SEARCH · PubMed Health

Results for “Norepinephrine”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources

PubMed1979

Possible role of brain norepinephrine in the hypothalamic hypophyseal adrenal system.

Intracisternal injection of bethanidine in rats decreased brain norepinephrine turnover without affecting its endogenous level, and increased both cardiac norepinephrine turnover and serum corticosterone level. A negative correlation was observed between brain norepinephrine turnover rate and serum corticosterone level. On the other hand, when cardiac norepinephrine turnover was suppressed by intraperitoneal injection of bethanidine, serum corticosterone did not change significantly. Next, ether inhalation was added after intracisternal injection of bethanidine. Then, serum corticosterone increased more even brain norepinephrine turnover was suppressed only slightly. These data may indicate that serum corticosterone increases by selective decrease in brain norepinephrine turnover via the humoral route; from the hypothalamus down to the adrenal cortex. Inversely, intracisternal injection of corticosterone increased brain norepinephrine turnover. These results suggest that brain norepinephrine may play an inhibitory role in the tonic regulation of CRF-ACTH secretion in the higher center than the hypothalamus and there may be a closed-loop feedback system between brain norepinephrine and serum corticosterone.

Animals↗

PubMed1975

Interaction of angiotensin with exogenous and neurally released norepinephrine on the cat nictitating membrane in vitro.

We have studied the effect of high (1-2.9 X 10(-5) M) and low 1.9 X 10(-9) M) concentrations of angiotensin on the retention and release of 3H-norepinephrine by the cat isolated nicititating membrane preparation in vitro in conjunction with their effect on the contractile responsiveness of the preparation to exogenous norepinephrine and transmural electrical stimulation. Both concentrations of angiotensin made the preparation contract, but only the high concentration affected the retention and spontaneous efflux of 3-H-norepinephrine. Retention was inhibited about 25% only when the preparation was preincubated with the angiotensin for 30 minutes (i.e., before adding 3H-norepinephrine). Under similar conditions cocaine, 2.9 X 10(-5) M, inhibited retention more than 90%. Spontaneous efflux was increased for as long as the high concentration of angiotensin was in contact with the preparation. Under similar conditions, tyramine, 5.7 X 10(-6) M, caused a much greater sustained increase in spontaneous efflux. Transmural stimulation of the preparation caused release of 3H-norepinephrine and frequency-dependent contractions. The contractions were selectively inhibited by phentolamine, 2.7 X 10(-6) M, or bretylium, 2.4 X 10(-5) M. Angiotensin had no effect on this neurally mediated 3H-norepinephrine release and contractile response or on contractions produced by exogenous norepinephrine. Since, as reported previously, angiotensin in vivo strongly inhibits contractile responses of the cat nicitating membrane to both neurally released and exogenous norepinephrine, the present results make it unlikely that such inhibition derives from angiotensin's relatively modest capacity for affecting the disposition of norepinephrine by this effector organ.

Angiotensin II↗

PubMed1978

alpha- and beta-receptor blockade of isoproterenol- and norepinephrine-induced effects on regional blood flow and blood flow acceleration.

The effects of the beta-receptor blocking agent propranolol (100 microgram/kg i.v.) and of the alpha-receptor blocking agent dihydroergotamine (50 microgram/kg i.v.) on hemodynamic responses to isoproterenol and norepinephrine (both 1--1024 ng/kg) were investigated in anesthetized dogs. The effects studied were: (1) flow in the ascending aorta and the coronary, common hepatic, gastroduodenal, splenic, cranial mesenteric, renal and femoral arteries: (2) maximal flow acceleration in the splenic, cranial mesenteric and femoral arteries; (3) maximal rate of change of left ventricular pressure (LV dP/dt max). Propranolol shifted the dose-response curves for the isoproterenol-induced flow increases in the common hepatic, gastro-duodenal, and cranial mesenteric arteries to the right. It did not influence the flow responses to isoproterenol in the ascending aorta or the coronary, splenic, renal and femoral arteries. Propranolol prevented the decrease of arterial pressure evoked by isoproterenol. Propranolol shifted the isoproterenol-induced increase of LV dP/dt max and maximal blood flow to the same extent. Propranolol blocked the flow to the liver and gastrointestinal tract to a greater extent than the LV dP/dt max and maximal flow acceleration. Propranolol had no effect on the norepinephrine-induced increases in flow in the splenic, femoral and coronary arteries, but blocked the norepinephrine-evoked increases of flow accelerations and LV dP/dt max to the same extent. Dihydroergotamine inhibited the norepinephrine-induced increase in flow in the femoral artery and the decreases in flow in the hepatic, splenic, cranial mesenteric and renal arteries, and reversed the reduction of flow in the gastroduodenal artery. It is argued that dihydroergotamine may inhibit the increase in femoral flow through two mechanisms: (1) blocking the flow reduction to norepinephrine in the abdomen, and thereby passively shunting blood from the abdomen in preference to the femoral bed; (2) attenuating the norepinephrine-evoked reflexogenic femoral vasodilatation. It is concluded that: (1) propranolol is a beta-receptor blocking agent with a preference for blockade of isoproterenol-induced vascular effects; (2) norepinephrine-induced flow increases are not direct actions on vascular beta-receptors; (3) the increase of maximal blood flow accelerations after isoproterenol and norepinephrine is mediated by stimulation of cardiac beta-receptors; (4) dihydroergotamine is an alpha-receptor blocking agent particularly in the splanchnic vascular region.

Adrenergic alpha-Antagonists↗

PubMed1977

Central and peripheral norepinephrine metabolism in rat strains selectively bred for differences in response to stress.

Rats of the Maudsley nonreactive (MNRA) strain were found to contain higher levels of norepinephrine in heart, spleen, and hypothalamus than animals of the Maudsley reactive (MR) strain. Total adrenal catecholamines were also greater in nonreactive animals. There was a trend toward higher endogenous norepinephrine concentration in MR rats in brainstem and telencephalon, but this was not statistically significant. Turnover measurements calculated from the fall of norepinephrine at 1 and 4 hours after a single dose of levo-alpha-methylparatyrosine showed no significant strain differences in telencephalon or brainstem, but MNRA animals had a faster rate of norepinephrine decline in heart than had MR rats. Possibly indicative of a higher rate of norepinephrine metabolism, the percentage of 3H-non-catechol metabolites relative to total counts was higher in brainstem of MNRA rats 90 min after intraventricular injection of 3H-norepinephrine. However, the disagreement between this estimate of norepinephrine metabolism and that provided by the alpha-methyl-paratyrosine technique prevents a conclusive statement about norepinephrine metabolism in the two strains. The results are discussed in the light of the established differences in behavior between the strains as well as other work exploring relationships between catecholamine metabolism and emotionality.

Adrenal Glands↗

PubMed1975

Interactions of 17beta-estradiol and L-norepinephrine on the rat uterus.

Norepinephrine increased the in vitro uptake of 3H-estradiol by the uterus of spayed rats. This effect was observed at 15 and 30 min but not at 90 min. Norepinephrine also increased the binding of 3H-estradiol by the nuclear (p less than 0.02) and the cytosol fractions (p less than 0.01) when incubated with uterine homogenates, suggesting that norepinephrine does not require the presence of the intact tissue to exert its effects. The in vivo uptake of 3H-estradiol and the determination of the number of binding sites were performed in the uterus of rats treated with estradiol and estradiol plus norepinephrine. Norepinephrine alone increased the uptake of 3H-estradiol and the number of binding sites. The highest increment in both parameters was observed in the uterus of rats treated with estradiol plus norepinephrine. The estradiol Ka of the rat uterus cytosol treated with estradiol alone or plus norepinephrine was higher than that observed in the group without estradiol, suggesting the presence of different proteins that bind estradiol. These results indicate that norepinephrine increases the entrance of estradiol into the rat uterus both in vitro and in vivo.

Animals↗

PubMedDate not supplied

Changes in plasma norepinephrine, blood pressure and heart rate during physical activity in hypertensive man.

We have investigated the changes in plasma norepinephrine and blood pressure and heart rate during a range of physical activities in eight hypertensive subjects in order to determine whether changes in plasma norepinephrine reflect changes in sympathetic activity. Blood pressure was recorded over 24 hours from an intra-arterial cannula. Plasma norepinephrine, measured by a sensitive radioenzymatic method, increased progressively with increasing levels of physical activity. In each subject a statistically significant linear relationship was observed between the logarithm of plasma norepinephrine and systolic blood pressure. Analysis of variance showed that 66% of the variance of plasma norepinephrine was associated with changes in blood pressure and heart rate. These observations support the hypothesis that plasma norepinephrine reflects short-term changes in sympathetic activity. Use of the quantitative relationship described, in conjunction with measurements of norepinephrine metabolism, may help to determine the significance of increased levels of plasma norepinephrine observed in some hypertensive patients.

Adult↗

PubMed1979

Vascular and metabolic effects of circulating epinephrine and norepinephrine. Concentration-effect study in dogs.

Vascular and metabolic effects of circulating epinephrine and norepinephrine have been studied in relation to the plasma concentration of these amines in dogs. Intravenous infusion of epinephrine or norepinephrine (0.1, 0.5, and 2.5 nmol x kg-1 x min-1) raised the plasma concentration of the infused amine by 2.5 , 13, and 63 nM from resting levels of 2.4 and 3.6 nM, respectively. Blood flow to isolated adipose tissue; skeletal muscle preparations; and plasma levels of glycerol, glucose, and cyclic AMP were measured. Epinephrine and norepinephrine displayed a distinct selectivity with regard to both vascular and metabolic effects. Epinephrine caused significant vasoconstriction in adipose tissue already at a plasma concentration of 5 nM, whereas no significant effect was seen on skeletal muscle vascular resistance. Norepinephrine, on the other hand, caused significant vasoconstriction in skeletal muscle at 5 nM but had no vasoconstrictor effect in adipose tissue. Epinephrine was more potent than norepinephrine in increasing plasma cyclic AMP and glucose, whereas the converse was true for plasma glycerol. Epinephrine had significant effects on plasma cyclic AMP at 5 nM and on plasma glucose and glycerol at 15 nM. Norepinephrine, on the other hand, had significant effects on plasma glycerol at 5 nM, plasma cyclic AMP at 15 nM and plasma glucose only at 65 nM. It is suggested that these response patterns are related to a preferential action of epinephrine on beta 2-adrenoceptors and a preferential action of norepinephrine on beta 1-adrenoceptors. Our results support the view that both epinephrine and norepinephrine may act as circulating hormones, because vascular and metabolic effects of both amines were seen at plasma concentrations encountered during various kinds of stress in animals and man.

Adipose Tissue↗

PubMed1979

Effects of nerve stimulation and drugs on the release of histamine and norepinephrine from the isolated heart.

Compound 48/80 and polymyxin B elicited prompt and sharp increases in histamine output from the isolated guinea pig heart and had no effect on norepinephrine output. Dextran decreased histamine output without affecting norepinephrine output. Bradykinin increased both histamine and norepinephrine output; the histamine output increased only after a latent period. Stimulation of both left and right stellate ganglia increased norepinephrine output, but only right ganglion stimulation increased histamine output, after a latency. Stimulation of the right but not the left vagus nerve decreased histamine output first, then increased it moderately, the peak of which came later than norepinephrine release. It was suggested that histamine release following nerve stimulation and bradykinin was secondary to norepinephrine release. Isoniazid decreased the output of both histamine and norepinephrine. Aminoguanidine increased histamine output but decreased norepinephrine output.

Adrenergic Fibers↗

PubMed1975

Inhibition of potassium uptake by low concentrations of norepinephrine and dibutyryl cyclic AMP.

(1) The inhibition of potassium uptake by low concentration of norepinephrine (3 X 10-8 M) and of dibutyryl cyclic AMP (DBcAMP, 10 minus5 M) was studied in cardiac Purkynĕ fibres. (2) The inhibitory action of DBcAMP on K uptake was abolished by the alpha blocker phentolamine. (3) Norepinephrine alone decreased K uptake and such inhibition was somewhat larger when DBcAMP was added. DBcAMP alone caused the usual decrease in K uptake but addition of norepinephrine abolished it. (4) The inhibition caused by norepinephrine reduced the increase in uptake caused by a high concentration (10 minus 3 M) of DBcAMP. (5) The inhibitory effect of norepinephrine was reversed in the presence of high concentration of magnesium (5.25 mM). (6) The inhibitory effect of norepinephrine was reversed by aminophylline and abolished by caffeine. (7) The inhibitory action of norepinephrine and BCcAMP was reversed or abolished, respectively, by imidazole. (8) It is concluded that the inhibition of potassium uptake by low concentration of DBcAMP is mediated by an alpha receptor mechanism and that possibly the "receptors" for this effect of norepinephrine and DBcAMP are located at different sites. Also it appears that DBcAMP may be acting at the membrane and that the action of methylxanthines and imidazole is not necessarily mediated only by a modification of phosphodiesterase activity.

Aminophylline↗

PubMed1976

[Effects of norepinephrine and phentolamine on acute intracranial hypertension].

It is accepted that cerebrovascular dilatation is a constant response during the advanced stage of intracranial hypertension. Severe intracranial hypertension ultimately associates with profound vasodilatation and reduces cerebral blood flow to zero. This irreversible state is called cerebral vasomotor paralysis by Langfitt et al (1965). The rich adrenergic nerve supply of the cerebral vessels suggests that pressor amines possibly affect the cerebral circulation and the cerebral vascular tone. This study is to investigate the reactivity of norepinephrine and phentolamine on intracranial pressure (ICP) in patients with severe intracranial hypertension. The ICP and systemic blood pressure (SBP) monitorings were carried out continuously after the evacuation of intracerebral hematomas due to ruptured intracranial aneurysms. Severe intracranial hypertension due to brain swelling was observed in these patients. Three stages were defined according to the reactivity to norepinephrine and phentolamine on the ICP. In Stage I, norepinephrine caused a transient decrease in the ICP and phentolamine caused a marked rise in the ICP. Stage II was marked by the absence of the ICP response to norepinephrine and phentolamine. During Stage III, the ICP changes synchronously with a variation of the SBP after the administration of norepinephrine and phentolamine. In Stage I patients, the mean ICP level was between 500-1000 mmH2O. Tracing of the ICP in this group showed transient rises called pressure waves and the waves were recurring increases in the ICP to value of 300-500 mmH2O superimposed on an elevated level of the ICP. On the other hand, in Stage II and III patients, the ICP level exceeded 1000 mmH2O. Tracing of the ICP in these groups showed only variations by the arterial pulses. The patients in Stage I had a well prognosis for life if proper treatments such as continuous ventricular drainage were carried out. The patients in Stage II and III had a poor prognosis for life inspite of continuous ventricular drainage. There are varying stages in cerebrovascular dilatation accompanying intracranial hypertension. We have no information on the mechanism of this cerebrovascular dilatation at present. However, we speculate that the pressor amines such as norepinephrine may partly participate in the mechanism responsible for the vasodilation. So, we attempt to grade the degree of this vasodilatation according to the reactivity of norepinephrine and phentolamine on the ICP. It is presumed that cerebrovascular dilatation is slight and reversible in Stage I patients, whereas cerebrovascular dilatation is profund and irreversible in Stage II and III patients. Continuous ICP recording and examination of the reactivity to norepinephrine and phentolamine on the ICP are valuable when considering the prognosis for life in patients with severe intracranial hypertension.

Adult↗

PubMed1975

The effects of 5-hydroxy-5(4'-chlorophenyl)-2, 3-dihydro-5H-imidazo (2, 1-a) isoindole (mazindol, SaH 42-548) on the metabolism of brain norepinephrine.

Mazindol, 5-hydroxy-5-(4'-chlorophenyl)-i, 3-dihydro-5H-imidazo-(2, 1-a) isoindole, has demonstrated anorexic activity and other pharmacological responses which suggest alterations in brain norepinephrine metabolism. Studies of the effects of mazindol on neuronal uptake and/or release of norepinephrine showed that mazindol, when given before cerebral intraventricular injection of 3-H-norepinephrine by a mechanism that increases 3-H-normetanephrine synthesis via catechol-O-methyl-transferase and provided no significant effect on deamination of the catecholamine. Studies designed to measure norepinephrine release showed that mazindol (in contrast to d-amphetamine) did not cause release of 3-H-norepinephrine from neuronal stores. Furthermore, mazindol did not inhibit norepinephrine synthesis, whereas d-amphetamine did. The effect of d-amphetamine on norepinephrine release and synthesis may be more important than effects on uptake of this catecholamine. In contrast, mazindol appears to produce its primary effect on norepinephrine metabolism by inhibition of neuronal uptake mechanism.

Animals↗

PubMed1978

Rat jugular vein relaxes to norepinephrine, phenylephrine and histamine.

Circular muscle of the rat external jugular vein contracted to serotonin, angiotensin and potassium chloride but not to norepinephrine, phenylephrine, histamine or carbamylcholine. In contrast, rabbit and guinea-pig jugular veins contracted to norepinephrine, phenylephrine and histamine, although contractions to norepinephrine were small in guinea-pig jugular veins. Norepinephrine, phenylephrine and histamine produced a concentration-dependent sustained relaxation of serotonin-induced contractions in the rat jugular vein, as did isoproterenol, nitroglycerin and papaverine. Propranolol blocked relaxation to norepinephrine, phenylephrine and isoproterenol whereas metiamide, a H2 receptor antagonist blocked relaxation to histamine. alpha adrenergic receptor blockade with phentolamine or prazosin resulted in greater relaxation to norepinephrine whereas cocaine did not enhance norepinephrine-induced vasodilation. This study supports the premise that norepinephrine may exert prominent beta adrenergic receptor stimulation in some blood vessels and that this effect may be more apparent in veins than arteries.

Adrenergic alpha-Antagonists↗

PubMedDate not supplied

Actions and interactions of norepinephrine and acetylcholine on sinus node potassium movements.

The influence of norepinephrine and/or acetylcholine on K uptake of the guinea pig sinus node was investigated. Both "high" (10(-6) M) and "low" (10(-9) M) mediator concentrations were employed. The following results were obtained: 1) high concentration of norepinephrine increased K uptake; 2) high concentration of acetylcholine had a similar effect; 3) simultaneous exposure to both mediators did not lead to summation of the effects; 4) low concentration of norepinephrine depressed K uptake; 5) high concentration of acetylcholine overcame the inhibitory effect of the small concentration of norepinephrine; 6) 2-deoxy-D-glucose did not abolish the stimulating effect of acetylcholine on potassium uptake; and 7) strophanthidin abolished the stimulatory effect of norepinephrine, but not that of acetylcholine. The following conclusions are drawn: 1) both neuromediators in suitable concentrations increase K uptake in the sinus node; 2) the mechanism of such an increase is different, norepinephrine increasing the active and acetylcholine increasing the passive potassium transport; 3) a low concentration of norepinephrine depresses K uptake; and 4) when the two mediators are administered together, acetylcholine suppresses the action of norepinephrine on K transport.

Acetylcholine↗

PubMed1977

Inhibition of norepinephrine uptake by phenoxybenzamine and desmethylimipramine in the isolated guinea-pig atrium.

The effects of phenoxybenzamine (PBZ) and desmethylimipramine (DMI) on 3H-norepinephrine uptake by sympathetic nerve terminals of isolated guinea-pig left atrium has been investigated in the absence and in the presence of norepinephrine, tyramine, cocaine and isoproterenol, used as protecting agents. PBZ blocked the uptake of 3H-norepinephrine by 50% at a concentration of 3 micronM. For DMI the ID50 was approximately 0.33 micronM. These doses were used for all subsequent protection experiments. When incubation with PBZ was carried out in the presence of tyramine (574 micronM) the blocking effects of PBZ were completely reversed. In contrast, tyramine was unable to protect against 3H-norepinephrine uptake blockade elicited by DMI. Norepinephrine (20 micronM) or cocaine (29 micronM) afforded no protection against DMI-induced 3H-norepinephrine uptake blockade, but both agents significantly protected against blockade of PBZ. Isoproterenol (40 micronM) was unable to protect against 3H-norepinephrine uptake blockade evoked either by PBZ or DMI. The results provide strong evidence for a different site and/or mechanism of action of PBZ and DMI on the norepinephrine uptake system at adrenergic nerve terminals.

Animals↗

PubMed1975

Norepinephrine in treatment of ocular hypertension and glaucoma.

Norepinephrine (4%) as free base produced a significant fall in intraocular pressure and resistance to outflow. This effect was sustained for up to 20 weeks. No significant difference could be shown between the effect of 2%, 3%, and 4% norepinephrine on the aquious humor dynamics. The effect on pressure and facility was shown in eyes with ocular hypertension and with glaucoma. An additive effect was observed after use of norepinephrine with pilocarpine in the treatment of glaucoma. Crossover studies between epinephrine borate 1% and norepinephrine borate 4% revealed no significant difference. Like epinephrine, norepinephrine produces a conjunctival hyperemia in many patients. However, there is an absence of tachycardia after use of norepinephrine, and one person in this study showed an allergic reaction to epinephrine that cleared promptly and completely when norepinephrine was substituted.

Aged↗

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↗

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↗