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PubMed1984

Chronic effects of norepinephrine and vasopressin on urinary prostaglandin E and kallikrein excretions in conscious rats.

To assess in vivo functional interactions of vasopressor substances, norepinephrine and vasopressin, with renal prostaglandins and kallikrein-kinin system which are responsible for the vasodepressor mechanism in the kidney, we evaluated chronic effects of norepinephrine (1.8 mg/kg/day ip) and vasopressin (7.2 U/kg/day ip) on urinary prostaglandin E excretion and urinary kallikrein excretion in conscious rats. Both norepinephrine and vasopressin induced a sustained increase in systolic blood pressure. Norepinephrine induced slight but significant increases in urinary prostaglandin E excretion and urinary kallikrein excretion which were sustained for up to 6 days. Vasopressin induced a marked increase in urinary prostaglandin E excretion which was sustained for up to 6 days, whereas it induced a sustained decrease in urinary kallikrein excretion. Circulating angiotensin II levels was not changed by norepinephrine, but was decreased by vasopressin. These results indicate that renal prostaglandin E may not correlate with renal kallikrein-kinin and renin-angiotensin system in the responses to norepinephrine and vasopressin, and that vasopressin may be a more potent stimulator of the synthesis or release of renal prostaglandin E.

Angiotensin II↗

PubMed1987

Diminished prostaglandin-mediated inhibition of norepinephrine release from the sympathetic nerve endings in spontaneously hypertensive rats.

This study was performed to investigate prostaglandin (PG)-mediated regulation of norepinephrine release from the sympathetic nerve endings in spontaneously hypertensive rats (SHR). The effects of PGE2 on the pressor responses and norepinephrine overflow during the periarterial nerve stimulation were examined in the perfused mesenteric vascular beds from SHR and age-matched Wistar Kyoto rats (WKY). In preliminary studies using normotensive Wistar rats, PGE2 inhibited the overflow of norepinephrine in response to the electrical nerve stimulation. On the contrary, when indomethacin was infused into the preparations, the norepinephrine overflow induced by the nerve stimulation was increased. In SHR, the neurogenic vasoconstriction and norepinephrine overflow during the nerve stimulation were significantly greater than in WKY. PGE2 in the medium inhibited the pressor responses and norepinephrine overflow during the nerve stimulation dose-dependently in WKY, while the inhibitory effects of PGE2 in SHR were blunted. These results suggest that PGE2 is an important hormone in regulating sympathetic vascular tone and that presynaptic inhibition of vascular adrenergic transmission by PGE2 is attenuated in SHR.

Animals↗

PubMed1992

Influence of age on control of norepinephrine release from the rat tail artery.

Stimulation-evoked norepinephrine release from the rat tail artery increases with age; therefore, the sensitivity of prejunctional alpha-2 adrenergic receptors to antagonists and agonists was compared in perfused tail arteries from Fischer-344 rats, aged 6 and 20 months. The increase in endogenous fractional norepinephrine release produced by blockade of alpha-2 adrenergic receptors with submaximal concentrations of either yohimbine or idazoxan was significantly greater in 6-month-old animals as compared to 20 months; however, the effect of a maximal concentration of idazoxan was not significantly different. Inhibition of norepinephrine release by the alpha-2 receptor agonist UK14304 was reduced in 20-month-old animals compared to 6 months. In contrast, there were no age-related differences in inhibition of contractile responses to nerve stimulation by the prejunctionally acting dopamine D2 agonist, N-0923. These data suggest that age-related changes in the sensitivity of prejunctional alpha-2 receptors to agonists and antagonists may not reflect any fundamental alteration in the function of this receptor system, but may be related to competition between alpha-2 agonists or antagonists and increased biophase concentrations of norepinephrine. This conclusion is supported by lack of an age-related change in function of prejunctional dopamine D2 receptors. Persistence of age-related increases in norepinephrine release when alpha-2 adrenergic receptors are fully blocked may reflect an alteration in other fundamental mechanisms that control norepinephrine release.

Adrenergic beta-Agonists↗

PubMed2004

Distinguishing roles for norepinephrine and serotonin in the behavioral effects of antidepressant drugs.

Antidepressant drugs have typically been classified into sets of compounds with actions targeted at serotonin (selective serotonin reuptake inhibitors [SSRIs]), norepinephrine (norepinephrine reuptake inhibitors [NRIs]), or both neurotransmitters (serotonin-norepinephrine reuptake inhibitors). Their classification has been based predominantly on their acute pharmacologic effects, usually determined by in vitro radioligand binding assays. The pharmacologic selectivity of antidepressants can be altered after their systemic administration, however, by dose, drug metabolism, physiologic interactions between neurotransmitters, and adaptive effects that emerge after chronic administration. This review examines whether pharmacologic selectivity is maintained by different types of antidepressants in vivo and whether pharmacologic selectivity matters for the production of their behavioral effects. Antidepressants increase extracellular levels of neurotransmitters according to their ability to inhibit presynaptic transporters, although physiologic interactions among neurotransmitters can influence antidepressants' selectivity in certain brain regions. Chronic administration of many antidepressants also causes down-regulation of postsynaptic and presynaptic receptors. The pattern of responses of presynaptic markers suggests that pharmacologic selectivity is maintained after chronic administration of many antidepressants. Behavioral tests indicate that depletion of serotonin (5-HT) is capable of preventing the effects produced by SSRIs but not NRIs. The depletion of catecholamines also inhibits the effects of NRIs, although test results can be complicated by inhibition of motor activity. Depletion of norepinephrine may also inhibit the effects of some SSRIs, but not highly selective SSRIs like citalopram. Although the pattern of results from in vivo tests supports the concept that parallel neurotransmitter mechanisms lead to antidepressant activity, norepinephrine may participate in the effects of some SSRIs. It is also possible that compounds with dual actions at 5-HT and norepinephrine systems may be effective under circumstances in which selective antidepressants are ineffective.

Antidepressive Agents↗

PubMed2004

Norepinephrine is a more potent inhibitor of tumor necrosis factor over a range of doses than dopamine.

In the current study, we test the hypothesis that norepinephrine has greater anti-inflammatory effects versus dopamine over a range of doses in a model of lipopolysaccharide (LPS)-stimulated cytokine release in human saphenous vein. Segments of saphenous vein were cut and separated into 1 mm x 1 mm squares and placed into two 24-well plates. These small segments of vessels were incubated in the presence of 20 microg/mL bacterial LPS, alone as a control or with 10x-6, 10x-5, 10x-4, 10x-3 concentration of dopamine or norepinephrine and LPS. The general linear models (GLM) statistical analysis for least squares means and adjustment for multiple comparisons was chosen to analyze the data. Both norepinephrine and dopamine were able to suppress the production of tumor necrosis factor (TNF) in a dose-dependent fashion. Over the range of doses, norepinephrine is a more potent inhibitor of TNF production than dopamine. This is a statistically significant linear trend (P < .0001). Both norepinephrine and dopamine are powerful anti-inflammatory agents. Norepinephrine is a more potent inhibitor of TNF than dopamine.

Dopamine↗

PubMed2005

The relationship between magnesium, epinephrine and norepinephrine blood concentrations during CABG with normovolemic hemodilution.

The effects of procedures with extracorporeal circulation on the disturbance of relationships between blood magnesium (Mg), epinephrine, and norepinephrine levels have not been explicitly explained. It is assumed that both hypomagnesemia and increased concentration of the above mentioned hormones exert adverse effects on the myocardium often causing life threatening disorders. This problem is particularly important in cases of stunned myocardium, observed after extracorporeal circulation procedures. The complex nature of the procedures and the intraoperative normovolemic hemodilution (NH) employed are likely to alter Mg, epinephrine, and norepinephrine concentrations, as well as the above mentioned relations. The aim of the study was to evaluate the changes in blood Mg, epinephrine and norepinephrine concentrations in patients undergoing extracorporeal circulation and normovolemic hemodilution. The study encompassed 16 men operated on for stable coronary disease (I or II degrees according to the Canadian Scale). The patients were divided into two groups according to body weight: A) patients weighing less than 75 kg and B) patients weighing more than 75 kg. The degree of NH caused by constant volume of priming (1800 mL) was determined on the basis of hematocrit measurements and in relation to body weight. The examinations were conducted in 5 stages: 1) after radial artery cannulation before anaesthesia and surgery, 2) during hemodilution and deepest hypothermia, 3) after surgery before sending the patient to Intensive Postoperative care Unit, 4) in the first postoperative day, 5) in the second postoperative day. The observations showed an increase in epinephrine levels in group A in the second stage and of norepinephrine levels in stage 4. Decreased blood Mg levels were noted in all the patients in the second stage, however in group A significantly lower values were also observed in stage 3. Moreover, the correlation between Mg level changes and blood epinephrine and norepinephrine levels were observed. The study revealed significant effects of extracorporeal circulation procedures on adrenergic reactions as well as blood magnesium concentrations. It seems that the degree of NH is the main factor determining blood levels of Mg, epinephrine and norepinephrine during the use of a heart-lung apparatus, which may be particularly relevant in patients with impaired heart function and low body weight.

Aged↗

PubMed1977

The presynaptic site of action of norepinephrine in the superior cervical ganglion of guinea pig.

Supramaximal preganglionic volleys did not elicit detectable postsynaptic potential in the curare-treated superior cervical ganglion cell of the guinea pig whereas, a tetanic stimulation (10-30 Hz, 1-5 seconds) consistently evoked a monophasic depolarizing potential resembling the slow excitatory postsynaptic potential. The depolarizing potential was not preceded by a detectable hyperpolarization. In non-curare-treated preparations, norepinephrine in concentrations of 1 to 10 muM consistently and reversibly suppressed the fast excitatory postsynaptic potential elicited by submaximal preganglionic stimulation without appreciably affecting the resting membrane potential, the total membrane resistance or the cell membrane excitability. Pretreating the ganglion with phenoxybenzamine (10 muM) completely prevented, whereas propranolol (30 muM) failed to antagonize, the ganglionic depressant action of norepinephrine. The amplitude and time course of the iontophoretically induced acetylcholine potential were not significantly altered by norepinephrine in concentrations which markedly attenuated the response of the fast excitatory postsynaptic potential. The frequency but not the amplitude of the miniature excitatory postsynaptic potentials was significantly reduced by norepinephrine (1-10 muM). These results demonstrate that norepinephrine inhibits ganglionic transmission in the guinea pig principally by reducing the output of acetylcholine from the presynaptic nerve terminals. These data are discussed with respect to their relation to the presence in the guinea pig superior cervical ganglion of norepinephrine-containing small intensely fluorescent cells which are not connected synaptically with the postganglionic neurons.

Acetylcholine↗

PubMed1991

Glucagon pharmacodynamics and modulation of sympathetic nerve and norepinephrine-induced constrictor responses in the superior mesenteric artery of the cat.

The aim of this study was to assess whether the pancreatic peptide glucagon was capable of inhibiting nerve- and norepinephrine-induced vasoconstrictor responses in the superior mesenteric artery of the anesthetized cat. Intra-arterial dose-response curves for glucagon and norepinephrine were analyzed by nonlinear regression to estimate the maximal response (maximal dilation, 163%; maximal constriction, 110%) in terms of percent change in superior mesenteric artery conductance and dose of glucagon or norepinephrine required to produce 50% of the maximal response (0.98 and 0.38 micrograms/kg/min, respectively). Constrictor responses (3-min duration) were only weakly inhibited by glucagon. Peak constrictor responses induced by low-dose i.a. infusions of norepinephrine were significantly inhibited (39%) by the high dose of glucagon, whereas the high-dose norepinephrine peak constrictor responses were unaffected by any dose of glucagon. Intermediate and high doses of glucagon significantly inhibited the low-frequency (2 Hz) nerve-induced peak constrictions (19% and 34%, respectively). The higher frequency (6 Hz) nerve-induced peak constrictor responses were not significantly affected by glucagon. Vascular escape from nerve- and norepinephrine-induced peak constrictor responses was not related to the degree of initial constriction nor were they affected by glucagon. Glucagon levels produced by our i.a. infusions were estimated to be well outside the pathophysiological range. We conclude that glucagon is not an effective inhibitor of constrictor responses in the superior mesenteric artery and is unlikely to have such an effect at physiological levels.

Animals↗

PubMed1990

Alpha-2 adrenergic inhibition of Ca(++)-evoked [3H]norepinephrine release from synaptosomes is blocked by depolarization.

The Ca(++)-evoked release of [3H]norepinephrine was used in these studies to investigate presynaptic regulation of norepinephrine release. In hippocampal synaptosomes, previously unexposed to Ca++ during isolation and superfusion, 1.25 mM Ca++ evoked a modest (4 to 7% of total stores) release of [3H]norepinephrine with 4.5 mM [K+] present. The alpha-2 adrenergic agonist clonidine inhibited 60% of the Ca(++)-evoked [3H]norepinephrine release. The alpha-2 adrenergic antagonists idazoxan and yohimbine reversed clonidine inhibition of release whereas the alpha-1 antagonist prazosin did not. Increasing the [K+] before Ca++ exposure increased [3H]norepinephrine release, and at 20 [K+] the release increased to over 20% of total stores. However, at [K+] above 9 mM, inhibition of Ca(++)-evoked release by clonidine decreased, and by 20 mM [K+] clonidine no longer inhibited release. Release was unaffected by 5 microM idazoxan or the opiate antagonist naloxone at 15 or 20 mM [K+]. The K+ channel blockers tetraethylammonium (5 mM) and 4-aminopyridine (0.1 mM) increased Ca(++)-evoked release almost 4-fold above control (4.5 mM [K+] present). Neither clonidine nor idazoxan affected Ca(++)-evoked release with the K+ channel blockers present. Therefore, even though K+ channel blockers and 20 mM [K+] increase neurotransmitter release, it is not autoreceptor activation by released endogenous norepinephrine that is responsible for blocking alpha-2 inhibition, but the depolarization produced by these treatments. The 20 mM [K+] blockade of alpha-2 inhibition was decreased by lowering the [Ca++] in the superfusion buffer. Therefore, synaptosomal accumulation of Ca++ may partially explain the loss of alpha-2 inhibition.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1977

Norepinephrine-stimulated cyclic AMP accumulation in brain slices in vitro after serotonin depletion or chronic administration of selective amine reuptake inhibitors.

These experiments demonstrate that altering serotonin availability in vivo does not influence the interaction of norepinephrine with adenylate cyclase in vitro. Neither reducing serotonin levels (parachloroamphetamine) nor increasing the availability of serotonin by blocking its reuptake (fluoxetine) affect the norepinephrine-induced elevation of cyclic AMP in slices of the limbic forebrain of rats. However, increasing norepinephrine availability by chronic administration of desipramine, a norepinephrine reuptake inhibitor, reduces cyclic AMP synthesis in the limbic forebrain. However, it is doubtful that blockade of norepinephrine reuptake alone accounts for the reduction in receptor sensitivity produced by desipramine since chronic administration of a new norepinephrine reuptake inhibitor, nisoxetine, does not decrease cyclic AMP accumulation.

Animals↗

PubMed1990

A comparison of N-methyl-D-aspartate-evoked release of adenosine and [3H]norepinephrine from rat cortical slices.

Tetrodotoxin reduced N-methyl-D-aspartate (NMDA)-evoked release of adenosine by 35% but virtually abolished [3H]norepinephrine release. Although [3H]norepinephrine release from rat cortical slices evoked by 500 microM NMDA was abolished by 1.2 mM Mg++, which produces a voltage-sensitive, uncompetitive block of NMDA-channels, adenosine release was increased in the presence of Mg++. Partial depolarization with 12 mM K+ relieved the Mg++ block of 500 microM NMDA-evoked [3H]norepinephrine release but did not affect adenosine release, indicating that a Mg++ requirement for the adenosine release process per se cannot account for this discrepancy. NMDA was 33 times more potent in releasing adenosine than [3H]norepinephrine. At submaximal concentrations of NMDA (10 and 20 microM), adenosine release was augmented in Mg+(+)-free medium. Although a high concentration of the uncompetitive NMDA antagonist MK-801 [(+)-5-methyl-10,11,dihydro-5H-dibenzo[a,d]cyclohepten-5-10-imine maleate] (3 microM) blocked NMDA-evoked release of [3H]norepinephrine and adenosine, a lower concentration (300 nM) decreased NMDA-evoked [3H]norepinephrine release by 66% without affecting adenosine release. These findings suggest that maximal adenosine release occurs when relatively few NMDA receptors are activated, raising the possibility that spare receptors exist for NMDA-evoked adenosine release. Rather than acting as a protectant against excessive NMDA excitation, released adenosine might provide an inhibitory threshold which must be overcome for NMDA-mediated neurotransmission to proceed.

Adenosine↗

PubMed1989

Thiophosphorylation causes Ca2+-independent norepinephrine secretion from permeabilized PC12 cells.

Adenosine-5'-O-(3-thiotriphosphate) (ATP gamma S) was used to examine the role of phosphorylation in the regulation of norepinephrine secretion by digitonin-permeabilized PC12 cells. While most kinases will use ATP gamma S to thiophosphorylate proteins, thiophosphorylated proteins are relatively resistant to dethiophosphorylation by protein phosphatases. Norepinephrine secretion by permeabilized PC12 cells was ATP- and Ca2+-dependent but resistant to calmodulin antagonists. Half-maximum secretion was obtained in 0.75 microM Ca2+. Permeabilized PC12 cells were incubated with ATP gamma S in the absence of Ca2+, the ATP gamma S was removed, and norepinephrine secretion was determined. Preincubation with ATP gamma S increased the amount of norepinephrine secreted in the absence of Ca2+, but it had no effect on the amount released in the presence of Ca2+. After a 15-min preincubation in 1 mM ATP gamma S, there was almost as much secretion in the absence of Ca2+ as in its presence. Inclusion of ATP in the preincubation inhibited the effect of ATP gamma S. Ca2+ stimulated the rate of modification by ATP gamma S as brief preincubations with ATP gamma S in the presence of Ca2+ resulted in higher levels of Ca2+-independent secretion than did preincubations with ATP gamma S in the absence of Ca2+. Similarly, brief preincubations of permeabilized cells with ATP in the presence of Ca2+ resulted in elevated levels of Ca2+-independent secretion. Secretion of norepinephrine from ATP gamma S-treated cells was ATP-dependent. These results suggest that norepinephrine secretion by PC12 cells is regulated by a Ca2+-dependent phosphorylation. Once this phosphorylation has occurred, secretion is still ATP-dependent, but it no longer requires Ca2+.

Adenosine Triphosphate↗

PubMed1988

Platelet-generated thromboxane A2 enhances norepinephrine release from adrenergic nerves.

Platelet-generated thromboxane A2 enhances norepinephrine release from adrenergic nerves. Microsomes were prepared from outdated human platelets and incubated with arachidonic acid to produce thromboxane A2. The incubate was added to isolated, electrically stimulated rabbit portal veins to determine its effect on adrenergic neurotransmission. Immunoreactive thromboxane B2 concentrations were measured to assess the generation of the precursor, thromboxane A2. Addition of microsomes in the presence of arachidonic acid (1 microM) caused a concentration-dependent increase in thromboxane B2 concentrations, electrically induced force and norepinephrine release. Inclusion of acetylsalicylic acid (10 microM) or the thromboxane synthase inhibitor, U63557A (100 micrograms/ml), in the arachidonic acid-microsome incubate eliminated the potentiation of force, norepinephrine release and thromboxane B2 generation. The thromboxane receptor antagonist, SQ30741 (1 microM), also eliminated the microsome effects on neurogenic force and norepinephrine release but not on thromboxane generation. The microsome-arachidonic acid incubate did not influence norepinephrine concentration-contractile response curves. These data are consistent with a potentiative action of thromboxane A2 on adrenergic neurotransmission, primarily mediated by enhanced release of norepinephrine. The physiological or pathological significance of this observation depends on the thromboxane concentrations in the vicinity of adrenergic nerves.

Animals↗

PubMed1988

Differential effects of (-)-norepinephrine and of (+/-)-isoproterenol on cardiac contraction, an uptake phenomenon.

Concentration-dependent inotropic effects of (-)-norepinephrine and of (+/-)-isoproterenol were compared in isometrically contracting guinea pig papillary muscles stimulated at a frequency of 0.2 Hz. (-)-Norepinephrine (0.1-100 mumol/l) elicited a positive inotropic effect that was not antagonized by carbachol, failed to produce a positive inotropic staircase after resumption of stimulation and shortened relaxation time in a concentration-dependent fashion.(+/-)-Isoproterenol had a dual action: at low and moderately effective concentrations (1-30 nmol/l), the positive inotropic effect was antagonized by carbachol, a positive inotropic staircase was elicited and time to peak force was shortened. At (+/-)-isoproterenol concentrations exceeding an EC80 for the positive inotropic effect (greater than 30 nmol/l), relaxation time became shorter, staircase and carbachol-induced antagonism became less pronounced until at 300 nmol/l inotropic effects of (+/-)-isoproterenol resembled closely those of (-)-norepinephrine. Cyclic AMP derivatives and the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine mimicked (+/-)-isoproterenol in their inotropic actions. Impairment of neuronal uptake caused (-)-norepinephrine 1) to produce (+/-)-isoproterenol-like effects on the isometric contraction, 2) to induce a positive inotropic staircase and 3) to become sensitive to carbachol-induced antagonism. The results are compatible with the concept that neuronal uptake produces a distribution of (-)-norepinephrine within the papillary muscle which allows predominantly high concentrations of (-)-norepinephrine to become effective in the receptor compartment.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1987

Actions of the alpha-1 adrenoceptor blocker bunazosin on the norepinephrine-induced contraction of smooth muscles in the rabbit proximal urethra.

Effects of bunazosin on the norepinephrine-induced electrical and mechanical activities of smooth muscles of the rabbit proximal urethra were investigated using microelectrode and tension recording methods. Responses to norepinephrine were mediated by activation of both alpha-1 and beta adrenoceptors. In the presence of propranolol, the norepinephrine-induced contraction increased and, with yohimbine, the phasic but not tonic contraction was only inhibited slightly. Contributions of the alpha-2 adrenoceptor to the norepinephrine-induced contraction were negligible. Bunazosin inhibited in a concentration-dependent manner both the phasic and tonic responses of the norepinephrine-induced contraction, and the concentration-response relationship for norepinephrine shifted to the right. The Schild plot obtained from measurements of tonic responses in this antagonism yielded a straight line with a slope of 0.96. The pA2 value for bunazosin was 8.39 and the KB value was 4.1 nM. Prazosin had similar effects (the corresponding values being 0.96, 8.21 and 6.2 nM, respectively). The mechanical response evoked by field stimulation was composed of cholinergic, noradrenergic alpha-1 and noncholinergic-nonadrenergic contractions and of a subsequent nonadrenergic-noncholinergic relaxation. Bunazosin inhibited the twitch contraction evoked by field stimulation more than did prazosin, albeit not completely. These results indicate that although the smooth muscle tone in the urethra is regulated by multiple neural factors, the elevation of the tone is regulated predominantly by activation of the alpha-1 adrenoceptors. Bunazosin has an antagonistic action on this receptor. The actions of bunazosin are discussed in relation to the clinical application in cases of inadequate micturition.

Acetylcholine↗

PubMed1987

Ouabain binding to brain (Na+,K+)-adenosine triphosphatase: interactions of K+, ethanol and norepinephrine with high- and low-affinity binding.

Effects of K+, ethanol and norepinephrine on the binding kinetics of ouabain to (Na+,K+)-adenosine triphosphatase in beef brain microsomes were examined. K+ reduced the rate and apparent affinity for ouabain binding markedly. Whereas ethanol and norepinephrine themselves inhibited ouabain binding slightly, they stimulated binding in the presence of K+. Norepinephrine enhanced the effect of ethanol. Dissociation of ouabain was biphasic, with fast and slow components corresponding to high and low apparent affinity. About 65% of the enzyme had high affinity, regardless of conditions. Norepinephrine and ethanol had differential effects on the rate of dissociation from high and low affinity enzyme, however. Alpha receptor blockade generally prevented the effects of norepinephrine. These results show that, although norepinephrine and ethanol have a modest effect on the amount of enzyme that can bind ouabain, their main effect on (Na+,K+)-adenosine triphosphatase is to antagonize the binding of K+ to its allosteric site that inhibits ouabain binding. The data support the hypothesis that ouabain binds rapidly to a K+-insensitive form of phosphorylenzyme or to its dephosphorylated analog and dissociates rapidly from E1.

Animals↗

PubMed1986

Changes in myocardial norepinephrine levels in response to stress, exercise and aging in control and T. cruzi-infected rats.

The effect of mild acute exercise (swimming for 1 h), restraint for 1 h and fasting for 48 h on myocardial norepinephrine concentration was compared with rats "at rest" using 320 control and chronically T. cruzi-infected rats at 50, 110, 200 and 380 days of age. Ventricular norepinephrine concentrations of control and similarly aged T. cruzi-infected rats were different for 2 of 4 "at rest" groups. Significant and opposite differences in ventricular norepinephrine were observed for restrained T. cruzi-infected rats when compared to controls (-35% in 50-day old rats and +40% in 110-day old rats). Exercised, "at rest" and fasted control rats presented a significant age-dependent decrease of ventricular norepinephrine concentration, which was not observed for restrained control rats. Norepinephrine levels of pooled atria from 120-day old "at rest" T. cruzi-infected rats were significantly lower than those from non-infected controls, whereas no difference was found in serotonin levels. The lability of myocardial norepinephrine levels in T. cruzi-infected rats suggests, but does not demonstrate, that there is a disturbance of the cardiac sympathetic control.

Animals↗

PubMed1988

Norepinephrine and potassium induced calcium translocation in rat vas deferens.

To understand calcium regulation in smooth muscle, we studied both potassium- and norepinephrine-mediated alterations in the movement of calcium in the smooth muscle of rat vas deferens. We employed 45Ca to measure agonist-mediated calcium influx and efflux, as well as tissue calcium content. In addition we labeled tissues with [3H]myoinositol to measure the effect of norepinephrine on inositol phosphate generation. Stimulation of the vas deferens with 50 mM potassium caused a rapid influx of 45Ca (6-fold). Norepinephrine stimulation, even at a concentration maximal for contraction of the tissue (1 mM), did not result in any alteration in 45Ca influx by itself but inhibited potassium-stimulated 45Ca influx (IC50 = 3 microM). This alpha receptor-mediated effect of norepinephrine was not diminished by either pretreatment with reserpine or adrenergic denervation. Studies of the efflux of 45Ca from vas deferens revealed that efflux was not affected by potassium but was significantly stimulated by norepinephrine. Alpha receptor stimulation of vas deferens smooth muscle caused a marked elevation in the appearance of inositol phosphates, particularly inositol trisphosphate, that was not dependent on extracellular calcium. We conclude that norepinephrine does not stimulate calcium influx in vas deferens smooth muscle but leads to the release of calcium from intracellular stores via formation of inositol trisphosphate and that the resulting increase in intracellular calcium may lead to inactivation of the potential-dependent calcium channel.

Animals↗