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Results for “Norepinephrine”

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PubMed1978

Resistance to endogenous norepinephrine in Bartter's syndrome: reversion during indomethacin administration.

In five patients with Bartter's syndrome, mean (+/-SE) plasma norepinephrine concentrations increased from 324 +/- 75 pg/ml with the patients in the supine position to 550 +/- 100 pg/ml, 753 +/- 104 pg/ml and 808 +/- 116 pg/ml after 2,5 and 10 minutes, respectively, in the standing position, levels significantly higher than normal. Plasma epinephrine concentrations were indistinguishable from normal. One patient was shown to resistant the pressor (but not the metabolic) effects of intravenously administered norepinephrine prior to treatment with reversion to normal pressor responsiveness during indomethacin administration. Similarly, that patient's exaggerated endogenous norepinephrine response to standing (10 minute plasma value of 1,110 pg/ml) reverted to normal (10 minute value of 462 pg/ml) during indomethacin administration. Thus, patients with Bartter's syndrome exhibit a hyperadrenergic state consisten with resistance to endogenous, as well as exogenous, norepinephrine. Since the metabolic responses to intravenously administered norepinephrine were normal in the patient studied, norepinephrine resistance would appear to be limited to the vasculare system. Reversion of norepinephrine resistance during administration of an inhibitor of prostaglandin synthesis suggests that this hyperadrenergic state is not a primary pathogenetic abnormality in Bartter's syndrome.

Adult↗

PubMed1976

Plasma levels of norepinephrine (NE) during the periovulatory period and after LH-RH stimulation in women.

In three normally cycling women studied daily from day 10 to 17 of the menstrual cycle, the levels of circulating norepinephrine showed a sharp rise preceding or concomitantly with the ovulatory LH surge. In two patients the norepinephrine peak took place 24 hr. previously to the LH rise and in the third one it occurred simultaneously. The simultaneous determination of ovarian hormones and norepinephrine showed no temporal correlation between this catecholamine and either estradiol or progesterone. On the other hand, after a single intravenous 100 mug dose of LH-RH, a significant rise in plasma norepinephrine, preceding the LH peak, was found in the four patients studied. The determination of norepinephrine at 3 minute intervals beginning one minute after LH-RH injection showed a significant rise in the amine levels ranging from 5 to 10 times in respect to basal values between 1 and 6 minutes after LH-RH stimulation. In these patients a second peak of norepinephrine occurred simultaneously with the maximal response of LH, which rose to peak levels after 18 minutes in one patient and after 24 minutes in the other. These findings are discussed with respect to the origin and role of increased amounts of plasma norepinephrine related to the LH surge.

Estradiol↗

PubMed1982

Monoamine oxidase type A: differences in selectivity towards l-norepinephrine compared to serotonin.

l-Norepinephrine and serotonin have been regarded as preferential substrates for monoamine oxidase (MAO) type A. A close comparative examination of a number of tissues from different species, however, indicated the following differences. Serotonin was a more selective substrate for MAO-A, being inhibited by low concentrations (less than 10(-7) M) of the irreversible MAO-A inhibitor, clorgyline, more consistently and to a greater extent (80-100%) than was l-norepinephrine (30-85%). These serotonin-norepinephrine differences were greater in humans and other primates than in rodents. Serotonin also had a 2- to 4-fold smaller apparent Km for MAO-A than l-norepinephrine and was deaminated 2- to 5-fold more readily by MAO in vitro in most tissues. In contrast, the MAO-B in human platelets deaminated l-norepinephrine more readily than serotonin. Thus, l-norepinephrine, like dopamine, should be regarded as a substrate for both MAO-A and MAO-B in vitro. The prominent role of MAO-B in norepinephrine degradation in primates may need to be considered in interpreting laboratory and clinical studies of clorgyline and other selective MAO-inhibiting drugs.

Animals↗

PubMed1990

Antinociception produced by interactions between intrathecally administered adenosine agonists and norepinephrine.

It is well-established that intrathecal injection of noradrenergic agonists produces dose-dependent antinociception in rats. Recently, the antinociceptive actions of norepinephrine in the central nervous system have been shown to be modulated by adenosine and adenosine analogs. This study examined whether there is an interaction between norepinephrine and adenosine analogs in the regulation of nociceptive transmission in the rat spinal cord using the tail flick and hot plate tests. The results indicate that dose-dependent antinociception was produced by intrathecal injection of norepinephrine (4.8-195 nmol), the A1/A2 adenosine agonist 5'-N-ethylcarboxamide adenosine (NECA; 0.97-4.9 nmol), and the A1 adenosine agonist R-phenylisopropyladenosine (R-PIA; 0.78-26 nmol). Furthermore, subeffective doses of NECA and norepinephrine interacted synergistically to produce potent antinociception. In contrast, no synergistic interaction was observed between norepinephrine and doses of R-PIA as high as 26 nmol. The antinociception produced by coadministration of norepinephrine and NECA appears to be mediated by adenosine receptors, since it was attenuated by pretreatment with theophylline, a non-selective adenosine antagonist. The synergistic interaction between NECA and norepinephrine did not appear to result from alterations in cardiovascular tone because blood pressure values were not significantly altered by drug administration. These results suggest that purinergic and noradrenergic systems interact synergistically to modify nociceptive transmission in the spinal cord. The purinergic component of this interaction may be mediated, in part, by adenosine A2 receptors.

Adenosine↗

PubMed1991

Microinjections of norepinephrine within the superficial laminae of trigeminal subnucleus caudalis evoke increases in plasma adrenocorticotropin in the rat.

To determine if local release of norepinephrine within the medullary dorsal horn influences autonomic responses often associated with nociception, microinjections of norepinephrine or of specific adrenergic receptor agonists were directed at the trigeminal subnucleus caudalis (Vc) in pentobarbital-anesthetized rats. Norepinephrine (20 nmol, 100 nl) evoked a significant increase (+ 233.8 +/- 89.5 pg/ml, P less than 0.01) in plasma concentrations of adrenocorticotropin (ACTH) after injections within the superficial laminae (I-II) of Vc, whereas mean arterial pressure or heart rate were not affected. Methoxamine (20 nmol), an alpha 1-adrenoceptor agonist, injections into laminae I-II also increased plasma ACTH (+ 90.6 +/- 32 pg/ml, P less than 0.025) without affecting arterial pressure or heart rate. Norepinephrine injections into the deeper laminae (III-V) of Vc caused a variable increase in plasma ACTH (+ 203.5 +/- 146.5 pg/ml, P less than 0.01) that was not mimicked by injections of methoxamine. Microinjections of alpha 2-(clonidine) or beta-(isoproterenol) adrenergic receptor agonists into Vc had no effect on plasma ACTH regardless of the laminar site of injection. The results suggest that norepinephrine acts within Vc to alter selected autonomic responses often associated with nociception. The involvement of an alpha 1-adrenergic receptor subtype within the superficial laminae of the medullary dorsal horn suggests a neural mechanism for norepinephrine-evoked increase in plasma ACTH that is distinct from the well known alpha 2-adrenergic receptor-mediated antinociceptive effects of norepinephrine.

Adrenocorticotropic Hormone↗

PubMed1991

Decreased norepinephrine release in anterior hypothalamus of NaCl-sensitive spontaneously hypertensive rats during high NaCl intake.

We previously demonstrated that dietary NaCl supplementation reduces endogenous norepinephrine stores and turnover in the anterior hypothalamic area (AHA) of male NaCl sensitive spontaneously hypertensive rats (SHR-S) but not in NaCl resistant control rats and have implicated this mechanism in the pathogenesis of NaCl sensitive hypertension. In the current study, we tested directly the hypothesis that dietary NaCl supplementation decreases the release of norepinephrine from nerve terminals in the AHA of SHR-S using the push-pull perfusion technique. Conscious, freely moving SHR-S and control Wistar-Kyoto (WKY) rats were studied after 2-3 weeks of 8% or 1% NaCl feeding. In the 1% NaCl fed SHR-S, 3-methoxy-4-hydroxyphenylglycol (MOPEG, the major metabolite of norepinephrine in brain) levels averaged 272 +/- 32 pg/10 min; norepinephrine levels, 17 +/- 2 pg/10 min; in the 8% NaCl fed SHR-S, MOPEG levels averaged 72 +/- 7 pg/10 min; norepinephrine levels were 6 +/- 1 pg/10 min. There was a positive linear correlation (r = 0.777; P less than 0.01) between MOPEG and norepinephrine levels in AHA perfusates, indicating that perfusate MOPEG levels provide a useful index of norepinephrine release from AHA nerve terminals. In contrast, MOPEG levels in AHA perfusates were not affected by dietary NaCl intake in control WKY, and in control posterior hypothalamic perfusates, were not affected by dietary NaCl intake in SHR-S.(ABSTRACT TRUNCATED AT 250 WORDS)

3,4-Dihydroxyphenylacetic Acid↗

PubMed1995

Dietary sodium intake modulates systemic but not forearm norepinephrine release.

INTRODUCTION: Sodium intake has profound effects on systemic and renal sympathetic activity, but its effects on sympathetic activity in skeletal muscle vascular beds, a site at which local regulatory mechanisms could alter vascular tone directly, are unclear. METHODS: To determine the effect of dietary sodium intake on basal and isoproterenol-stimulated systemic and forearm norepinephrine kinetics, we studied seven healthy male volunteers twice, 4 weeks apart, while they were receiving a low-sodium (10 mmol sodium/24 hours) diet and a high-sodium diet (250 mmol sodium/24 hours). Forearm blood flow, measured by plethysmography, and systemic and forearm norepinephrine spillover, measured by radioisotope dilution, were determined before and after intra-arterial infusion of 60 and 400 ng/min isoproterenol. RESULTS: Baseline (before isoproterenol) systemic norepinephrine spillover was higher when subjects received the low-sodium diet (448.1 +/- 55.7 ng/min) compared with the high-sodium diet (269.7 +/- 42.7 ng/min; p < 0.05). In contrast, sodium intake did not affect local forearm norepinephrine spillover, either at baseline (low-sodium diet, 2.05 +/- 0.48 ng/min versus high-sodium diet, 2.63 +/- 0.79 ng/min; p = 0.50) or after stimulation with isoproterenol in doses of 60 ng/min (low-sodium diet, 8.84 +/- 2.2 ng/min versus high-sodium diet, 6.1 +/- 1.9 ng/min; p = 0.38) or 400 ng/min (low-sodium diet, 16.4 +/- 4.5 ng/min versus high-sodium diet, 16.7 +/- 2.5 ng/min; p = 0.93). CONCLUSIONS: Under conditions of low sodium intake, systemic norepinephrine spillover was increased but forearm norepinephrine spillover was not, suggesting that alteration in sodium intake may produce a differential effect on norepinephrine spillover in different tissues but that decreased local sympathetic activity in skeletal muscle is not the likely mechanism by which a low-sodium diet may lower blood pressure or attenuate stress-induced pressor responses.

Adrenergic beta-Agonists↗

PubMed1976

The effect of tricyclic antidepressants and neuroleptics on the peripheral and central action of norepinephrine in reserpine-treated mice.

The effect of exogenous norepinephrine on the ptosis induced by reserpine and its modification by tricyclic antidepressants and neuroleptics were studied in reserpine-pretreated mice. S.c injection of norepinephrine (0.3-5 mg/kg) reversed dose-dependently the ptosis induced by reserpine. The maximal effect was obtained 15 min after norepinephrine administration. Tricyclic antidepressants (2.5 and 5 mg/kg i.p.) potentiated the effect of norepinephrine. In contrast neuroleptics (1 and 5 mg/kg i.p.) antagonized it. Intracerebral injection of norepinephrine (5-20 mug) also reversed dose-dependently the ptosis induced by reserpine, and the maximal effect was obtained within 5 min. Tricyclic antidepressants potentiated the effect of norepinephrine, but neuroleptics antagonized it. Among tricyclic antidepressants, the potentiating action of secondary amines was stronger than that of tertiary amines. Chlorpromazine blocked the action of norepinephrine more strongly than did the same dose of haloperidol.

Animals↗

PubMed1980

Comparison of 3H-norepinephrine and 3H-metaraminol accumulation as indices of adrenergic nerve density in rabbit blood vessels.

The possibility that accumulation of 3H-metaraminol, which is not metabolized, would provide a better estimate of adrenergic nerve density than 3H-norepinephrine accumulation was examined in a series of rabbit blood vessels. Accumulation of 3H-metaraminol was linear for up to 10 min. Norepinephrine accumulation was correlated with metaraminol acumulation in the vessels studied, but the relationship was not a simple one. The findings suggest that, even with short incubation times, metabolism may significantly alter the amount of norepinephrine retained by the tissue. Nevertheless, accumulation of metaraminol was still not well-correlated with endogenous norepinephrine content. Norepinephrine contents of the basilar artery, mesenteric artery and mesenteric vein were quite similar: 2.7, 2.8 and 2.8 micrograms/g respectively. However, values for metaraminol accumulation in these vessels ranged from 8.7 to 1.78 ml cleared/g. These findings suggest that norepinephrine content of a single adrenergic varicosity may vary from tissue to tissue. The relationship between norepinephrine content, storage capacity, uptake activity and transmitter release needs to be more carefully examined. No single parameter can provide an adequate estimate of adrenergic nerve density.

Adrenergic Fibers↗

PubMed1996

Inhibitory effect of phorbol 12,13-dibutyrate on norepinephrine-induced contraction in rabbit iris dilator muscle.

The hypothesis that the increase in Ca2+ sensitivity on norepinephrine-induced contraction of smooth muscles and also the decrease of the norepinephrine-induced sustained level of intracellular Ca2+ concentration are produced by the activation of protein kinase C was tested. Phorbol 12,13-dibutyrate (PDB; 10(-6) M) relaxed the norepinephrine-induced sustained contraction in a concentration-dependent manner. On pretreatment with PDB a transient contraction was produced by the application of norepinephrine, but the sustained contraction was significantly reduced. The sustained elevations of intracellular Ca2+ concentration ([Ca2+]i) and the contraction induced by norepinephrine in fura-2-loaded preparations were decreased by the application of PDB. These inhibitory effects were antagonized by potent protein kinase inhibitors, 2-(1-(3-dimethylaminopropyl)-indol-3-yl)-3-(-indol-3-yl)-maleimide (GF 109203X) (10 (-6) M) and 1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride (H-7) (10 (-6) M), but were not affected by a protein kinase A/G inhibitor, N-(2-cinnamylaminoethyl)-5-isoquinolinesulfonamide (H-88) (10(-6) M). The slope of the regression line for norepinephrine for [Ca2+]i and tension was significantly steeper than those obtained with high K+. Also, on pretreatment with PDB the Ca2+ sensitivity of the K(+)-induced contraction was decreased, but the Ca2+ sensitivity of norepinephrine-induced contraction tended to be increased. These observations indicate that PDB induces a decrease of [Ca2+]i on Ca2+ mobility and an increase of Ca2+ sensitivity on contraction of smooth muscle through the activation of protein kinase C.

Adrenergic alpha-Agonists↗

PubMed1988

Alpha-adrenoceptor-mediated effects of norepinephrine on the guinea pig sinus node.

The significance of alpha-adrenergic-mediated effects of norepinephrine on cardiac pacemakers is still controversial. Sinus node preparations (SN) from guinea pig hearts were superfused with Tyrode's solution (36 degrees C) to investigate such actions. Intracellular microelectrodes were used to monitor sinus node rate and membrane potentials of SN subsidiary pacemaker fibers (SP). Membrane potentials were recorded before, during, and after 10 minutes of exposure to norepinephrine in low (10(-13)-10(-10) M) or high (10(-6) M) concentrations. Low norepinephrine did not modify the sinus node rate or the membrane potentials. High norepinephrine increased the sinus node rate as expected. In the presence of propranolol, high norepinephrine did not modify the sinus node rate, but the action potential duration of SP was increased, whereas the membrane resting potential and the amplitude of the action potential were unchanged. The alpha-adrenergic agonist methoxamine did not depress the automaticity of the sinus node preparations, but the antagonist phentolamine blocked the effect of high norepinephrine on the action potential duration. In summary, norepinephrine did not have an alpha-mediated action on the automaticity of the guinea pig sinus node preparations, but it did prolong the action potential duration through alpha-receptor stimulation. The conflicting results reported in the literature regarding the effects of alpha-adrenoceptor stimulation in the heart appear to be due to species differences in the number and/or affinity of receptors.

Animals↗

PubMed1989

Effect of reperfusion on the cardiac acetylcholine and norepinephrine contents in rat hearts.

The effects of ischemia, reperfusion and hypoxia on the cardiac acetylcholine, choline, norepinephrine and cyclic AMP contents were investigated in isolated, spontaneously beating rat hearts perfused under constant pressure (100 cm H2O) with Krebs-Henseleit solution gassed with 95% O2-5% CO2. Acetylcholine, choline and norepinephrine were determined by high performance liquid chromatography with electrochemical detection. Cyclic AMP was determined by radioimmunoassay. One min reperfusion following 15 min ischemia (termination of perfusion) caused a significant decrease in both cardiac acetylcholine (P less than 0.05) and norepinephrine (P less than 0.01) contents, but had no significant effect on the cardiac norepinephrine/acetylcholine content ratio, or choline or cyclic AMP content. By contrast, 16 min ischemia did not significantly affect the cardiac acetylcholine, norepinephrine, choline or cyclic AMP content. Also, 16 min hypoxia (perfusion with Krebs Henseleit solution gassed with 95% N2 5% CO2) decreased the cardiac norepinephrine content significantly (P less than 0.01) and norepinephrine/acetylcholine content ratio slightly but not significantly. However, hypoxia had no significant effect on the cardiac acetylcholine, choline or cyclic AMP content. Pre-treatment with 10 microns atropine sulfate prevented the decrease in the cardiac acetylcholine content caused by reperfusion but caused a significant depletion in the cardiac norepinephrine content in the control (P less than 0.01) and ischemia (P less than 0.05) groups and a significant decrease in the norepinephrine/acetylcholine content ratio in all three groups (all, P less than 0.05). Extending the reperfusion period to 5 and 10 min following 15 min ischemia also caused a significant decrease in both cardiac acetylcholine and norepinephrine contents compared with the control groups. However, no significant difference in these contents was found between 1 min reperfusion group and 5 or 10 min reperfusion group. Twenty or 25 min ischemia alone did not significantly affect these contents. These findings suggest that reperfusion disturbs both the sympathetic and parasympathetic nervous systems in the heart and that pre-treatment with atropine adversely affects the balance of the autonomic nervous system.

Acetylcholine↗

PubMed1990

Interactive alpha- and beta-adrenergic actions of norepinephrine in rat cardiac myocytes.

We investigated the effects of the physiological neurotransmitter norepinephrine on the contractile properties and Ca2+ dynamics of isolated cardiac myocytes, with particular emphasis on possible interactions between alpha- and beta-adrenergic effects. Individual rat ventricular myocytes were electrically stimulated at a frequency of 1 Hz. Norepinephrine (10(-9) to 10(-5) M) increased extent and velocity of shortening and decreased the contraction duration. beta-Adrenergic activation gave a greater enhancement of extent and velocity of shortening than did norepinephrine alone (i.e. alpha plus beta). Neither alpha 1 nor alpha 2 adrenergic activation individually produced a significant impact upon contraction. Using suspensions of myocytes loaded with Quin-2, we also studied resting levels of cytosolic Ca2+ ([ Ca2+]c), the increase of [Ca2+]c due to caffeine-addition (as an index of sarcoplasmic reticulum Ca2+ content) and the subsequent increase in [Ca2+]c due to depolarization with 30 mM K+ (as an index of sarcolemmal voltage-dependent Ca2+ channel activity). Norepinephrine decreased resting [Ca2+]c, increased sarcoplasmic reticulum Ca2+ content and increased Ca2+ channel activity. beta-Adrenergic activation produced the same effect on resting [Ca2+]c and sarcoplasmic reticulum content, but gave significantly greater activation of sarcolemmal Ca2+ channel activity, than did norepinephrine (alpha plus beta). By contrast, alpha-adrenergic stimulation had no effect on resting [Ca2+]c or sarcoplasmic reticulum Ca2+ content. We conclude that beta-mediated effects predominate in the action of the physiological agonist norepinephrine on cardiac myocytes. However, alpha (specifically alpha 1)-adrenergic effects are significant in diminishing the potentiation of the extent and velocity of shortening, and of depolarization-induced entry of Ca2+ into the cell, which is seen on beta-stimulation alone. Thus, there may be an intrinsic feedback effect in the actions of norepinephrine on the cardiac myocyte.

Animals↗

PubMed1991

Influence of diabetes on norepinephrine-induced inositol 1,4,5-trisphosphate levels in rat aorta.

The effects of norepinephrine on total tissue levels of inositol 1,4,5-trisphosphate were measured by protein binding assay in aortas from rats with chronic streptozotocin-induced diabetes and from age-matched control rats. In both control and diabetic aortas, norepinephrine induced a rapid, transient and concentration-dependent elevation of inositol 1,4,5-trisphosphate content during contraction. Maximum production of inositol 1,4,5-trisphosphate in response to norepinephrine was greater in diabetic than in control aortas. However, the sensitivities of control and diabetic aortas to norepinephrine for inositol 1,4,5-trisphosphate production were not significantly different. Enhanced norepinephrine-induced production of inositol 1,4,5-trisphosphate in diabetic aortas may contribute to the increased maximum contractile responsiveness of these arteries to the agonist. However, since enhanced contractile responses of diabetic aortas to norepinephrine were also detected at times when inositol 1,4,5-trisphosphate levels were not significantly increased, other factors also appear to be involved in mediating enhanced contractions of diabetic arteries to norepinephrine.

Animals↗

PubMed1993

Anticonvulsant effects of intracerebroventricularly administered norepinephrine are potentiated in the presence of monoamine oxidase inhibition in severe seizure genetically epilepsy-prone rats (GEPR-9s).

Pharmacological and neurochemical evidence indicates that brain noradrenergic systems play an important role in the determination of audiogenic seizure severity in genetically epilepsy-prone rats (GEPRs). In earlier studies, intracerebroventricular (ICV) injections of norepinephrine suppressed convulsions in a now extinct moderate seizure GEPR colony. Also, ICV noradrenergic agonists are known to produce dose-related anticonvulsant effects in the extant moderate seizure GEPRs (GEPR-3s). The present experiments were undertaken to determine whether ICV norepinephrine also suppresses audiogenic seizures in the extant GEPR-3s and in the severe seizure genetically epilepsy-prone rats (GEPR-9s). Injections of norepinephrine or vehicle were made into the lateral ventricle through implanted guides. GEPR-9s were pretreated systemically either with the monoamine oxidase inhibitor pargyline or with saline. GEPR-3s received no pretreatment. In pargyline pretreated GEPR-9s, seizure severity fell and the fraction of animals exhibiting an anticonvulsant response increased progressively as the dose of norepinephrine was increased. In saline pretreated GEPR-9s, the anticonvulsant dose response curve for norepinephrine was shifted to a higher dose range. Accordingly, the anticonvulsant dose50 for norepinephrine was significantly greater in saline pretreated GEPR-9s than in pargyline pretreated animals. Moreover, the dose required to produce the anticonvulsant effect in GEPR-9s was approximately 10 fold greater than in the earlier studies in the extinct moderate seizure GEPRs. Also, the current experiment with extent GEPR-3s, showed that ICV norepinephrine was anticonvulsant in the same dose that was effective in the extinct colony of moderate seizure GEPRs. In general terms, these observations provide additional evidence that noradrenergic influences are anticonvulsant in the GEPR. The neurobiological factors responsible for reduced responsiveness of the GEPR-9 are presently unknown.

Animals↗

PubMed1994

Neuropeptide Y potentiates norepinephrine-stimulated inositol phosphate production in the rat tail artery.

We have recently demonstrated the ability of neuropeptide Y to augment norepinephrine-stimulated contractions of the rat tail artery. In [3H]myo-inositol labeled segments of rat tail artery, addition of a concentration of neuropeptide Y (10(-8) M) known to potentiate contractile responses produced no effect on the basal accumulation of [3H]inositol phosphates. Addition of norepinephrine (10(-7) M), however, resulted in the rapid accumulation of [3H]inositol 1,4,5-trisphosphate to 325 +/- 29% of basal levels within 5 min. This effect of norepinephrine on [3H]inositol 1,4,5-trisphosphate accumulation was mirrored by significant increases (274 +/- 25% of control) in total [3H]inositol phosphates. When neuropeptide Y and norepinephrine were added together, the norepinephrine-stimulated increase in [3H]inositol 1,4,5-trisphosphate was significantly augmented (467 +/- 35% of control) as was the increase measured in total [3H]inositol phosphates (366 +/- 21% of control). We suggest that the ability of neuropeptide Y to augment norepinephrine-induced contraction of the rat tail artery is due, at least in part, to the ability of neuropeptide Y to increase norepinephrine-stimulated phospholipase C activity in vascular smooth muscle and may represent the mechanism of action of this co-neurotransmitter in vivo.

Animals↗

PubMed1975

Effects of norepinephrine on cyclic nucleotide levels in the ductus deferens of the rat.

The effect of 1-norepinephrine on cyclic nucleotide levels was studied in rat ductus deferens. Norepinephrine (0.01-0.3 mM) increased cyclic AMP and cyclic GMP levels in a concentration-dependent manner. Cyclic GMP was increased by about two-fold and cyclic AMP by 30%-40% by 0.1 mM norepinephrine after 3 min. Phenylephrine (0.1 mM) increased cyclic GMP levels about twofold without affecting cyclic AMP. Cyclic GMP was maximally increased by norepinephrine or phenylephrine after 3-10 min, but was not significantly changed after 20 sec, when contraction was fully developed. Atropine did not affect the norepinephrine-induced changes in cyclic nucleotide levels; phentolamine blocked the effect of norepinephrine on cyclic GMP, and propanolol blocked that on cyclic AMP. These findings indicate that in the ductus deferens alpha-adrenergic receptors are involved in the effect of catecholamines on cyclic GMP, and beta-adrenergic receptors are involved in the effect on cyclic AMP levels. The presence of Ca-2+ was required for the effect of norepinephrine on cyclic GMP, but not on cyclic AMP.

Acetylcholine↗

PubMed1986

Effect of physical training on norepinephrine turnover in tissues of normal and diabetic rats.

This study was designed to examine the influence of physical training on the norepinephrine turnover rate in heart, pancreas, liver, and gastrocnemius muscles of normal and diabetic male rats at rest. Diabetes was induced with the IV injection of streptozotocin (45 mg/kg) and physical training was done on a treadmill according to a ten-week program. Norepinephrine turnover rate of tissues was estimated by following over time the decay in the specific activity of norepinephrine after a single IV bolus of tritiated norepinephrine (30 microCi/kg). Plasma glucose, insulin, and glucagon levels were also measured at the time of death. Although training caused a reduction in the plasma glucose values of diabetic rats, no changes in norepinephrine turnover rate were observed after the conditioning program. On the other hand, diabetes was associated with a significant 30% to 40% decrease in the pancreatic norepinephrine turnover rate. It is concluded that the beneficial effects of physical training on diabetes mellitus cannot be explained by adaptive changes in the sympathetic nervous system activity and that further work will be necessary to elucidate the mechanism whereby streptozotocin diabetes diminishes the pancreatic norepinephrine turnover.

Animals↗