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Biomedical subjects

A Philippu

Publications and source records attributed to A Philippu.

At least 109 records · Page 6Linked to original sources
PubMed1981

The release of endogenous catecholamines in the cat hypothalamus is affected by spinal transection and drugs which change the arterial blood pressure.

1. In anesthetized cats, posterior and anterior hypothalamic areas were superfused with CSF through double-walled cannulae. The release of endogenous catecholamines (dopamine, noradrenaline and adrenaline) was determined in the superfusate by a radioenzymatic assay. 2. Transection of the brain caudal to the hypothalamus almost abolished the release of catecholamines in the posterior hypothalamic area, while that in the anterior hypothalamic area was moderately decreased. A circular transection around the hypothalamus greatly reduced the release of catecholamines in the anterior hypothalamic area. It is concluded that the catecholaminergic nerve endings of the anterior hypothalamic area do not originate entirely from cell bodies located in the brain stem. 3. Spinal transection elicited a pressor response which was followed by a fall of the arterial blood pressure. The pressor response was associated with increased rates of release of the catecholamines in the anterior hypothalamic area, while the release of catecholamines in the posterior hypothalamic area was reduced. The fall of blood pressure enhanced the rates of release of the catecholamines in the posterior hypothalamic area and reduced their release in the anterior hypothalamic area. 4. Chlorisondamine i.v. caused a fall of blood pressure which was associated with an increased release of catecholamines in the posterior hypothalamic area and a decrease in the rates of release in the anterior hypothalamic area whilst i.v. tramazoline elicited a pressor response and enhanced the rates of release of the catecholamines in the anterior hypothalamic area. 5. It is concluded that pronounced changes in the arterial blood pressure affect the release of catecholamine in opposite direction in the two hypothalamic areas to counteract the blood pressure change.

Animals↗
PubMed1980

Rise in blood pressure increases the release of endogenous catecholamines in the anterior hypothalamus of the cat.

In anaesthetized cats, anterior and posterior hypothalamic areas were simultaneously superfused with artificial CSF using two push-pull cannulae. The rates of release of endogenous catecholamines were determined in the superfusates which were continuously collected in periods of 10 seconds. In both areas, the rate of release of dopamine was higher than the rates of release of noradrenaline and adrenaline. Electrical stimulation of the splanchnic nerve elicited a rise in the arterial blood pressure and increased the rates of release of noradrenaline, adrenaline and dopamine in the anterior hypothalamic area. The rates of release of the catecholamines in the posterior hypothalamic area were not influenced by the pressor response to stimulation of the splanchnic nerve. Transection of the brain caudal to the hypothalamus reduced the rates of release of the catecholamines in the anterior hypothalamus and abolished the releasing effect of the stimulation of the splanchnic nerve. The results indicate that acute rise in blood pressure activates catecholamine cell bodies in the lower brain stem, which in turn stimulate the anterior hypothalamus to counteract the pressor response.

Animals↗
PubMed1980

Failure of isoprenaline and beta-receptor blocking drugs to modify depressor response and bradycardia induced by electrical stimulation of the anterior hypothalamus of cats.

The role of the hypothalamic beta-adrenoceptors in the depressor response and bradycardia induced by stimulation of the anterior hypothalamus was studied in cats. In chloralose and urethane anaesthetized cats the anterior hypothalamus was superfused with artifical cerebrospinal fluid through a push-pull cannula. Electrical stimulation of the anterior hypothalamus with the tip of the cannula elicited a fall of systemic blood pressure and a decrease in heart rate. Superfusion of the anterior hypothalamus with isoprenaline did not change the depressor response and bradycardia induced by electrical stimulation of the anterior hypothalamus. Superfusion with atenolol or butoxamine also failed to modify the responses. Superfusion with (+/-)-propranolol significantly suppressed the responses. However, superfusion with (+)-propranolol suppressed the responses to the same extent. The resting systemic blood pressure and heart rate were not significantly changed by superfusion of the hypothalamus with these drugs. These results suggest that beta-adrenoceptors of the anterior hypothalamus are not involved in the depressor response and bradycardia elicited by hypothalamic stimulation.

Adrenergic beta-Antagonists↗
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↗
PubMed1976

Inhibition by locally applied alpha-adrenoreceptor blocking drugs of the depressor response to stimulation of the anterior hypothalamus.

Cats were anaesthetized with pentobarbital sodium and the anterior hypothalamus was superfused with artificial cerebrospinal fluid through a push-pull cannula. Electrical stimulation of the superfused area with the tip of the cannula elicited a fall of the arterial blood pressure which was dependent on frequency and voltage. Maximal depressor response was obtained at 60 Hz with 2-4V; further increase of the voltage often led to a rise of the arterial blood pressure. Superfusion of the anterior hypothalamus with the alpha-adrenoreceptor blocking drugs tolazoline, piperoxan, yohimbine or phentolamine caused a dose-dependent inhibition of the depressor response to hypothalamic stimulation. Tolazoline was less effective than the other drugs. Superfusion of the anterior hypothalamus with the alpha-sympathomimetic drug phenylephrine prior to and during superfusion with phentolamine abolished the inhibitory action of the latter drug. It is concluded that alphaadrenoreceptors are present in the anterior hypothalamus and involved in the depressor response to electrical stimulation of this hypothalamic area.

Adrenergic alpha-Antagonists↗
PubMed1975

Uptake of dopamine into fractions of pig caudate nucleus homogenates.

Homogenates of the caudate nucleus of the pig were submitted to differential centrifugation. The 20000 g and 80000 g fractions were isolated and a part of them was osmotically shocked. The highest dopamine content per mg protein was found in the intact 80000 g fraction. Incubation experiments with the intact and the osmotically shocked fractions at 25 degrees C revealed that the particles of the intact 20000 g fraction took up dopamine, the influx of the amine was not enhanced by addition of ATP and magnesium to the incubation medium. On the other hand after osmotic shock the uptake of dopamine into the particles of this fraction was greatly enhanced by addition of ATP and magnesium. The uptake of dopamine into the particles of both intact and osmotically shocked 80000 g fractions was likewise enhanced by ATP and magnesium. The uptake in all fractions was not influenced by ouabain. The influx of dopamine into the particles of the intact 80000 g fraction was competitively inhibited by reserpine (Ki0.96 x 10-8M) and prenylamine (Ki1.74 x 10-8M). It is concluded that the intact 20000 g fraction contains intact synaptosomes; the uptake of dopamine is independent of the presence of ATP and magnesium. The shocked 20000 g fraction and the 80000 g fractions contain synaptic vesicles; the uptake of dopamine into these vesicles is enhanced by ATP and magnesium.

Adenosine Triphosphate↗
PubMed1975

Uptake of serotonin, gamma-aminobutyric acid and histamine into synaptic vesicles of the pig caudate nucleus.

Dopamine-containing vesicles were isolated from the caudate nucleus of the pig by differential centrifugation and incubated with 14-C-serotonin (14-C-5-HT), 14-C-gamma-aminobutyric acid (14-C-GAGA), 14-C-dopamine or 14-C-histamine. At 25 degrees C the uptake of 14-C-5-HT and 14-C-GABA was enhanced by ATP and magnesium. The Km for the uptake of 14-C-5-HT in the presence of ATP and magnesium was 0.67 x 10-6M, that of 14-C-GABA 1.33 x 10-4M. 14-C-Histamine was also taken up into the vesicles but its uptake was not incluenced by ATP and magnesim. The ATP-magnesium-dependent uptake of 14-C-5-HT and 14-C-GABA was abolished at 0 degrees C. At 37 degrees C the accumulation of 14-C-GABA in the presence of ATP and magnesium reached a steady state after 20 min, while the accumulation of 14-C-5-HT reached a maximum after 2.5 min of incubation and then gradually declined. Osmotic lysis of the vesicles followed by sonication abolished the enhanced uptake of 14-C-GABA, 14-C-5-HT and 14-C-dopamine in the presence of ATP and magnesium. Determination of the endogenous contents of the vasicles revealed 14.6 pmoles per mg protein for 5-HT and 22.7 nmoles per mg protein for GABA. It is concluded that the caudate nucles preparation used in this study contains not only dopamine-storing vesicles able to take up biogenic amines but also GABA-containing vesicles which take up GABA by an ATP-magnesium-dependent process.

Adenosine Triphosphate↗