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PubMed1985

Systemic and uterine responsiveness to angiotensin II and norepinephrine in estrogen-treated nonpregnant sheep.

Pregnancy is associated with uterine and systemic vasodilation and reduced vascular reactivity to angiotensin II and perhaps norepinephrine. The uteroplacental vasculature is relatively refractory to angiotensin II but very sensitive to norepinephrine. To investigate the possible role of the high levels of estrogen in pregnancy mediating these hemodynamic changes, we examined systemic and uterine vascular responsiveness to angiotensin II and norepinephrine in eight chronically instrumented nonpregnant sheep treated with 17 beta-estradiol. In these animals, 17 beta-estradiol produced significant systemic and uterine vasodilation without changing arterial pressure; cardiac output increased from 5.3 +/- 0.3 to 6.7 +/- 0.4 L/min, and uterine blood flow increased from 26 +/- 3 to 218 +/- 13 ml/min (mean +/- SE). Treatment with 17 beta-estradiol reduced the increases in systemic vascular resistance produced by angiotensin II and norepinephrine by 25% and 35%, respectively. After 17 beta-estradiol treatment, the uterine vascular responses were compared to the systemic vascular responses; the uterine responses to angiotensin II were only half the systemic responses, whereas the uterine responses to norepinephrine were six times greater than the systemic responses and were associated with decreases in uterine blood flow of 35% to 40%. These hemodynamic features of nonpregnant sheep treated with estrogen are strikingly similar to previous observations in sheep during pregnancy.

Angiotensin II↗

PubMed1987

Norepinephrine regulation of fetal heart rate: multiple mechanisms of action.

Norepinephrine was infused intravenously for 30 minutes into chronically catheterized sheep fetuses averaging 133 days' gestation. At infusion rates of 3.9, 12, and 39 micrograms/min, heart rate initially decreased as much as 40 bpm and then gradually increased to 50 bpm above the control value by the end of the infusion. Thereafter, heart rate increased further, and by the end of a 30-minute recovery period, heart rate was still 66 bpm above the control value. In fetuses pretreated with either a ganglionic blocker or a parasympathetic blocker, norepinephrine caused a large and sustained rise in heart rate by 124 bpm, which declined rapidly when the infusion was terminated. These results suggest that circulating norepinephrine affects fetal heart rate by several mechanisms: a baroreceptor-mediated suppression, a direct stimulation by norepinephrine, a gradual weakening of the vagal and an increase in cardiac sensitivity to sympathetic stimulation. In addition, there appears to be a long-term positive correlation between fetal heart rate and circulating norepinephrine levels.

Animals↗

PubMed1983

Regulation of gluconeogenesis by norepinephrine, vasopressin, and angiotensin II: a comparative study in the absence and presence of extracellular Ca2+1.

In hepatocytes isolated from fasted rats, vasopressin and angiotensin II stimulate the rate of gluconeogenesis from lactate or pyruvate in a Ca2+-dependent manner similar to that previously reported for norepinephrine. Actions of the peptide hormones on gluconeogenesis from glycerol or sorbitol, reduced substrates that require oxidation before they enter the gluconeogenic pathway at triosephosphate, also resemble those of norepinephrine. Stimulation of glucose production from these substrates is observed only in the presence of extracellular Ca2+. Actions of the peptide hormones on gluconeogenesis from dihydroxyacetone or fructose, the oxidized counterparts of glycerol and sorbitol, respectively, do not resemble those of norepinephrine. While norepinephrine enhances rates of glucose production from dihydroxyacetone or fructose in the absence of extracellular Ca2+, vasopressin and angiotensin II are ineffective either in the absence or presence of extracellular Ca2+. When the oxidation-reduction state in hepatocytes metabolizing dihydroxyacetone is altered by adding an equimolar concentration of ethanol (to provide cytosolic reducing equivalents), the results are similar to those obtained when cells are incubated with the reduced counterpart of dihydroxyacetone, glycerol, i.e., the peptide hormones cause an apparent increase in the rate of glucose production in a Ca2+-dependent manner. If, on the other hand, hepatocytes are incubated with glycerol or sorbitol and an equimolar concentration of pyruvate (to provide a cytosolic hydrogen acceptor), the peptide hormones, unlike norepinephrine, are ineffective in stimulating gluconeogenesis in the absence of extracellular Ca2+. These results indicate that whereas many of the actions of vasopressin and angiotensin II are similar to those of alpha 1-adrenergic agents, there are major differences in the manner in which the hormones act at various sites to regulate gluconeogenesis.

Angiotensin II↗

PubMed1990

Norepinephrine stimulation of sodium transport in Necturus urinary bladder.

Norepinephrine alters the transepithelial electrical properties of an open-circuited urinary bladder from the mud puppy, Necturus maculosus. When 10(-5) M norepinephrine is superfused over the serosa of the epithelium, the transepithelial voltage (Vt) and short-circuit current (Isc) increase as the resistance (Rt) decreases. The norepinephrine-mediated changes are reversed by the addition of amiloride (5.10(-5) M) to the mucosal Ringer's solution. The serosal adrenoceptors mediating the Na+ transport are more sensitive to norepinephrine (EC50 = 1.2.10(-6) M) than to epinephrine or isoproterenol. Since the Isc is blocked selectively by the antagonist, phenoxybenzamine, stimulation of active transepithelial Na(+)-flux by catecholamines is mediated by an alpha-adrenoceptor. The apical cell membrane voltage (Va) and fractional resistance (fRa) were recorded using conventional KCl-filled microelectrodes. Untreated tissues have Va close to 0 mV while the basolateral membrane voltage (Vb) is between -85 and -95 mV. About 90% of Rt is apical cell membrane resistance (fRa). When amiloride inhibits sodium transport, Va becomes negative, Vb hyperpolarizes slightly and fRa increases to 97%. On the other hand, if the bladders are treated with norepinephrine, fRa decreases to 79% as Va becomes positive and Vb depolarizes. When Rt changes, the resistance of the paracellular pathway (Rp) is unaltered. Changes in the electrical properties of the tissue appear to be mediated primarily by alterations in Ra. Since the Necturus bladder does not respond to antidiuretic hormone, this study implies that biogenic amines regulate Na+ transport in the epithelium.

Animals↗

PubMed1990

Vasopressin and norepinephrine stimulation of inositol phosphate accumulation in rat hepatocytes are modified differently by protein f1nase C and protein kinase A.

Rat hepatocytes were maintained in primary monolayer culture for 24 h in the presence of serum. Treatment of hepatocytes with 1 microM 4 beta-phorbol 12 beta-myristate 13 alpha-acetate (PMA) for 5-15 min increased membrane-associated protein kinase C activity and concomitantly decreased soluble activity. Membrane protein kinase C activity returned to basal values within 1 h then decreased by more than 50% within 2 h. Prolonged (2-18 h) incubation with PMA did not further decrease protein kinase C activity. Pretreatment of hepatocytes with PMA for 5-15 min had little effect on the subsequent actions of 100 nM vasopressin but abolished the stimulation of inositol phosphate accumulation by 3 nM vasopressin and 20 microM norepinephrine. Long-term exposure (2-18 h) of hepatocytes to 1 microM PMA actually enhanced the effects of vasopressin and 20 microM norepinephrine. The stimulation by norepinephrine (20 microM) of inositol phosphate accumulation was abolished by the alpha 1-adrenergic antagonist prazosin (1 microM), whereas the beta-adrenergic antagonist propranolol (30 microM) had little effect. Addition of 8Br-cAMP (100 microM) or glucagon (10 nM) for 5 min or 8 h had no significant effect alone, but enhanced the subsequent vasopressin stimulation of inositol phosphate accumulation. There was no effect of 8Br-cAMP or glucagon on norepinephrine stimulation of phosphoinositide breakdown. These data indicate that the stimulation of phospholipase C activity in rat hepatocytes by 3 nM vasopressin is enhanced by cyclic AMP-dependent kinase but inhibited by protein kinase C. In contrast, down regulation of protein kinase C markedly enhanced the maximal phosphoinositide response due to both vasopressin and norepinephrine.

Animals↗

PubMed1993

Regulation of [3H]norepinephrine release by N-methyl-D-aspartate receptors in minislices from the dentate gyrus and the CA1-CA3 area of the rat hippocampus.

It has been reported previously that N-methyl-D-aspartic acid induces a significant release of [3H]norepinephrine preaccumulated in slices from the hippocampus. In the present study, we investigated whether there are regional differences in the hippocampus regarding this N-methyl-D-aspartate effect. In the absence of Mg2+, N-methyl-D-aspartate (10-200 microM) induced the release of [3H]norepinephrine from superfused minislices containing the dentate gyrus area or the CA1-CA3 region of the hippocampus. Such N-methyl-D-aspartate effects on [3H]norepinephrine release were significantly higher in the dentate gyrus than in the CA1-CA3 area. The N-methyl-D-aspartate effects in both hippocampal areas were also reduced significantly by D-2-amino-5-phosphonovaleric acid (50 microM), an antagonist of the N-methyl-D-aspartate receptor, and by tetrodotoxin, a blocker of the voltage-dependent Na+ channels. The extent of this reduction was the same in the dentate gyrus and the CA1-CA3 area. Further experiments, conducted in the presence of Mg2+, demonstrated that N-methyl-D-aspartic acid increased K(+)-induced release of [3H]norepinephrine from dentate gyrus minislices but not from the CA1-CA3 area. The results are consistent with the existence of a higher density and/or different subtypes of N-methyl-D-aspartate receptors modulating [3H]norepinephrine release in the dentate gyrus as compared with the CA1-CA3 hippocampal area.

Animals↗

PubMed1978

Ontogeny of (--)-[3H]norepinephrine uptake properties of synaptic storage vesicles of rat brain.

The ontogeny of[3H]norepinephrine uptake mechanisms has been examined in synaptosomes and storage vesicles isolated from rat whole brain. The [3H]norepinephrine accumulated by synaptosomes was low in neonates, but reached adult levels by 15 days of age. In contrast, development of[3H]norepinephrine uptake into isolated rat brain storage vesicles was not complete until 38 days of age. Kinetic analysis of the developing vesicular uptake mechanism revealed no change in Km, while maximal uptake increased progressively from birth to maturity. Storage vesicles from immature and adult rats exhibited similar energy requirements for uptake as determined by their dependence on ATP-Mg2+ concentration; furthermore, the degree of inhibition of [3H]norepinephrine uptake by other amines was the same in both vesicle preparations. Thus, storage vesicles isolated from adult and developing rats display an in vitro[3H]norepinephrine uptake mechanism with properties that are kinetically and pharmacologically similar. The results suggest that, while the number of storage vesicles in the central nervous system increases during development, those vesicles that are present possess a fully functional amine uptake system.

Adenosine Triphosphate↗

PubMed1981

Beta-endorphin-induced increases in plasma epinephrine, norepinephrine and dopamine in rats: inhibition of adrenomedullary response by intracerebral somatostatin.

Synthetic human beta-endorphin, 7.25 nmol intracisternally, in unanesthetized, freely moving, chronically cannulated, adult male rats increased plasma concentrations of all 3 catecholamines: epinephrine, norepinephrine and dopamine, for the 2 h period studied. Blockade of these endorphin effects by the prior systemic administration of naloxone supports mediation of the effects at opioid receptors. Acute systemic administration of guanethidine, which decreases norepinephrine release induced by sympathetic nerve stimulation, blunted the plasma norepinephrine response to intracerebral beta-endorphin. Thus, it seems likely that in addition to secretion by adrenal medulla a considerable portion of the beta-endorphin-induced increase in norepinephrine is derived from sympathetic nerve endings. Simultaneous intracisternal administration of another neuropeptide, somatostatin, together with beta-endorphin markedly inhibited the plasma epinephrine response to beta-endorphin, while decreasing the dopamine and norepinephrine responses to a much lesser degree. The dats suggest that beta-endorphin stimulates central sympathetic outflow to both adrenal medulla and sympathetic nerve endings, and further that somatostatin inhibits the effect of endorphin to stimulate outflow to adrenal medulla but does not affect outflow to sympathetic nerve endings.

Adrenal Medulla↗

PubMed1981

Norepinephrine depletion alters cerebral oxidative metabolism in the "active" state.

Unilateral chemical lesion of the nucleus locus coeruleus in rats produced unilateral depletion of ipsilateral cortical norepinephrine. Norepinephrine depletion was not associated with changes in "resting" metabolic balance of the cerebral cortex, as determined by in situ reflection spectrophotometry of the redox state of cytochrome oxidase. Norepinephrine depletion, however, caused slowing of the transient metabolic response to sudden increases in energy demand produced by direct cortical electrical stimulation. The effect was apparent in the redox state of both cytochrome oxidase and NAD, the latter being measured, also in situ, by reflection microfluorometry. These results demonstrate that norepinephrine has a role in modulating the response to increased metabolic demand in the cerebral cortex. Norepinephrine may mediate its effect by potentiating Na+, K+-ATPase or through its effects on vascular reactivity, or both.

Animals↗

PubMed1991

Estrogen modulates stimulation of inositol phospholipid hydrolysis by norepinephrine in rat brain slices.

The influence of estrogen on stimulation of inositol phospholipid hydrolysis by norepinephrine and carbamylcholine has been studied by measuring the accumulation of [3H]inositol-monophosphate ([3H]InsP) in cortical, hippocampal and striatal slices from ovariectomized rats. Repeated (but not a single) subcutaneous injections of estradiol benzoate (EB) (2 micrograms/animal once every 2 days for 10 days) markedly reduced stimulation of inositol phospholipid hydrolysis by norepinephrine in hippocampus and corpus striatum. Conversely, the efficacy of norepinephrine was increased in cortical slices. Estrogen treatment did not affect basal or carbamylcholine-stimulated [3H]InsP formation. In vitro addition of 17 beta-estradiol (1-100 nM) failed to modify norepinephrine- or carbamylcholine-induced [3H]InsP production in all regions examined. An increased density of alpha 1-adrenergic binding sites in cortical membranes paralleled the enhanced responsiveness of inositol phospholipid hydrolysis to norepinephrine induced by EB treatment in this area, whereas no significant changes in [3H]prazosin binding were found in membranes from hippocampus and corpus striatum. These results indicate that estrogen may affect inositol phospholipid hydrolysis in discrete brain areas, suggesting a complex role for estradiol in modulating noradrenergic receptor activity in the central nervous system.

Animals↗

PubMed1995

Biphasic pressor responses to norepinephrine in humans.

We investigated pressor responses to intravenous bolus infusion of norepinephrine in seven healthy volunteers. Norepinephrine (1, 2, and 4 micrograms/kg) elevated blood pressure in a concentration-dependent manner and decreased heart rate. The pressor response to norepinephrine was biphasic (early and late). Intravenous administration of phentolamine (10 mg) completely abolished the pressor response to norepinephrine, and prazosin (5 mg, given orally) inhibited the early and late responses to a same extent. Continuous intravenous infusion of nicardipine (2 micrograms/kg/min) inhibited the late pressor response but not the early one. These data suggest that bolus infusion of norepinephrine evoked the biphasic pressor response and that the late response depends on vasoconstriction by calcium influx through nicardipine-sensitive calcium channels.

Adult↗

PubMed1977

Inhibition of [3H]norepinephrine uptake in peripheral organs of some mammalian species by ouabain.

In order to demonstrate the possible involvement of (Na+ + K+)-ATPase in the high affinity uptake of [3H]-norepinephrine in the sympathetic nerve endings, the effect of ouabain on [3H]norepinephrine uptake in spleen and heart slices of five mammalian species was examined. The ouabain sensitivity of [3H]norepinephrine uptake in the heart slices form various species, as determined by the estimation of IC52, was, in increasing order, lamb (2,3 muM) less than calf (2.5 muM) less than guinea pig (4 muM) less than rabbit (10muM) less than rat (greater than 500 muM). The IC50 values in the spleen slices were: lamb (1 muM) less than calf (3.2 muM) less than rabbit (9.5 muM) less than guinea pig (25 muM) less than rat (greater than 500 muM). The IC50 values for the inhibition of specific [3H]ouabain binding in the microsomal fractions of spleen and heart of the five mammalian species by ouabain were similar to the IC50 values for the inhibition of [3H]norepinephrine uptake by the cardiac glycoside. Since ouabain is known to bind exclusively to (Na+ + K+)-ATPase of a microsomal fraction, these results suggest that the inhibition of [3H]norepinephrine uptake in the sympathetic nerve endings by ouabain is mediated by the inhibition of (Na+ + K+)-ATPase.

Animals↗

PubMed1977

Anesthesia-induced alteration of small vessel response to norepinephrine.

Closed-circuit television microscopy was used to quantitate the in vivo response of small arteries (approximately 100 micron) and small veins (approximately 150 micron) to topically applied norepinephrine in the rat cremaster muscle. Rats were anesthetized with pentobarbital (50 mg/kg), or urethane (1200 mg/kg) or a combination of urethane (800 mg/kg) and chloralose (60 mg/kg). Complete concentration-response curves were obtained for an artery and vein pair in each rat and pD2 values (-log ED50) were used to evaluate the vascular sensitivity to norepinephrine. Both the artery and the vein in urethane-anesthetized animals had decreased sensitivity to norepinephrine in comparison to the vessels of animals anesthetized with pentobarbital or urethane-chloralose. Pretreatment with cocaine (10(-5) M) significantly increased the sensitivity of both the artery and vein in pentobarbital-anesthetized animals but did not affect the vessels in urethane-chloralose-anesthetized animals. These results are consistent with two opposing effects of the urethane-chloralose combination. The first is an increased sensitivity to norepinephrine via blockade of neuronal uptake and the second is a decreased sensitivity of norepinephrine via a vascular inhibitory effect of urethane.

Anesthetics↗

PubMed1978

The role of calcium in supersensitivity to the inotropic effects of norepinephrine.

Experiments using electrically stimulated rabbit left atria have demonstrated that supersensitivity to the inotropic effects of norepinephrine can be induced by either chronic reserpine pretreatment or hypothermia (lowering the temperature of the bathing medium). These two experimental conditions for inducing supersensitivity were not additive implying that they shared a common mechanism of action. Norepinephrine had no significant effect on the amplitude of a potentiated contraction of the rabbit atrium when the temperature was reduced from 37 to 30 degrees C or following pretreatment with reserpine (30 or 37 degrees C). Under these same conditions the ED50 of norepinephrine on the normal contraction was reduced. It is concluded that both reserpine pretreatment and hypothermia induce supersensitivity to the inotropic effects of norepinephrine by enhancing the cellular store of activator calcium while not affecting the ability of norepinephrine to release activator calcium.

Animals↗

PubMed1980

Contraction velocity analysis of norepinephrine and angiotensin-II activation of vascular smooth muscle.

The contractile response of vascular smooth muscle is known to consist of fast and slow components of contraction. We investigated the effect of norepinephrine and angiotensin-II on these functional properties of vascular smooth muscle in a quantitative fashion by analyzing the velocity of isometric tension development in rabbit aortic strips as a function of time. Basic premises for contraction velocity analysis are: (1) tension development is proportional to agonist concentration and relates to the amount of calcium fixed by the contractile proteins; (2) the rate of tension development (Qt) reflects the rate calcium is mobilized; (3) the rate at which calcium is made available relates to agonist concentration; (4) calcium is available from internal and external sites; (5) the calcium source)s) activated are characteristic of the mechanism of action of a particular agonist, and (6) the source of calcium activated is identifiable. Aortic strips were contracted maximally with norepinephrine and the velocity of contraction found to decrease with time according to the empirical expression Qt = phi 1e-phi 2t + theta 1e-the 2t. Experiments in calcium-free medium served to identify the tonic component of norepinephrine-induced contraction as the second term while angiotensin demonstrated only one term (phasic) which was independent of extracellular calcium. Strips contracted with different concentrations of norepinephrine or angiotensin showed dose-dependent actions on these functional properties of vascular smooth muscle as revealed by their effects on the contraction velocity parameters. An expression describing the contribution of each component to total tension developed was derived by integrating the above expression to give Qtot = phi 1 (1--e-phi 2tmax)/phi 2 + theta 1 (1--e-theta 2tmax)/theta 2. The contribution of each component to total tension development was donse-dependent and their sum gave the total tension observed experimentally with norepinephrine. For angiotensin, the first term of the preceeding expression gave the observed tension response. It is concluded that contraction velocity analysis affords a new approach for studying the effects of vasoactive agents on the functional properties of vascular smooth muscle.

Angiotensin II↗

PubMed1981

Calcium-sensitive accumulation of norepinephrine in rat cerebral cortex.

The accumulation of high and low concentrations of [3H]-norepinephrine has been examined in a crude synaptosomal preparation of rat cerebral cortex in the presence and absence of uptake1 inhibitors. When uptake1 was blocked, [3H]-norepinephrine accumulation exhibited very rapid initial rates. It was not inhibited by 10 mM normetanephrine, a potent inhibitor of peripheral uptake2, but it was inhibited by 10 mM metaraminol. This accumulation was markedly reduced when calcium ions were omitted from the incubation medium, and is named here 'calcium-sensitive accumulation' (CSA) to distinguish it functionally from the sodium-dependent, high affinity, uptake1 process. CSA may be localized in nerve endings since it was found predominantly i the synaptosomal fraction of homogenates subjected to density gradient centrifugation in sucrose or in Ficoll-in-sucrose. At high concentrations of [3H]l-norepinephrine (1.0 microM) and short incubation times, CSA accounted for most of the total accumulation of [3H]l-norepinephrine whereas uptake1 contributed only a small portion. Since extracellular concentrations of brain norepinephrine are thought to reach levels in excess of 1.0 microM, CSA may be a significant factor in noradrenergic neuronal transmission.

Animals↗

PubMed1987

Effects of potassium and norepinephrine on calcium influx in guinea-pig vas deferens.

The effects of potassium (K+) and adrenoceptor agonists on 45Ca influx and contraction of isolated vas deferens from reserpine-treated guinea-pigs has been investigated. K+ (18-84 mM) increased 45Ca influx with the maximum influx occurring at 50 mM K+. The rate of influx upon exposure to K+ was highest in the first 2 min and decreased thereafter. In contrast to K+, norepinephrine, methoxamine and xylazine did not increase the rate of 45Ca influx. Norepinephrine and methoxamine, but not xylazine, inhibited 45Ca influx induced by high K+. The inhibitory effect of norepinephrine was also present in denervated tissues. Prazosin, but not yohimbine or propranolol, blocked the inhibitory effect of norepinephrine. Potassium-induced contractions were significantly potentiated in the presence of norepinephrine, especially at low calcium concentrations. We conclude that K+ contracts the guinea-pig vas deferens by increasing the influx of calcium whereas stimulation of alpha 1-adrenoceptors prevents 45Ca influx elicited by high potassium.

Adrenergic alpha-Agonists↗

PubMed1992

Endothelium-accelerated hyporesponsiveness of norepinephrine-elicited contraction of rat aorta in the presence of bacterial lipopolysaccharide.

The role of the endothelium in the hyporesponsiveness of alpha-adrenoceptor-mediated contractions of the rat aorta was investigated. The norepinephrine-induced maximal contraction was diminished after repeated addition of the agonist. The hyporesponsiveness of the maximal contraction was endothelium dependent, being prevented by NG-monomethyl-L-arginine (0.5 mM), L-argininosuccinic acid (0.5 mM), puromycin (IC50 = 100 microM), actinomycin D (IC50 = 80 nM) but not by indomethacin, which suggests that nitric oxide (NO) synthase is induced. The sensitivity of the rings to NO-induced relaxation remained unchanged. The above-mentioned hyporesponsiveness of norepinephrine-induced maximal contractions of aorta rings was also observed after a 5-h incubation without norepinephrine. The agonist-independent hyporesponsiveness was also prevented by NG-monomethyl-L-arginine, puromycin and actinomycin D, which suggests that NO synthase is induced. Moreover, the norepinephrine-independent hyporesponsiveness was prevented by polymyxin B (10 micrograms/ml), which suggests that bacterial lipopolysaccharide (LPS) might be involved. The concentration of contaminating LPS was 89 +/- 11 ng/ml. When the concentration of contaminating LPS was reduced to 40-70 pg/ml, the hyporesponsiveness of the maximal contraction did not occur after repeated addition of norepinephrine or alter a 5-h incubation without the agonist. An addition of 30 or 100 ng/ml of E. coli lipopolysaccharide to the organ bath reproduced the hyporesponsiveness of the maximal contraction. After a 5-h incubation of aortic rings with 30 ng/ml LPS, only the endothelium-intact ring showed a reduced contraction. However, a 24-h incubation reduced the contraction even in the absence of endothelium.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Oxidoreductases↗