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Biomedical subjects

V E Nahmod

Publications and source records attributed to V E Nahmod.

At least 55 records · Page 3Linked to original sources
PubMed1988

Serotonin and melatonin synthesis in peripheral blood mononuclear cells: stimulation by interferon-gamma as part of an immunomodulatory pathway.

Serotonin and melatonin inhibit phytohemagglutinin- (PHA) induced interferon-gamma (IFN-gamma) production by lymphocytes. In this paper, it is shown that IFN-gamma-increased tryptophan uptake by lymphocytes and macrophages led to an enhanced production of serotonin. When IFN-gamma and serotonin were added together to a lymphocyte culture, N-acetyl serotonin and melatonin production was increased, whereas the path to 5-hydroxy-indoleacetic acid remained unchanged. Therefore, the stimulated IFN-gamma production of serotonin and melatonin by lymphocytes and macrophages and the inhibition of IFN-gamma synthesis by these indoleamines suggest a hypothesis for an immunoregulatory circuit.

Cells, Cultured↗
PubMed1988

Differential release of enkephalin and enkephalin-containing peptides from perfused cat adrenal glands.

We have compared the enkephalin-like material derived from proenkephalin released from perfused cat adrenal glands stimulated with pilocarpine (5 X 10(-4)M) and nicotine (5 X 10(-6) M). In addition, two doses of acetylcholine (10(-5) and 10(-4) M) and 50 mM K+ were tested. Free Met-enkephalin immunoreactivity and total Met-enkephalin immunoreactivity, as determined by enzymatic digestion of large enkephalin-containing fragments, were coreleased with catecholamines. Free Met-enkephalin immunoreactivity represented 13% of total immunoreactivity for nicotinic stimulation, 46% for pilocarpine, 33% for 10(-5) M acetylcholine, 22% for 10(-4) M acetylcholine, and 16% for 50 mM K+. Analysis of the perfusate by gel filtration showed that 80% of the total Met-enkephalin immunoreactivity whose release was induced by pilocarpine was eluted in fractions corresponding to fragments of low molecular weight, whereas these fractions accounted only for 10% of the total Met-enkephalin immunoreactivity whose release was induced by nicotine. HPLC analysis of low-molecular-weight peptide fractions revealed that Met-enkephalin, Met-enkephalin-Arg-Gly-Leu, and Met-enkephalin-Arg-Phe represented 69% of total Met-enkephalin immunoreactivity whose release was induced by pilocarpine. These results indicate that selective activation of muscarinic receptors is followed by release of low-molecular-weight material, whereas nicotine application also yielded high-molecular-weight peptides. Furthermore, increasing the acetylcholine concentration from 10(-5) to 10(-4) M and using 50 mM K+ increased proportionally the high-molecular-weight peptide secretion. Results are discussed in relation to the existence of a heterogeneous population of granules either in the same cell or in different cells, containing proenkephalin-derived peptides. (ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1988

Adrenal proenkephalin-derived peptides during postnatal development in spontaneously hypertensive rats.

Adrenal enkephalin and enkephalin-containing peptides were studied during postnatal development in normotensive (WKY) and spontaneously hypertensive rats (SHR). The effect of chronic treatment with the ganglionic blocker chlorisondamine (5 mg/kg) was also assessed. Free enkephalin immunoreactivity and total enkephalin immunoreactivity, as determined by enzymatic digestion of large enkephalin containing fragments, were quantitated in the adrenal glands at 11 days and 7, 16, and 24 weeks of age. Both total and free metenkephalin were significantly diminished in the adrenal of SHR when compared to WKY at all ages tested. The analysis of the chromatographic profile showed that SHR displayed reduced levels of high and low molecular weight materials at 11 days and 16 weeks of age; however intermediate compounds were high in the glands of these animals. Similar increased values for free met-enkephalin were found in adrenals of WKY and SHR after ganglionic blocker treatment, which means that the relative increase was larger in SHR than WKY; while for total enkephalin the relative increase and the concentration reached in SHR was about half of those presented in WKY. These and other results presented suggest that the basic alteration of the adrenal proenkephalin system of SHR may be due to a genetic reduction of proenkephalin levels. Otherwise, the free enkephalin decrease could be related to changes in nervous input to the adrenal gland.

Adrenal Glands↗
PubMed1988

Low TRH-TSH responses in human essential hypertension.

Thirty female and male essential hypertensive patients and eighteen normotensive controls were submitted to the TRH-TSH conventional test (200 ug intravenously, bolus injection of TRH). Supramaximal doses of 400 and 600 ug were repeated with a week interval to each subject. Hypertensives showed a significant lower response to both conventional and supramaximal TRH doses. Hypothalamic-pituitary-thyroid axis abnormalities, secondary to TRH-receptor alterations, could account for this result.

Adult↗
PubMed1988

Angiotensin converting enzyme activity in the amygdaloid complex in a neurogenic hypertensive model.

The bilateral destruction of the ventral noradrenergic pathway induced by 6-hydroxydopamine (6-OHDA) administration into the ventral pons led to an increase in arterial blood pressure (ABP) and norepinephrine depletion in the amygdaloid complex, nucleus accumbens, septal area and olfactory bulb. Specific angiotensin converting enzyme (ACE) activity was significantly increased only in the amygdaloid complex (Control: 4.56 +/- 0.95; Vehicle: 4.08 +/- 1.07; 6-OHDA: 11.76 +/- 1.84). A significant correlation between arterial blood pressure and specific ACE activity levels in the amygdaloid complex was observed (r: 0.775; p less than 0.002). These results suggest that an increase in specific ACE activity of the amygdaloid complex after norepinephrine depletion could play a role in the development of hypertension in this model.

Amygdala↗
PubMed1987

Serotonin mediates cardiovascular responses to acetylcholine, bradykinin, angiotensin II and norepinephrine in the lateral septal area of the rat brain.

The infusion of acetylcholine, bradykinin, angiotensin II, norepinephrine and serotonin into the lateral septal area produced a dose-dependent increase of arterial blood pressure and heart rate. A pattern of inhibition of these cardiovascular responses, produced by pretreatment of the lateral septal area with phentolamine, 6-hydroxydopamine, methysergide and 5,7-dihydroxytryptamine was disclosed. These results suggest that the effects of acetylcholine, bradykinin and partially of angiotensin II, depend on the release of norepinephrine and the actions of this neurotransmitter in turn depend on the integrity of the serotonergic system in the lateral septal area.

5,7-Dihydroxytryptamine↗
PubMed1987

Angiotensin II regulates interferon-gamma production.

An extensive literature links the immune responses to neuroendocrine regulation. We have examined the effects of the neuropeptide hormone angiotensin II on the production of the immunomodulatory lymphokine interferon-gamma (IFN-gamma). Angiotensin II (10(-6)-10(-8) M) stimulated (three- to fivefold) the IFN-gamma production in human blood lymphocytes obtained from normal individuals. At 10(-9) M angiotensin II stimulation disappeared and was reestablished at physiological concentrations of the neuropeptide (10(-10)-10(-11) M). Stimulation by angiotensin II was compared with the classical effect of the lectin phytohemagglutinin, and it was seen that both actions are mediated by external calcium (as they are blocked by EGTA 2.5 mM) and that the stimuli follow different kinetics, reaching the steady state at 6 h with angiotensin II and later (18 h) when the lectin was used. The effect of angiotensin II over the IFN-gamma production was blocked by its analog sarcosine 1-isoleucine 8-angiotensin II, showing the specificity of angiotensin II action. These findings demonstrate a selective biological regulation of IFN-gamma production by angiotensin II and suggest another regulation pathway of immune responses.

Angiotensin II↗
PubMed1986

Interaction between acetylcholine and bradykinin in the lateral septal area of the rat brain: involvement of muscarinic receptors in cardiovascular responses.

The lateral septal area was used as a model to study the interaction between acetylcholine (Ach) and bradykinin on arterial blood pressure, since both mediators are present in this region. In the lateral septal area, the administration of the peptide or Ach produced a long-lasting, sympathetic-mediated increase of arterial blood pressure which was blocked by atropine. Pretreatment of the lateral septal area with hemicholinium-3, which depletes stores of acetylcholine, partially blocked the pressor effect of bradykinin but not that of Ach. Captopril--an inhibitor of kininase II--enhanced the pressor effects of bradykinin and Ach. Synaptosomal studies showed that bradykinin increased sodium-dependent, high-affinity uptake of choline and the conversion of [3H]choline to [3H]acetylcholine. Competition experiments using the highly specific muscarinic antagonist [3H]quinuclidinyl benzilate, demonstrated that bradykinin displaced the muscarinic antagonist from its receptor-ligand complexes. These results suggest that in the lateral septal area acetylcholine and bradykinin interact in a positive feed-back which amplifies pressor responses.

Acetylcholine↗
PubMed1986

Saralasin blocks the effect of angiotensin II and extracellular fluid saline expansion on the Na-K-ATPase inhibitor release in rats.

A low molecular weight substance which behaves like ouabain as inhibitor of brain membrane Na-K-ATPase and 3H-ouabain binding was found in plasma after saline expansion of extracellular fluid or angiotensin II infusion into the third brain ventricle in the rat. Intracerebroventricular infusion of angiotensin II antagonist, saralasin, blocks the increase of the Na-K-ATPase inhibitor produced by infusion of angiotensin II into the third ventricle or extracellular fluid saline expansion.

Angiotensin II↗
PubMed1984

Increase in muscarinic receptors in rat intestine by thyrotropin releasing hormone (TRH).

The effect of Thyrotropin Releasing Hormone (TRH) on the contractile activity elicited by acetylcholine and electric stimulation in the rat ileus terminalis was investigated. TRH did not show any intrinsic contractile activity but, after a 30 minute latency period, the peptide caused a shift to the left of the dose-response curve for both acetylcholine and electric stimulation. The binding of 3H-quinuclidinylbenzilate (3H-QNB) assayed on ileum slices disclosed that the addition of TRH increased the number of muscarinic cholinergic receptors without changes in affinity when incubation was performed at pH 7.8, but no effect TRH was demonstrated at pH 7.4. Therefore, in spite of its neural and direct actions on intestine motor activity, TRH may affect the acetylcholine induced contraction by increasing the number of muscarinic receptors at a specific pH.

Acetylcholine↗
PubMed1984

Changes in plasma aldosterone levels and renin activity after bilateral superior cervical ganglionectomy in two strains of rats.

Superior cervical ganglionectomy (SCGx) of Wistar rats brought about a significant increase of plasma renin activity (PRA) 9 or 15 days later, an effect not observed 48 days after surgery. The same surgical procedure performed in Chbb Tom rats did not result in significant modification of PRA. In both strains of rats immobilization stress induced a 2.3-3.3-fold increase of PRA regardless of whether the animals had intact superior cervical ganglia. The injection of the angiotensin-converting enzyme inhibitor captopril to SCGx Wistar rats at the time of elevated PRA induced a severe hypotension, while it did not affect blood pressure in sham-operated animals. In both strains of rats SCGx resulted in depressed circulating aldosterone levels at all studied times after surgery.

Aldosterone↗
PubMed1983

Thyrotropin-releasing hormone increases the number of muscarinic receptors in the lateral septal area of the rat brain.

Stereotactic injection of acetylcholine (0.5-2 micrograms) into the lateral septal region of the rat brain produces a long-lasting sympathetic-mediated increase of the arterial blood pressure. This effect is mediated by muscarinic receptors since 1 microgram atropine abolishes this response. In this same brain region, TRH (0.5-4 micrograms) did not elicit any significant change in the arterial blood pressure, but potentiated the effect of acetylcholine. This phenomenon is apparently due to an increase of the number of muscarinic receptors in the lateral septal area of the rat brain.

Acetylcholine↗
PubMed1983

Neurogenic hypertension after depletion of norepinephrine in anterior hypothalamus induced by 6-hydroxydopamine administration into the ventral pons: role of serotonin.

Destruction of the ventral noradrenergic pathway elicited by administration of 6-hydroxydopamine (6-OHDA, 5 micrograms into each side of the ventral pons) reduced the content of norepinephrine (NE) in the anterior hypothalamus (-80%) and induced an increase in arterial blood pressure (ABP) and in heart rate. These hypertensive rats, showed hypersensitivity to the hypotensive effect of NE (0.5-2 micrograms) and clonidine (0.75-1.5 micrograms) administered into the anterior hypothalamic preoptic (AH/PO) region. Methysergide (1-2 micrograms) and, to a lesser extent, ketanserin (1-2 micrograms) administered into the anterior hypothalamic preoptic region also reduced the arterial blood pressure in these rats treated with 6-OHDA. Bilateral administration of 5,7-dihydroxytryptamine (5,7-DHT, 8 micrograms) into the median forebrain bundle decreased the content of serotonin (5-HT) in the hypothalamus (-85%) without change in arterial blood pressure but largely prevented the development of hypertension after treatment with 6-OHDA in the ventral pons. These results suggest that neurogenic hypertension is produced after the removal of NE tonic depressor activity in the anterior hypothalamus and that serotonergic mechanisms play a major role in the development of the increased arterial blood pressure in this preparation.

5,7-Dihydroxytryptamine↗
PubMed1982

Circadian rhythm and neural regulation of rat pineal angiotensin converting enzyme.

Angiotensin converting enzyme was detectable in rat pineal gland and exhibited a circadian rhythm in activity with maximum at the end of the light phase of daily photoperiod. Superior cervical ganglionectomy (SCGx) or exposure to light for 6 days increased enzyme activity and obliterated morning-evening differences, whereas injection of the beta-agonist isoproterenol depressed the high values observed in SCGx animals. These results indicate that angiotensin converting enzyme in the pineal gland is under negative control by the norepinephrine released from pineal sympathetic nerves.

Animals↗
PubMed1981

Changes in drinking behavior caused by superior cervical ganglionectomy and pinealectomy in rats.

The effect of superior cervical ganglionectomy (SCGx) or pinealectomy (Px) on drinking behavior was examined in rats subjected to a restricted photoperiod (i.e. 4 h of light per day). Both in male and female rats SCGx depressed water intake significantly from 1 to 3 days after surgery. After osmolar (i.p. 5% NaCl) or non-osmolar stimuli (s.c. isoproterenol) SCGx female rats exhibited a depressed response in water and NaCl intake, an effect not observed in male rats. Castration of male or female rats did not change their drinking behavior response to thirst stimuli. Px did not mimic SCGx in its effects on drinking behavior; moreover in sham-Px rats the water intake fell significantly after craniotomy. Following the injection of isoproterenol or i.p. hypertonic saline, the drinking behavior was the same in Px or sham-Px animals. To assess whether the effects of SCGx needed the presence of the pineal gland, Px or sham-Px rats were subjected to SCGx 9 days later. In both groups SCGx depressed water intake; however the inhibition that followed ganglia removal in Px rats was greater than that observed in animals with a pineal gland. Water and NaCl intake following isoproterenol or i.p. hypertonic saline were similar in both experimental groups. These results suggest that SCGx affects drinking behavior in part by pathways other than pineal denervation.

Animals↗