PubMed Health⌕ Search

Biomedical subjects

A Philippu

Publications and source records attributed to A Philippu.

At least 19 recordsLinked to original sources
PubMed1992

Pulsatile release of histamine in the hypothalamus of conscious rats.

The pattern of histamine release was investigated in the hypothalamus of the conscious, freely moving rat over 20 h. Under anaesthesia, a guide cannula was stereotaxically inserted into the posterior hypothalamus. In the conscious animal, the stylet of the guide cannula was replaced by a push-pull cannula, and the hypothalamus was superfused with artificial cerebrospinal fluid. Histamine was determined radioenzymatically in the superfusate which was continuously collected in time periods of 20 min. The release rate of histamine fluctuated according to an ultradian rhythm (frequency: 1 cycle per 83 min) and a circadian rhythm with the highest release rate of histamine between 11:00 p.m. and 1:00 a.m. The release rate of histamine during darkness was higher than that during the light period. The results demonstrate that, in the brain, neuronal histamine is released according to rhythms with various frequencies.

Animals↗
PubMed1992

Nitric oxide releases acetylcholine in the basal forebrain.

In conscious rats, the basal forebrain was superfused through a push-pull cannula and the release of acetylcholine was determined in the superfusate. Superfusion with the nitric oxide (NO) synthase inhibitor, NG-nitro-L-arginine, diminished the release of acetylcholine. Subsequent superfusion with the NO donor, 3-morpholino-sydnonimine, enhanced the release of the neurotransmitter. It is concluded that endogenous NO enhances the release of acetylcholine from its neurons.

Acetylcholine↗
PubMed1992

Blood pressure changes modify the release rates of catecholamines in the intermediate nucleus of the solitary tract.

In anaesthetized cats, the intermediate aspect of the nucleus of the solitary tract (NTS) was bilaterally superfused with artificial CSF through push-pull cannulae. The release of the endogenous catecholamines dopamine, noradrenaline and adrenaline was determined in the superfusates radioenzymatically. Blood pressure changes were elicited by intravenous injections of drugs (noradrenaline or chlorisondamine), or electrical stimulation of the intermediate NTS with the tip of the push-pull cannula. Intravenous injections of noradrenaline (3 or 10 micrograms/kg) elicited a rise in the arterial blood pressure which was associated with a decrease in the release rate of adrenaline in the intermediate NTS. The release rates of dopamine and noradrenaline were not influenced. The intravenous injection of chlorisondamine (3 mg/kg) lowered blood pressure and diminished the release rate of dopamine in the intermediate NTS. The release rate of noradrenaline was not modified by chlorisondamine. Electrical stimulation of the intermediate NTS contralateral to the superfused nucleus increased moderately the arterial blood pressure and decreased the release rate of noradrenaline and dopamine, while the release of adrenaline was not influenced. The findings suggest that experimentally induced changes in the arterial blood pressure by drugs injected intravenously modify the release rates of adrenaline and dopamine in the intermediate NTS so as to counteract the blood pressure change. In the intermediate NTS, release of adrenaline from adrenergic nerve terminals seems to act hypertensive. The results obtained with chlorisondamine point to a hypotensive function of endogenous dopamine in the intermediate NTS.

Animals↗
PubMed1992

Effects of gamma-vinyl GABA (vigabatrin) on blood pressure and body weight of hypertensive and normotensive rats.

Inactivation of GABA was inhibited by gamma-vinyl GABA (GVG) and the effects of the increased GABA level in the brain on blood pressure and body weight of spontaneously hypertensive rats (SHR) and normotensive rats (WKY) were investigated. When started at the age of 8 weeks or 5 weeks, treatment of SHR and WKY with GVG (150 mg/kg, s.c.) for several weeks did not influence systolic blood pressure. In 1-week old SHR, treatment with GVG (up to 150 mg/kg, s.c.) abolished the rise in blood pressure until animals were 8 weeks old. Thereafter, arterial blood pressure started to increase but it remained distinctly lower than that in untreated animals. When started at the age of 1 week, treatment with GVG for 7 weeks did not influence arterial blood pressure in WKY. GVG delayed increase in body weight in SHR and WKY, irrespective of their age. GVG greatly increased GABA levels in the hypothalamus, frontal cortex, brainstem and rest of the brain in both WKY and SHR. It is concluded that an increase in the GABA level in the brain leads to a delay in the development of hypertension in young SHR. Hence, development of genetic hypertension seems to be susceptible to activation of the GABAergic system in a very early critical phase only.

4-Aminobutyrate Transaminase↗
PubMed1992

Release of endogenous acetylcholine in the hypothalamus of conscious rats.

The release of endogenous acetylcholine was investigated by the push-pull technique. The posterior hypothalamus of conscious rats was superfused through a push-pull cannula with artificial cerebrospinal fluid (ACSF) which contained 1 mumol/l neostigmine. Acetylcholine was determined in the superfusate by high pressure liquid chromatography and electrochemical detection. Hypothalamic superfusion with potassium-rich (100 mmol/l) ACSF led to a pronounced increase in the release rate of acetylcholine. Tetrodotoxin (1 mumol/l) almost abolished the basal release of the neurotransmitter. Superfusion of the hypothalamus with atropine (10 or 50 mumol/l) led to a concentration-dependent increase, whereas superfusion with oxotremorine (50 mumol/l) inhibited the release rate of acetylcholine. It is concluded that acetylcholine released into the superfusate of the hypothalamus originates from cholinergic neurons. Furthermore, the release of acetylcholine seems to be modulated by muscarinic acetylcholine receptors, probably located on cholinergic neurons of the hypothalamus.

Acetylcholine↗
PubMed1991

Involvement of catecholaminergic neurones of the nucleus of the solitary tract (NTS) in blood pressure regulation.

Determination of the release of catecholamines in the rostral and intermediate aspects of the NTS before, during and after termination of a bilateral carotid occlusion revealed that increases in blood pressure elicited by the occlusion reduce the release rates of noradrenaline and adrenaline, while occlusion-induced decreases in blood pressure diminish the release rate of dopamine. These findings demonstrate that, in response to blood pressure changes elicited by carotid occlusion, in both aspects of the NTS noradrenaline and adrenaline act to increase blood pressure when released from their neurones, while the release of dopamine lowers blood pressure. Noradrenergic neurones of the NTS receive impulses from baroreceptors of carotid sinus and aortic arch.

Animals↗
PubMed1991

In vivo modulation of the histamine release in the hypothalamus by adrenoreceptor agonists and antagonists.

The modulation of the histamine release from histaminergic neurons by noradrenergic neurons was investigated by the push-pull technique. The posterior hypothalamus of the conscious, freely moving rat was superfused with artificial CSF through a push-pull cannula and the release of endogenous histamine was determined in the superfusate. Hypothalamic superfusion with a potassium-rich CSF enhanced the release rate of histamine. Superfusion with the alpha 2-agonists noradrenaline or clonidine diminished the release rate of histamine. Moreover, clonidine abolished the potassium-induced increase in the histamine release. Superfusion with the alpha 2-antagonists yohimbine or idazoxan enhanced the release rate of histamine. It is concluded that noradrenaline released from noradrenergic neurons of the hypothalamus modulates the release of histamine from histaminergic neurons by stimulating alpha 2-adrenoreceptors located on histaminergic nerve terminals.

Adrenergic alpha-Agonists↗
PubMed1991

Release of endogenous catecholamines in two different regions of the nucleus of the solitary tract as influenced by carotid occlusion.

The effects of carotid occlusion on the release of catecholamines in the nucleus of the solitary tract (NTS) were investigated in anaesthetized cats. Two aspects of the nucleus (rostral or intermediate NTS) were superfused bilaterally through push-pull cannulae with artificial CSF and the release of the endogenous dopamine, noradrenaline and adrenaline was determined in the superfusate radioenzymatically. The superfusion rate was 150 microliters/min or 800 microliters/min. In some experiments, superfusion of the intermediate NTS was carried out after denervation of the aortic arch. In the rostral NTS superfused at a rate of 150 microliter/min, bilateral carotid occlusion led to a rise in blood pressure and decreased the release rate of dopamine. These changes continued after occlusion termination. The release rate of noradrenaline was transiently diminished during occlusion. The release of this amine was also decreased after occlusion termination. The release rate of adrenaline was not influenced during carotid occlusion, but it was found to be diminished after termination of the occlusion. Superfusion of the rostral NTS at a rate of 800 microliters/min also reduced the release rate of adrenaline after termination of carotid artery occlusion. In the intermediate NTS (superfusion rate 150 microliters/min) similar effects of the carotid occlusion on the release rates of dopamine and noradrenaline were observed. In this aspect of the NTS, denervation of the aortic arch abolished the decrease in the noradrenaline release during carotid occlusion, while the release rates of dopamine and adrenaline were decreased during and after termination of the carotid occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Does brain histamine contribute to the development of hypertension in spontaneously hypertensive rats?

Histaminergic neurons of the brain have been implicated in genetic hypertension. We investigated the effect of inhibition of histamine synthesis by alpha-fluoromethylhistidine (alpha-FMH), the irreversible inhibitor of histidine decarboxylase, on the development and maintenance of hypertension in spontaneously hypertensive rats. Young (3-week-old) and adult (7-week-old) rats were treated with alpha-fluoromethylhistidine for 29 and 13 days, respectively. Treatment of spontaneously hypertensive rats and normotensive Wistar-Kyoto rats with alpha-fluoromethylhistidine led to a pronounced decrease in the histidine decarboxylase activity and in the histamine concentration in the brain (hypothalamus, brainstem, cortex-midbrain). In adult spontaneously hypertensive rats, the development of hypertension was not influenced by alpha-fluoromethylhistidine. In young spontaneously hypertensive rats, alpha-fluoromethylhistidine led to a transient delay in the development of hypertension which was followed by a transient tendency to increased blood pressure. It is concluded that histaminergic neurons of the brain play only a subordinate role, if any at all, in the development of hypertension in spontaneously hypertensive rats.

Animals↗
PubMed1991

Patterns of histamine release in the brain.

The pattern of histamine release has been investigated in various brain areas of anaesthetized cats and conscious, freely moving rats by the push-pull technique. In the hypothalamus, medial amygdaloid nucleus and mamillary body of the anaesthetized cat, histamine was found to be released according to an ultradian rhythm with a frequency of 1 cycle per 1-2 h. Additionally, oscillations have been observed in the medial amygdaloid nucleus and mamillary body with a frequency of 1 oscillation per 10 min. In the posterior hypothalamus of the conscious rat, histamine is also released rhythmically with a frequency of 1 cycle per 1.5 h. Moreover, the release rate of histamine is increased in the night.

Amygdala↗
PubMed1979

In vivo release of endogenous catecholamines in the hypothalamus.

The posterior hypothalamus of anaesthetized cats was superfused with a push-pull cannula and the release of the endogenous catecholamines noradrenaline, adrenaline and dopamine was determined in the superfusate. The rate of release of the three catecholamines followed an ultradian rhythm, the time interval between two adjacent phases of high rate of release being about 70 min. Pretreatment of the animals with reserpine decreased the levels of catecholamines in the hypothalamus and rest of the brain and reduced their rate of release into the superfusate. Hypothalamic superfusion with superfusing fluid of high concentration of potassium and low concentration of sodium enhanced the rate of release of noradrenaline and adrenaline; this effect was abolished when the hypothalamus was superfused with calcium-free solution. Electrical stimulation of the locus coeruleus ipsilateral to the superfused hypothalamus increased the release of noradrenaline and adrenaline, stimulation of the contralateral locus coeruleus enhanced the release of noradrenaline, adrenaline and dopamine. In both cases, the rate of release of adrenaline was enhanced to a lesser extent than the rate of release of noradrenaline. The release of noradrenaline and adrenaline was increased to a higher extent on stimulation of the ipsilateral locus coeruleus than on stimulation of the contralateral one.

Animals↗
PubMed1979

In vivo release of endogenous GABA in the cat hypothalamus.

The posterior hypothalamus of anaesthetized cats was superfused with artificial cerebrospinal fluid through a push-pull cannula and the release of endogenous GABA from the hypothalamus into the superfusate was studied. The resting release of GABA varied rhythmically, since phases of high rate of release were separated from each other by phases of low rate of release. The time interval between two adjacent phases of high rate of release was about 70 min. Electrical stimulation of the posterior hypothalamus with the tip of the cannula enhanced the rate of release of GABA in a frequency-dependent way. Superfusion of the hypothalamus with CSF which contained a high concentration of potassium and a low concentration of sodium increased the rate of release of GABA; this effect was dependent on the presence of calcium ions in the superfusing fluid. Pretreatment of the cats with reserpine reduced the levels of GABA in hypothalamus and rest of brain and the concentration of GABA in the superfusate as well. Stimulation of the locus coeruleus with a bipolar electrode elicited an increased release of GABA in the hypothalamus.

Animals↗
PubMed1978

beta-Adrenoreceptors of the posterior hypothalamus.

Cats were anaesthetized with pentobarbital sodium. A push-pull cannula was inserted into the posterior hypothalamus which was superfused through the cannula and electrically stimulated with its tip. Electrical stimulation elicited a frequency-dependent pressor response and tachycardia. Superfusion with orciprenaline, isoprenaline (beta 1- and beta 2-stimulants) or tazolol (beta 1-stimulant) led to a concentration-dependent enhancement in the pressor response. Superfusion with terbutaline caused a slight and late increase in the pressor response, while salbutamol (beta 2-stimulants) was ineffective. The tachycardia elicited by the hypothalamic stimulation was slightly increased by the hypothalamic stimulation was slightly increased by orciprenaline, tazolol and terbutaline. Superfusion with atenolol (beta 1-adrenoreceptor blocking drug) or butoxamine (beta 2-adrenoreceptor blocking drug) inhibited the pressor response and the tachycardia caused by hypothalamic stimulation. Superfusion with butoxamine prior to isoprenaline reduced the enhancing effect of isoprenaline on the pressor response, while superfusion with atenolol abolished or even reversed it. It is concluded that beta 1 and beta 2-adrenoreceptors are present in the posterior hypothalamus; apparently, beta 1- rather than beta 2-adrenoreceptors are involved in the rise of blood pressure elicited by stimulation of the hypothalamus.

Adrenergic beta-Agonists↗
PubMed1977

Presence of beta-adrenoreceptors in the hypothalamus; their importance for the pressor response to hypothalamic stimulation.

The posterior hypothalamus of cats anaesthetized with pentobarbital sodium was superfused and electrically stimulated with a push-pull cannula. Superfusion of the hypothalamus with (+/-)-, (-)-propranolol, sotalol, practolol or metoprolol caused a concentration-dependent inhibiton of the pressor response to hypothalamic stimulation. (+/-)-Propranolol and a procaine concentration equi-anaesthetic to the concentration of (+/-)- and (-)-propranolol were ineffective. Lower concentrations of propranolol and metoprolol were needed to inhibit the pressor response than of sotalol or practolol. Superfusion with practolol and tolazoline impaired the pressor response to a greater extent than did superfusion with each of the drugs alone. Hypothalamic superfusion with isoproterenol elicited a concentration-dependent enhancement of the rise of blood pressure during electrical stimulation of the hypothalamus. It is concluded that beta-adrenorecptors are present in the posterior hypothalamus and that they are involved in the pressor response elicited by electrical stimulation of the hypothalamus. Propranolol and metoprolol seemed to possess a higher affinity to the beta-receptors of the hypothalamus than sotalol or practolol.

Animals↗
PubMed1977

Hypothalamic action of adrenoreceptor blocking agents.

In cats anaesthetized with pentobarbital sodium, the posterior hypothalamus was superfused and electrically stimulated with a push-pull cannula. The pressor response to stimulation of this hypothalamic area was inhibited when the hypothalamus was superfused with drugs blocking either alpha-adrenoreceptors (piperoxan, tolazoline), or beta-adrenoreceptors--(+/-)-propranolol, (-)-propranolol, practolol, sotalol, metoprolol. (+)-Propranolol and a concentration of procaine equianaesthetic to propranolol were ineffective. During superfusion with tolazoline in the presence of practolol the inhibition was twice as that when the hypothalamus was superfused with either tolazoline or practolol. In another series of experiments the push-pull cannula was inserted into the anterior hypothalamus. The depressor response to stimulation of this area was inhibited by the hypothalamic superfusion with the alpha-adrenoreceptor blocking drugs phentolamine, tolazoline, piperoxan or yohimbine. Hypothalamic superfusion with phenylephrine abolished the inhibitory effect of phentolamine on the depressor response. The results indicate that adrenoreceptors are present in the hypothalamus and that they are involved in blood pressure changes elicited by hypothalamic stimulation.

Adrenergic alpha-Antagonists↗
PubMed1976

Competition of some biogenic amines for uptake into synaptic vesicles of the striatum.

Synaptic vesicles were isolated from the caudate nucleus of the pigs by differential centrifugation and incubated with labelled monoamines in the absence or in the presence of ATP-Mg(2+). Addition of ATP-Mg(2+) enhanced the uptake of (14)C-dopamine into the vesicles. Serotonin competitively inhibited the ATP-Mg(2+)-dependent uptake of (14)C-dopamine without influencing the uptake which took place in the absence of ATP-Mg(2+). Likewise, dopamine caused a dose-dependent inhibition of the ATP-Mg(2+)-dependent uptake of (14)C-serotonin without inhibiting the uptake in the absence of ATP-Mg(2+). Incubation of the vesicles with equal concentrations of(3)-dopamine and (14)C-serotonin revealed that the presence of the one amine competitively inhibited the ATP-Mg(2+)-dependent uptake of the other. Tyranimine competitively inhibited the ATP-Mg(2+)-dependent uptake of (14)C-dine, (14)C-serotonin and (14)C-noradrenaline into the vesicles; the uptake of the amines which took place in the absence of ATP-Mg(2+) was not impairedby tyramine. Analysis of the amine uptake by the ABC test showed that a mutual inhibition exists between dopamine and serotonin for the uptake into the synaptic vesicles. GABA did not influence the uptake of (14)C-dopamine either in the absence, or in the presence of ATP-Mg(2+)...

Adenosine Triphosphate↗
PubMed1976

Hypothalamic superfusion with muscarinic drugs: their effects on pressor responses to hypothalamic stimulation.

The posterior hypothalamus of cats anaesthetized with pentobarbital sodium was superfused with artificial cerebrospinal fluid through a push-pull cannula and electrically stimulated with the noninsulated tip of the cannula. The effects of muscarinic drugs on the pressor response to stimulation of the hypothalamus were investigated. Superfusion with muscarine, oxotremorine or N-benzyl-3-pyrrolidyl acetate methobromide (AHR 602) decreased the pressor responses to hypothalamic stimulation. Superfusion with methylatropine did not influence the pressor responses to hypothalamic stimulation; however, superfusion with methylatropine 60 min prior to and during superfusion with the muscarinic drugs abolished the inhibitory effects of muscarine and oxotremorine and temporarily reversed that of AHR 602 on the pressor responses. Superfusion of the posterior hypothalamus with arecoline enhanced the rise of blood pressure elicited by hypothalamic stimulation. When the hypothalamus was superfused with hexamethonium 60 min prior to and during superfusion with arecoline, arecoline reduced the pressor responses to electrical stimulation of the hypothalamus. Superfusion with methylatropine prior to and together with an ineffective concentration of arecoline increased the rise of blood pressure elicited by hypothalamic stimulation. From the drugs studied here only oxotremorine caused a fall of the "resting" arterial blood pressure; it was abolished by the intravenous injection of methylatropine. From these results it was concluded that superfusion of the posterior hypothalamus with muscarinic drugs impairs the pressor responses to hypothalamic stimulation. Drugs possessing both nicotinic and muscarinic properties either enhance or diminish the pressor responses according to their relative potencies on the two types of receptor.

Alkaloids↗