Prolonged vibration of cutaneous artery: Absence of persisting aftereffects

Summary 1–3 h after prolonged (3–16 h) vibration (120 Hz, 0.2–0.3 mm amplitude) of rings of canine saphenous arteries there was no significant change in the contractile response to electrical stimulation, exogenous norepinephrine or of neuronal uptake of tritium labeled norepinephrine. These results did not provide evidence for persistent aftereffects of prolonged vibration.Acknowledgments. Supported in part by NIH grant HL 05883 and the Swedish Work Environmental Fund.     

Alpha 1-adrenergic stimulation of ketogenesis and fatty acid oxidation is associated with inhibition of lipogenesis in rat hepatocytes

The effect of norepinephrine on fatty acid synthesis (3H2O incorporation into fatty acids), on fatty acid oxidation to CO2 and on ketogenesis was studied in isolated hepatocytes of fed rats. After incubation with norepinephrine (50 microM), lipogenesis was lower (5.7 +/- 1.1 nmoles 3H2O incorporated into fatty acids/mg dry weight/30 min) than in controls (7.5 +/- 1.7; n = 6, p less than 0.02). In contrast, (1-14C) palmitate conversion into total ketone bodies was increased to 10.9 +/- 1.8 nmoles/mg/30 min with norepinephrine, vs 8.5 +/- 1.6 in controls (p less than 0.05), and more (1-14C) palmitate was converted to 14CO2 with norepinephrine than in controls (1.48 +/- 0.10 nmoles/mg/30 min vs 1.06 +/- 0.11, p less than 0.05). The inhibitory effect of norepinephrine on lipogenesis was abolished by addition of the alpha 1-receptor blocker prazosin, but not by alpha 2 or beta-blockers. The results demonstrate that the ketogenic effect of norepinephrine is coupled with an inhibitory effect on lipogenesis which may be explained by diminished activity of acetyl-CoA carboxylase, diminished formation of malonyl-CoA and decreased activity of carnitine palmitoyl transferase I.     

Beta-adrenergic stimulation of androgen production by fetal mouse Leydig cells in primary culture

The responsiveness of fetal mouse Leydig cells to catecholamines (epinephrine, norepinephrine), a beta-agonist agent (L-isoproterenol) and hCG was investigated in vitro. Fetal Leydig cells when freshly isolated were unable to respond to L-isoproterenol (10(-5) M). However, L-isoproterenol, epinephrine and norepinephrine significantly stimulated androgen production by fetal Leydig cells after 24 h of primary culture. Androgen production was increased in both conditions and to a greater extent by hCG. Propranolol blocked the stimulatory effect of L-isoproterenol and epinephrine. It is concluded that catecholamines can regulate fetal testosterone biosynthesis.     

Depletion of hypothalamic norepinephrine reduces the fever induced by polyriboinosinic acid: polyribocytidylic acid (Poly I:Poly C) in rats

Administration of either Poly I:Poly C (0.05-0.50 micrograms) or norepinephrine (2-8 micrograms) into the anterior hypothalamic area produced a dose-related fever in rats. The fever induced by Poly I:Poly C was attenuated after selective depletion of norepinephrine in the hypothalamus. However, selective depletion of hypothalamic norepinephrine did not affect the fever induced by intrahypothalamic norepinephrine. The data indicate that Poly I:Poly C may act to induce fever through the endogenous release of norepinephrine from the rat's hypothalamus.     

Interaction of CDP-choline with synaptosomal transport of biogenic amines and their precursors in vitro and in vivo in the rat corpus striatum.

Added to a striatal synaptosomal homogenate of rat brain, CDP-choline 10(-4) M inhibits the uptake of norepinephrine (NE), dopamine (DA) and serotonin (5 HT) in a competitive fashion and enhances the uptake of tyrosine and tryptophan; administered to animals, CDP-choline (50 mg/kg/l h/i.v.) inhibits only the in vitro uptake of DA but enhances the uptake of precursors.     

Modification of theophylline-induced lipolysis in human fat cells after trypsination.

Trypsin-treatment of human fat cells results in the potentiation of the lipolytic response and the cAMP accumulation induced by theophylline (5 . 10(-4) M) but not of those induced by theophylline (5 . 10(-3) M). The amount of cAMP formed after exposure to theophylline (5 . 10(-3) M) plus norepinephrine (5 . 10(-6) M) remains, however, 2.6 fold higher in trypsin-treated human fat cells than in the control ones.     

Antihypertensive activity of some novel pyridinylidene arylurea derivatives in spontaneously hypertensive rats.

3 novel pyridinylidene arylurea derivatives were found to lower arterial pressure in spontaneously hypertensive rats. Their relative oral potency ranged from 6 to 32 times that of guanethidine. The onset of antihypertensive action following their oral administration was less than 1 h and the duration of action ranged from 8 to over 24 h. The antihypertensive activity of the pyridinylidene arylureas was found to be assoicated with depletion of tissue catecholamines. Compound C depleted cardiac norepinephrine with little or no effect on total brain norepinephrine levels. It is suggested that compound C may have useful antihypertensive properties without CNS depressant activity.     

Norepinephrine in fetal and neonatal rabbit brain.

In the first hour after parturition, the newborn rabbit brain norepinephrine content is about 37% less than that of the fetus of 30th or 31st day. Later on, within 2 to 4 h, the norepinephrine level returns to the prenatal value and remains unchanged between 8 to 12 h. This transitory fall of the brain norepinephrine seems to be linked to the stress conditions which occur during parturition.     

Moderate cooling depresses the accumulation and the release of newly synthesized catecholamines in isolated canine saphenous veins

Moderate cooling (from 37 degrees to 24 degrees C) depressed the formation of 3H-dopamine and 3H-norepinephrine from 3H-tyrosine by isolated canine saphenous veins. Cooling reduced the evoked release of newly synthesized catecholamine to the same extent as that of stored norepinephrine. Hence the augmentation by cold of the contractile response to sympathetic nerve stimulation observed in earlier work is not accompanied by an augmented release of newly synthesized norepinephrine.     

Activation by S-adenosylhomocysteine of norepinephrine and serotonin in vitro uptake in synaptosomal preparations from rat brain.

S-Adenosylhomocysteine (10(-7)-10(-5) M) activated norepinephrine (NE) and serotonin (5HT) in vitro uptake in synaptosomal preparations from rat brain, but did not affect dopamine (DA) uptake. When administered to rats (7 mg/kg i.p.), it has the same effect on in vitro NE and 5HT uptake. It did not affect NE and 5HT release.     

Hormonal facilitation in the release of sperm from the spermatheca of the red-spotted newt

Several neurotransmitters and hormones with potential to trigger a simultaneous contraction of the oviducts and the spermathecal myoepithelium were examined. Saline (0.05 ml), or 0.05 ml saline plus acetylcholine (9 mg), norepinephrine (50 micrograms), arginine-vasotocin (25 units), prostaglandin F2 alpha (3 micrograms) were injected into the spermathecal region of female newts (n = 24 per group). The numbers of sperm present in the cloacae of prostaglandin-injected animals (107 +/- 30 SEM) were significantly greater than the numbers detected in saline (27 +/- 5 SEM) and in uninjected (14 +/- 3 SEM) controls. Smaller and less consistent increases in the numbers of sperm were detected in the vasotocin- and norepinephrine-injected groups. Study of sections from ovulating female newts failed to produce evidence that pressure from the passage of ova through the posterior portion of the oviduct forced sperm from the spermatheca. Observations indicate an active role for the spermathecal myoepithelium in the discharge of stored sperm and of a role for prostaglandin F2 alpha in triggering that discharge.     

Alpha-adrenoceptor blocking action of hymenin, a novel marine alkaloid

In the rabbit isolated aorta, hymenin (10(-6) M), a novel marine alkaloid, caused a parallel rightward shift of the dose-response curve for norepinephrine without affecting that for histamine or KCl, suggesting that hymenin is a competitive antagonist of alpha-adrenoceptors in vascular smooth muscles.     

Inhibitory action of bradykinin on release of the adrenergic transmitter in the isolated lapine kidney

Summary In the isolated lapine kidney perfused with tyrode solution and prelabeled with [³H] norepinephrine, bradykinin (10 ng/ml) decreased the overflow of tritium elicited by sympathetic nerve stimulation both in the presence and absence of indomethacin. These observations indicate that bradykinin acts at presynaptic sites reducing release of the adrenergic transmitter in the isolated lapine kidney.This study was supported by American Heart Association Grant 77-803, and U.S. Public Health Service Grant HL-16134 from the National Heart and Lung Institute.     

Effet inhibiteur de la tétrabénazine sur l'influence corticosurrénalienne de la réserpine

Summary Reserpine provokes an intense and long-lasting (more than 20 h) stimulation of the adrenocortical activity of the rat. Tetrabenazin (50 mg/kg) also produces an adrenocortical stimulation which is, however, of a much shorter duration. The injection of tetrabenazin 1 h before the injection of reserpine (5 mg/kg) prevents the prolonged stimulating effect of reserpine on the adrenal cortex. This effect can be compared with the blocking effect of tetrabenazin, a short-acting central depressant with monoamine-liberator properties, against the prolonged central sedative influence of reserpine.     

β-Adrenergic stimulation of androgen production by fetal mouse Leydig cells in primary culture

Summary The responsiveness of fetal mouse Leydig cells to catecholamines (epinephrine, norepinephrine), a-agonist agent (L-isoproterenol) and hCG was investigated in vitro. Fetal Leydig cells when freshly isolated were unable to respond to L-isoproterenol (10^–5M). However, L-isoproterenol, epinephrine and norepinephrine significantly stimulated androgen production by fetal Leydig cells after 24 h of primary culture. Androgen production was increased in both conditions and to a greater extent by hCG. Propranolol blocked the stimulatory effect of L-isoproterenol and epinephrine. It is concluded that catecholamines can regulate fetal testosterone biosynthesis.     

Interaction of CDP-choline with synaptosomal transport of biogenic amines and their precursors in vitro and in vivo in the rat corpus striatum

Summary Added to a striatal synaptosomal homogenate of rat brain, CDP-choline 10^–4 M inhibits the uptake of norepinephrine (NE), dopamine (DA) and serotonin (5 HT) in a competitive fashion and enhances the uptake of tyrosine and tryptophan; administered to animals, CDP-choline (50 mg/kg/l h/i.v.) inhibits only the in vitro uptake of DA but enhances the uptake of precursors.This research was supported by CNRS grant (ERA No. 560) and Inserm grant (FRA 5).     

Close relation between hypothalamic and cardiac norepinephrine during stress and its role in acute myocardial infarction disrhythmias

Summary The decrease of the norepinephrine levels in hypothalamus and heart caused by stress is prevented by pargyline and imipramine. Such a decrease in spleen and adrenals is not affected. Chlorpromazine and lithium only prevent the norepinephrine decrease in the spleen. The uptake of H³norepinephrine by isolated atria of guinea-pig increases during anoxia; the change to a normal oxygen situation decreases these norepinephrine levels by more than 50%.     

Depletion of hypothalamic norepinephrine reduces the fever induced by polyriboinosinic acid: polyribocytidylic acid (Poly I:Poly C) in rats

Summary Administration of either Poly I:Poly C (0.05–0.50 g) or norepinephrine (2–8 g) into the anterior hypothalamic area produced a dose-related fever in rats. The fever induced by Poly I:Poly C was attenuated after selective depletion of norepinephrine in the hypothalamus. However, selective depletion of hypothalamic norepinephrine did not affect the fever induced by intrahypothalamic norepinephrine. The data indicate that Poly I:Poly C may act to induce fever through the endogenous release of norepinephrine from the rat's hypothalamus.This work was supported by grants from the National Science Council (Taipei, Republic of China).     

Antihypertensive activity of some novel pyridinylidene arylurea derivatives in spontaneously hypertensive rats

Summary 3 novel pyridinylidene arylurea derivatives were found to lower arterial pressure in spontaneously hypertensive rats. Their relative oral potency ranged from 6 to 32 times that of guanethidine. The onset of antihypertensive action following their oral administration was less than 1 h and the duration of action ranged from 8 to over 24 h. The antihypertensive activity of the pyridinylidene arylureas was found to be associated with depletion of tissue catecholamines. Compound C depleted cardiac norepinephrine with little or no effect on total brain norepinephrine levels. It is suggested that compound C may have useful antihypertensive properties without CNS depressant activity.Acknowledgments. The authors express their gratitude to Mr L. Flataker for the preliminary behavioral studies in mice and to Dr N. Bohidar for statistical evaluation of the antihypertensive data.     

α1-Adrenergic stimulation of ketogenesis and fatty acid oxidation is associated with inhibition of lipogenesis in rat hepatocytes

Summary The effect of norepinephrine on fatty acid synthesis (³H₂O incorporation into fatty acids), on fatty acid oxidation to CO₂ and on ketogenesis was studied in isolated hepatocytes of fed rats. After incubation with norepinephrine (50 M), lipogenesis was lower (5.7±1.1 nmoles³H₂O incorporated into fatty acids/mg dry weight/30 min) than in controls (7.5±1.7; n=6, p<0.02). In contrast, (1-¹⁴C) palmitate conversion into total ketone bodies was increased to 10.9±1.8 nmoles/mg/30 min with norepinephrine, vs 8.5±1.6 in controls (p<0.05), and more (1-¹⁴C) palmitate was converted to¹⁴CO₂ with norepinephrine than in controls (1.48±0.10 nmoles/mg/30 min vs 1.06±0.11, p<0.05). The inhibitory effect of norepinephrine on lipogenesis was abolished by addition of the ₁-receptor blocker prazosin, but not by ₂ or -blockers. The results demonstrate that the ketogenic effect of norepinephrine is coupled with an inhibitory effect on lipogenesis which may be explained by diminished activity of acetyl-CoA carboxylase, diminished formation of malonyl-CoA and decreased activity of carnitine palmitoyl transferase I.