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Biomedical subjects

S Finkielman

Publications and source records attributed to S Finkielman.

At least 73 records · Page 4Linked to original sources
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↗
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↗
PubMed1978

Angiotensin regulates release and synthesis of serotonin in brain.

Angiotensin II released serotonin from neuron terminals and accelerated synthesis of the serotonin. This increase in synthesis depended on the activation of tryptophan hydroxylase. A biphasic effect was observed: at high doses the stimulatory effect depended on conversion of angiotensin II to angiotensin III. At low doses an inhibitory effect was found, possible dependent on an angiotensin II metabolite. These actions represent a subtle regulation of the open-loop serotonin system.

Angiotensin II↗