferator-activated receptor gamma, coactivator 1 alpha and mitochondrial DNA. The effect of NA treatment was less evident than that of NAM 100. These results demonstrate that NAM is more effective than NA on the regulation of glucose metabolism and the NAD-sirtuin pathway, which may relate to the altered mitochondrial biogenesis.     

Clonidine Prevents Transient Loss of Noradrenaline in Response to Cholinergic Hypofunction Induced by Ethylcholine Aziridinium (AF64A)

Intracerebroventricular injection of ethylcholine aziridinium (AF64A) (2 nmol/ventricle) induced a considerable decrease in the level of acetylcholine (ACh) in hippocampus (from 21.14 +/- 0.84 to 10.04 +/- 0.59 pmol/mg of tissue; p less than 0.001) 4 days after application. The reduction of cholinergic function was accompanied by a decrease in the level of noradrenaline (NA) (from 1.96 +/- 0.08 to 1.41 +/- 0.06 pmol/mg of tissue; p less than 0.001). Two days after administration of AF64A (1 or 2 nmol/ventricle), the dose-dependent decrease in NA level was associated with an increase in the level of its major metabolite, 3-methoxy-4-hydroxyphenylglycol (MHPG), resulting in a considerable increase in the MHPG/NA molar ratio (from 0.84 +/- 0.06 to 1.62 +/- 0.17; p less than 0.002). Chronic treatment of AF64A-injected rats with clonidine (0.02-0.2 mg/kg, i.p., every 8-12 h) had no significant effect on the loss of ACh content, whereas the decrease in NA content in hippocampus was completely prevented. Clonidine induced aggressive behavior in the AF64A-treated rats, in contrast to sedation in vehicle-injected rats. The response to clonidine under these experimental conditions and the increased MHPG/NA molar ratio in response to AF64A suggest that the transient loss of NA content following AF64A administration results from increased NA release. The increased noradrenergic activity in hippocampus may be linked to the reduction of tonic inhibitory cholinergic input. These results are discussed in relation to possible implications for senile dementia of the Alzheimer type.     

海马内NA能神经损毁对抗急性低氧诱发皮质酮分泌

本工作观察了６羟多巴胺（６ｈｙｄｒｏｘｙｄｏｐａｍｉｎｅ,６ＯＨＤＡ）损毁大鼠腹侧海马去甲肾上腺素能神经对急性低氧诱发皮质酮分泌的影响。结果显示,吸入１０４％Ｏ２３０ｍｉｎ后血浆皮质酮水平显著升高,６ＯＨＤＡ注入腹侧海马致使海马内去甲肾上腺素（ＮＡ）含量降低（－３８５％）;血浆皮质酮水平也较未损毁组为低（－３３２％）。吸入１０４％Ｏ２后,皮质酮对低氧刺激的反应性升高现象消失。结果提示：海马内ＮＡ可能参与急性低氧应激引发血浆皮质酮分泌的调节活动。     

The effect of cocaine on kinetics of α<Subscript>1</Subscript>-adrenergic contractile response in different portions of the rat vas deferens

The effect of cocaine (10 μM) on the kinetics of contractile response to noradrenaline (NA) was studied in the rat epididymal and prostatic vas deferens. Cocaine caused an acute increase in vas deferens adrenergic sensitivity primarily due to blockage of NA neuronal capture. The presynaptic action prevailed in the epididymal half: the EC 50 value decreased 32-fold with a slight increase of the maximum adrenergic response more evident in the prostatic half. In the presence of cocaine, the prostatic contraction to NA was mediated not by a single pool of α₁-adrenoceptors like in epididymal vas deferens but by two. Its high affinity pool had the same affinity as α₁-adrenoceptors of the epididymal half, the affinity value of the low one was 36-fold less, and the total maximal response of both pools increased 4.5-fold. The differences in cocaine effect on the rat epididymal and prostatic vas deferens contractions to NA appear to be caused by the different sources of Ca²⁺ involved in these responses.     

免疫应答期间脑和淋巴器官中去甲肾上腺素含量的变化

应用高效液相色谱－电化学检测法（ＨＰＬＣ－ＥＣＤ）测定大鼠在用绵羊红细胞（ＳＲＢＣ）免疫后第２－７天期间,下丘脑、海马、脑干、胸腺和脾脏中去甲肾上腺素（ＮＡ）含量的变化。实验结果表明,下丘脑内ＮＡ含量在免疫后第４－７天明显增加,其中第７天有回降趋势。海马内ＮＡ含量在第４－５天显著增多。而胸腺和脾脏中ＮＡ水平在第４－５天均明显降低。脑干在免疫应答期间无明显改变。以上结果说明,体液免疫应答可影响脑和淋     

The effects of pertussis toxin-treatment on integrated vasoactive response of vascular system in spontaneously hypertensive rats

We investigated the effect of pertussis toxin (PTX) on hypotensive response induced by acetylcholine (ACh) and bradykinin (BK) and on noradrenaline (NA)-induced pressor response in spontaneously hypertensive rats (SHR). Fifteen-week-old Wistar rats and age-matched SHR were used. Half of SHR received PTX (10 microg/kg/i.v.) and the experiments were performed 48 h later. After the anesthesia the right carotid artery was cannulated in order to record blood pressure (BP). The hypotensive response to ACh was enhanced in SHR compared to Wistar rats. After pretreatment of SHR with PTX the hypotensive response to ACh was reduced compared to untreated SHR and it was also diminished in comparison to Wistar rats. Similarly, the hypotensive response to BK was also decreased after PTX pretreatment. The pressor response to NA was increased in SHR compared to Wistar rats. NA-induced pressor response was considerably decreased after PTX pretreatment compared to untreated SHR. In conclusion, the enhancement of hypotensive and pressor responses in SHR was abolished after PTX pretreatment. Our results suggested that the activation of PTX-sensitive inhibitory G(i) proteins is involved in the regulation of integrated vasoactive responses in SHR and PTX pretreatment could be effectively used for modification of BP regulation in this type of experimental hypertension.     

Hypothalamic monoamines in the cold stress during changes in activity of nitric oxide system

Effects of NO-synthase inhibitor N(omega)-nitro-L-arginine (LNA) and donor sodium nitroprusside (SNP) on alteration in body temperature, plasma corticosterone level and hypothalamic monoamines in response to cold exposure, were studied. Drop of the body temperature in cold exposure in rats treated with LNA or SNP was the same as in the control group. Administration of SNP (2 mg/kg i.p.) significantly increased the basal level of corticosterone (CS). Cold exposure elevated CS in all groups of rats. LNA did not markedly alter the hypothalamic noradrenaline (NA) while SNP significantly decreased the NA. Cold exposure resulted in additional decrease of the NA in SNP-treated rats. NA was found to significantly increase within 48 hrs following the cold exposure in the LNA as well as in the SNP groups. SNP significantly increased basal dopamine and DOPAC levels. Cold exposure did not affect hypothalamic dopamine. In the experiments, NO changes of serotonin and 5-hydroxyindoleacetic acid were observed. The findings suggest that antagonistic effects of the NO-synthase inhibitor and NO donor postulated in literature for various kinds of stress do not occur in experiments with cold stress.     

Modulation of noradrenaline-induced vasoconstriction in isolated perfused mesenteric arterial beds from obese Zucker rats in the presence and absence of insulin

The genetically obese Zucker rat (fa/fa) is an insulin-resistant animal model with early-onset severe hyperinsulinemia that eventually develops mild hypertension. Thus, it represents a model in which the effect of hyperinsulinemia - insulin resistance associated with hypertension on vascular reactivity can be examined. The purpose of this study was to investigate the contribution of endogenous nitric oxide (NO) and prostaglandins to reactivity to noradrenaline (NA) in the presence and absence of insulin in mesenteric arterial beds (MAB) from 25-week-old obese Zucker rats and their lean, gender-matched littermates. In the absence of insulin, bolus injection of NA (0.9-90 nmol) produced a dose-dependent increase in perfusion pressure in MAB from both lean and obese rats. Although there was no significant difference in NA pD2 (-log ED50) values, the maximum response of MAB from obese rats to NA was slightly but significantly reduced compared with that of MAB from lean rats. The nitric oxide synthase inhibitor NG-monomethyl-L-arginine (L-NMMA, 300 microM) enhanced and indomethacin (20 microM) inhibited pressor responses to NA in MAB from both obese and lean rats. Perfusion with insulin (200 mU/L, a level similar to that in obese rats in vivo) potentiated only the responses of the obese MAB to the two lowest doses of NA tested (0.9 and 3 nmol). In the presence of L-NMMA, insulin further potentiated the NA response in MAB from obese rats. Indomethacin, the prostaglandin H2/thromboxane A2 receptor antagonist SQ 29548 (0.3 microM), and the nonselective endothelin-1 (ET-1) receptor antagonist bosentan (3 microM) all abolished insulin potentiation of the NA response in obese MAB. These data suggest that concurrent release of NO and vasoconstrictor cyclooxygenase product(s) in MAB from both obese and lean Zucker rats normally regulates NA-induced vasoconstrictor responses. Furthermore, insulin increases the release of contracting cyclooxygenase product(s) and enhances reactivity to low doses of NA in MAB from obese rats. The effects of insulin may be partially mediated by ET-1 via ET receptors and are buffered to some extent by concomitant NO release. This altered action of insulin may play a role in hypertension in this hyperinsulinemic - insulin-resistant model.     

Release of [3H]noradrenaline from perfused rat hearts by potassium and its modifications by 6-hydroxydopamine and reserpine.

The sources of noradrenaline (NA) released by excess potassium from isolated perfused rat hearts were investigated by labelling the hearts from normal, reserpine-treated, and 6-hydroxydopamine-treated (6-OHDA-treated) rats with [3H]HA, and measuring the increased rate of efflux induced by perfusion with a Krebs solution containing varying amounts of excess potassium. The [3H]NA and its metabolites in the effluent were separated by adsorption on alumina and a cation-exchange resin (Dowex-50). The release induced by potassium was a linear function of the log of the increased potassium concentration. Following a 1-h efflux period after labelling with [3H]NA, the hearts from reserpine-treated rats retained 1/5 as much [3H]NA, and released, in response to a 56mM elevation in the potassium concentration, less than 1/6 as much tritium label as the hearts from untreated (control) animals. In contrast, the hearts form 6-OHDA-treated animals retained 1/15 of the amount of [3H]NA and released 1/50 of the 3H label as did the control hearts. The potassium-induced increase of 3H-labelled substances in the effluent from the control hearts showed a large (threefold) percentage increase in the [3H]NA fraction, whereas the effluents from the hearts of reserpine- and 6-OHDA-treated animals contained only small increases in the [3H]NA fraction. Based on the assumptions that reserpine prevented retention of NA in the storage granules whereas 6-OHDA prevented almost all neuronal storage, it was concluded that more than 80% of the NA released by potassium excess from perfused normal hearts originated from the storage vesicles of the nerves, the remainder being largely from the cytoplasm of the nerves, with only a small portion from extraneuronal sources.     

Central vasopressin in the modulation of catecholamine release in conscious rats

Neurons containing arginine vasopressin (AVP) have been shown to project from the paraventricular nucleus of the hypothalamus to the nucleus tractus solitarius (NTS) in the medulla. We investigated whether AVP acts in brain stem regions to influence sympathoadrenal outflow. Cannulae were implanted into the fourth ventricle of rats 7 days prior to the experiment. The effects of intracerebroventricular (icv) injections of AVP, the vehicle, and AVP antagonist, d(CH2)5Tyr(Me)AVP, on mean arterial pressure (MAP) and plasma noradrenaline (NA) and adrenaline (A) levels were determined in conscious unrestrained rats. Injections of AVP (icv, 23 and 73 ng/kg) but not the vehicle increased MAP and plasma NA and A levels. In contrast, iv injection of AVP increased MAP but decreased plasma concentrations of A and NA. The pressor response to icv injection of AVP was abolished by prior icv injection of AVP antagonist. Injection of AVP antagonist (icv, 0.5 and 1.5 microgram/kg) had no effect on MAP or plasma NA or A levels. These results show that centrally injected AVP activates sympathoadrenal outflow, possibly via an inhibition of baroreceptor reflexes. Since centrally administered AVP antagonist did not influence MAP or plasma NA or A levels, it appears that endogenously released AVP does not have a tonic influence on central cardiovascular reflex system in conscious, unrestrained rats.     

Breast Feeding Increases Vasoconstriction Induced by Electrical Field Stimulation in Rat Mesenteric Artery. Role of Neuronal Nitric Oxide and ATP

Objectives

The aim of this study was to investigate in rat mesenteric artery whether breast feeding (BF) affects the vasomotor response induced by electrical field stimulation (EFS), participation by different innervations in the EFS-induced response and the mechanism/s underlying these possible modifications.

Methods

Experiments were performed in female Sprague-Dawley rats (3 months old), divided into three groups: Control (in oestrous phase), mothers after 21 days of BF, and mothers that had recovered their oestral cycle (After BF, in oestrous phase). Vasomotor response to EFS, noradrenaline (NA) and nitric oxide (NO) donor DEA-NO were studied. Neuronal NO synthase (nNOS) and phosphorylated nNOS (P-nNOS) protein expression were analysed and NO, superoxide anion (O₂ ^.–), NA and ATP releases were also determined.

Results

EFS-induced contraction was higher in the BF group, and was recovered after BF. 1 µmol/L phentolamine decreased the response to EFS similarly in control and BF rats. NA vasoconstriction and release were similar in both experimental groups. ATP release was higher in segments from BF rats. 0.1 mmol/L L-NAME increased the response to EFS in both control and BF rats, but more so in control animals. BF decreased NO release and did not modify O₂ ^.– production. Vasodilator response to DEA-NO was similar in both groups, while nNOS and P-nNOS expressions were decreased in segments from BF animals.

Conclusion

Breast feeding increases EFS-induced contraction in mesenteric arteries, mainly through the decrease of neuronal NO release mediated by decreased nNOS and P-nNOS expression. Sympathetic function is increased through the increased ATP release in BF rats.     

Aδ afferent fiber stimulation activates descending noradrenergic system from the locus coeruleus

We compared the noradrenaline (NA) level in the dorsal horn following electrical stimulation of Aδ afferent nerve fibers in the peripheral nervous system between rats with bilateral lesions of the locus coeruleus (LC) and non-operated control rats by using a microdialysis technique combined with high performance liquid chromatography. Prior to Aδ afferent fiber stimulation, the NA content in the dialysate did not differ between the LC-lesioned and the control rats. During Aδ afferent fiber stimulation, in the LC-lesioned rats, the NA level did not change significantly compared to that before Aδ afferent fiber stimulation, whereas the NA level increased significantly in the control rats. There was a significant difference in the NA levels during Aδ afferent fiber stimulation between the two groups of rats. The result suggests that descending noradrenergic neurons from the LC is involved in the increase of the NA level in the spinal cord dorsal horn produced by Aδ afferent fiber stimulation.     

Paraventricular noradrenergic systems participate in angiotensin II-induced drinking

The present study was designed to examine the role of noradrenergic systems in the hypothalamic paraventricular nucleus (PVN) in the drinking response induced by microinjection of angiotensin II (ANG II) into the subfornical organ (SFO) in the awake rat. Intracerebral microdialysis techniques were utilized to quantify the extracellular concentration of noradrenaline (NA) in the region of the PVN. Injections of ANG II (10⁻⁶ M, 0.2 μl) into the SFO significantly increased NA release in the PVN area. The increase in the NA concentration caused by the ANG II injection was significantly attenuated by water ingestion. In urethane-anesthetized rats, injections of ANG II into the SFO elicited an elevation in mean arterial pressure (MAP). On the other hand, intravenous injections of the -agonist metaraminol (5 μg) slightly decreased the release of NA in the PVN area that accompanied an elevation in MAP. These results show that the noradrenergic system in the PVN area may be involved in the dipsogenic response induced by ANG II acting at the SFO.