Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dopamine (DA) and noradrenaline (NA) levels and activities of the enzymes metabolizing catecholamines were determined in the rat brain and kidneys during prolonged (4 weeks) administration of lysine vasopressin (LVP) and 2 weeks after its withdrawal. DA level was elevated during the whole period of experiment. NA level increased mainly after LVP withdrawal. Dopa-decarboxylase activity was elevated in all the experimental animals. Tyrosine and dopamine-beta-hydroxylase activities increased at the final period of LVP administration and after its withdrawal. Activities of MAO and COMT were markedly increased only after 3 weeks of LVP administration.
Acta Physiol Pol
PMID:The effect of prolonged vasopressin administration on the level and metabolism of catecholamines in the rat brain and kidneys. 0 18

The experiments were performed on male rats, drinking 2% NaCl solution ad libitum for 12 days instead of tap water. The pituitary gland was exposed by the transpharyngeal approach under urethane-chloralose anaesthesia. The posterior lobe remained in neural and partial vascular connection with the hypothalamus, whereas the anterior lobe was entirely removed. Samples of the outflow medium from the incubated in situ rat posterior pituitary lobe were collected during 30 min intervals. Substance P-like peptides and vasopressin activities were assayed by the biological tests. Injections of hypertonic solution into the internal carotid artery did not change vasopressin release, but induced an increase in Substance P release from the posterior pituitary lobe into the incubation medium. Under conditions of unexcitability of the osmosensitive cells, triggering vasopressin release, the injection of hypertonic solution into the internal carotid artery stimulated the Substance P-like peptides release from the posterior pituitary lobe.
Acta Physiol Pol
PMID:Substance P-like peptides and vasopressin release from posterior pituitary lobe incubated in situ after intracarotid injections of hypertonic solution in rats. 2 85

The effect of increased concentration of vasopressin and oxytocin in the cerebrospinal fluid on the excitability of the hypoglossal nerve nucleus was investigated. The experiments were carried out on rats under chloralose anaesthesia. Retractory jerks of the outstretched tongue were evoked by supra- or infraorbital nerve stimulation during perfusion of the cerebral ventricles with McIlwain-Rodnight solution. The solution contained synthetic arginine vasopressin 0.05 U/ml or synthetic oxytocin 0.05 U/ml. Perfusion of the ventricles with vasopressin increased and perfusion with oxytocin decreased the evoked tongue jerks.
Acta Physiol Pol
PMID:Effect of vasopressin and oxytocin perfusion of the cerebral ventricles on evoked tongue jerks. 21 38

Rats dehydrated up to 8 days were treated with diphenylhydantoin given intraperitoneally in daily doses of 10 mg/100 g of the initial body weight. The single dose of diphenylhydantoin diminished the vasopressin content in the hypothalamus and neurohypophysis of normally hydrated rats. Under conditions of severe dehydration (8 days), DPH treatment resulted in a more marked decrease of vasopressin in the hypothalamo-neurohypophysial system.
Acta Physiol Pol
PMID:The hypothalamic and neurohypophysial vasopressin content as influenced by diphenylhydantoin in dehydrated rats. 49 39

The effect of intraventricular 6-hydroxydopamine on the content of oxytocin and vasopressin in the hypothalamus and pituitary gland of water deprived rats. Acta Physiol. Pol., 1977, 28 (6): 497-504. Rats received one infusion of 200 microgram 6-hydroxydopamine with 25 microgram of ascorbic acid into the lateral cerebral ventricle. After 57 days some rats were deprived of water for 4, 8 or 12 days. Then, the animals were sacrificed by decapitation. Oxytocin was determined in extracts from the posterior pituitary lobe and hypothalamus by the method of Van Dongen and Hays, while the vasopressin content was determined by the method of Dekanski. It was found that 6-hydroxydopamine injection into the cerebral ventricles causes a rise in oxytocin content in the hypothalamus and prevents its fall during--4--12 days of dehydration.
Acta Physiol Pol
PMID:The effect of intraventricular 6-hydroxydopamine on the content of oxytocin and vasopressin in the hypothalamus and pituitary gland of water-deprived rats. 61 34

Content of vasopressin in the neurohypophysis of long-term dehydrated rats as influenced by carbachol treatment. Acta Physiol. Pol., 1977, 28 (1): 71-75. Rats dehydrated up to 12 days were treated with carbachol given intraperitoneally in daily doses of 20 microng/100 g of the initial body weight. Under extreme dehydration (8 and 12 days) the vasopressin depletion in the neurohypophysis was significantly inhibited in the carbachol-treated animals.
Acta Physiol Pol
PMID:Content of vasopressin in the neurohypophysis of long-term dehydrated rats as influenced by carbachol treatment. 86 26

About 2000 bovine hypothalami were homogenized, extracted, purified and three times filtrated on Sephadex G - 25 column. During the first and second filtration the fractions with vasodepressor activity were collected for further purification. During the third filtration about 40 fractions possessing vasodepressor activity were found. The fractions emerging before vasopressin decreased the arterial blood pressure and induced transient bradycardia in rats. The results indicate that some fractions of hypothalamic extract produce vasodepressor response by vasodilatation only and the other ones by simultaneous vasodilatation and heart rate decrease.
Acta Physiol Pol
PMID:Cardiodepressor and vasodepressor activities of partially purified bovine hypothalamic extract. 94 86

Turnover of noradrenaline (NA) and dopamine (DA) in some regions of the rat brain was determined after 1 and 3 weeks of daily injections of lysine vasopressin (LVP) and 2 weeks after the termination of 28-day LVP injections. Disappearance of 3H-DA was estimated in the hemispheres, brain stem and striatum and of 3H-NA in the hemispheres and brain stem after intraventricular injection of 3H-tyrosine. A significant acceleration of 3H-NA disappearance from the hemispheres was found in all the experimental animals and from the brain stem 3 weeks after LVP adminstration and 2 weeks after its withdrawal. No marked changes in dopamine turnover in the examined regions of the rat brain were found. Since prolonged vasopressin administration produces hypertension in the rat it seems likely that central NA, but not DA, plays a role in the vasopressin-induced hypertension.
Acta Physiol Pol
PMID:Turnover of catecholamines in some regions of the rat brain during prolonged vasopressin administration and after its withdrawal. 94 87

The blood pressure was investigated in the common left carotid artery (LC), in the left atrium (LA), in the pulmonary artery (PA) and in the right atrium (RA). After adrenaline injection the blood pressure rised rapid and simulatneously in all four regions. After vasopressin injection the blood pressures rised sequence in LC, in LA and PA. The blood pressure in RA in this time was unchanged. These results indicate that primary causes of the lung oedema after adrenaline or vasopressin are different.
Pol J Pharmacol Pharm
PMID:Haemodynamic changes accompanying lung oedema produced by iv injection of adrenaline or vasopressin into rats. 98 Oct 23

Low doses of apomorphine (20-50 micrograms/kg) induced an increase in the activity of an endogenous inhibitor of cAMP dependent protein Kinases (type I inhibitor) in the striatum, anterior and posterior hypothalamus of normotensive rats by stimulating D2-dopamine receptors. In contrast, high doses of the compound (2-10 mg/kg) produced a dose dependent decrease in type I inhibitor activity. In the posterior hypothalamus of vasopressin hypertensive rats and SHR the maximal increase of type I inhibitor activity was markedly higher than in normotensive animals. Moreover, apomorphine induced the increase of type I inhibitor activity in a much wider range of doses. Only as high dose of the compound as 10 mg/kg was able to decrease type I inhibitor activity. This points to a marked supersensitivity of D2 receptors and suggests the subsensitivity of D1 receptors in this brain area of hypertensive rats. In contrast, in the striatum and anterior hypothalamus of hypertensive rats the apomorphine dose response curves were similar to those in normotensive rats. Thus, it seems tha hypertension is associated with the alteration in sensitivity of D2 and D1 receptors in the posterior hypothalamus, the brain area involved in regulation of blood pressure.
Pol J Pharmacol Pharm
PMID:The responsiveness of D1- and D2-dopamine receptors in the striatum and hypothalamus of spontaneous and vasopressin hypertensive rats. 128 99


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