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1

TGLP-1 and release of vasopressin and oxytocin from the isolated rat hypothalamo-neurohypophysial system: effects of a TGLP-1 receptor agonist and antagonist

100%

Bojanowska E., Stempniak B.

Journal of Physiology and Pharmacology

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2001

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tom 52

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nr 4,2

To date, glucagon-like peptide–1 (7-36) amide (tGLP-1) has been found to enhance the vasopressin and oxytocin secretion in vivo but not in vitro (i.e., when the isolated neurointermediate lobe of the pituitary was used for experiments). The goal of this study was to investigate whether tGLP-1 can influence the function of the hypothalamo-neurohypophysial complex in vitro. Also, the effect of a tGLP-1 agonist, exendin-4, and antagonist, exendin-(9-39), on the release of vasopressin/oxytocin from the isolated rat hypothalamo-neurohypophysial complex was tested. tGLP-1 enhanced the basal but not the potassium-stimulated release of vasopressin and oxytocin from the hypothalamo-neurohypophysial complex. On the other hand, tGLP-1 failed to affect the release of both hormones from the isolated neurointermediate lobe. The tGLP-1 agonist increased the secretion of oxytocin and vasopressin from the hypothalamo-neurohypophysial system whilst the tGLP-1 antagonist completely abolished the stimulatory effect of tGLP-1 on the secretion of both hormones. It is concluded that tGLP-1 affects the function of vasopressin- and oxytocinergic neurones through specific hypothalamic receptors.

2

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Studies on the vasopressin and oxytocin storage in the hypothalamus and neurohypophysis

88%

Guzek J. W.

Acta Physiologica Polonica

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1987

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tom 38

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nr 6

3

Intracerebroventricular insulin affects the neurohypophysial vasopressin content in euhydrated and dehydrated rats

88%

Stempniak B., Guzek J. W.

Acta Physiologica Polonica

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1990

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tom 41

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nr 7

Stempniak В. and Guzek J. W.: Intracerebroventricular insulin affects the neurohypophysial vasopressin content in euhydrated and dehydrated rats. Acta Physiol. Pol., Rats euhydrated or dehydrated for four days were given intracerebroventricular insulin once daily in a dose of 100 ng (not affecting blood sugar level). In euhydrated rats, insulin decreased significantly the neurohypophysial vasopressin content. In dehydrated animals the neurohypophysial content depleted by deprivation of water could be further reduced by intracerebroventricular treatment with insulin. These results may suggest a possible regulatory role of brain insulin in the mechanisms of vasopressin release.

4

Effect of a prostacyclin analogue on the vasopressin and oxytocin secretion in vitro

75%

Bojanowska E., Guzek J. W.

Acta Physiologica Polonica

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1990

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tom 41

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nr 7

Bojanowska E. and Guzek J. W.: Iloprost (ZK 36374; a stable prostacyclin analogue) increases basal as well as potassium-evoked vasopressin and oxytocin secretion from rat neurointermediate lobes in vitro. This finding suggests a possible regulatory role of endogenous prostacyclin in the release of neurohypophysial hormones.

5

Thyrotropin-releasing hormone modulates vasopressin and oxytocin synthesis and release from the hypothalamo-neurohypophysial system of different age male rats

75%

Ciosek J., Izdebska K.

Journal of Physiology and Pharmacology

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2009

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tom 60

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nr 2

63-70

Thyrotropin-releasing hormone (TRH) is engaged in the modulation of the hypothalamo-neurohypophysial system activity. Effects of repeated intravenously injections of TRH in a dose of 100 ng/100 g b.w. on vasopressin (VP) and oxytocin (OT) biosynthesis and release from the hypothalamo-neurohypophysial system was investigated in rats in different age (1-, 3- or 7-months of the life). To estimate the biosynthesis rate of both neurohormones the colchicine procedure was used (the dose of 5 µg/5 µl icv 20 hours before the decapitation). It has been observed that vasopressin synthesis in the hypothalamus increased gradually with maturation of rats, while OT biosynthesis decreased in the same animals. Hypothalamic biosynthesis rate of VP and OT is most effective in youngest rats and declines during the adolescence of animals. Thyrotropin-releasing hormone directly affects VP-ergic and OT-ergic hypothalamic neurons activity and both neurohormones biosynthesis process. This effect, however, is opposed: TRH acts as a stimulator of vasopressin biosynthesis most of all in young male rats and as an inhibitor for oxytocin biosynthesis especially in mature animals.

6

Centrally applied vasopressin intensifies hypotension and bradycardia after hemorrhage in SHR rats

75%

Dobruch J., Paczwa P., Lon S., Szczepanska-Sadowska E.

Journal of Physiology and Pharmacology

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2002

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tom 53

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nr 2

Spontaneuosly hypertensive rats (SHR) have been shown to exhibit several alterations in function of the intrabrain vasopressinergic system. The present study was designed to find out whether centrally administered vasopressin (AVP) may influence the cardiovascular adaptation to hypotensive hypovolemia in SHR rats. Two series of experiments were performed on conscious 17 SHR rats chronically implanted with lateral cerebral ventricle (LCV) cannulas and with femoral artery catheters. Mean arterial pressure (MAP) and heart rate (HR) were monitored before and after arterial bleeding (1,3% body weight) performed during LCV infusion of 1) artificial cerebrospinal fluid 5µl/hour (aCSF); and 2) arginine vasopressin, 100ng/hour/5µl of aCSF (AVP). Central administration of aCSF and AVP had no effect on MAP and HR under resting conditions. Hemorrhage evoked significant hypotension (p<0.001) and bradycardia (p<0.001). During central infusion of AVP hemorrhage resulted in significantly greater hypotension than during central infusion of aCSF alone (p<0,05). The results provide evidence that centrally applied vasopressin significantly modulates cardivascular adjustments to hypotensive hemorrhage in SHR.

7

Galanin influences vasopressin and oxytocin release from the hypothalamo-neurohypophysial system of salt-loaded rats

75%

Cisowska-Maciejewska A., Ciosek J.

Journal of Physiology and Pharmacology

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2005

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tom 56

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nr 4

Galanin is a peptide present in the nervous system and peripheral tissues which exerts a broad range of physiological functions. The influence of centrally administered galanin (Gal; 100 pM i.c.v.) on arginine vasopressin (AVP) and oxytocin (OT) content in the hypothalamus and neurohypophysis as well as on their blood plasma concentration was estimated in male Wistar rats drinking ad libitum 2% solution of natrium chloride per 48 hours. In euhydrated rats and subsequently applied i.c.v. with Gal a significant fall in the hypothalamic and neurohypophysial content of OT but not AVP was observed, however, without simultaneous changes in these neurohormones blood plasma concentration. On the contrary, i.c.v. injection of Gal to salt-loaded rats caused a marked raise in AVP and OT level in the hypothalamus and neurohypophysis with subsequent diminution of both neurohormones concentration in blood plasma. These results suggest that in euhydrated rats Gal has an inhibitory influence on the biosynthesis as well as axonal transport of OT, but not AVP. On the contrary, in salt-loaded rats galanin restricts secretion of both neurohormones into the systemic circulation.

8

Enhanced pressor response to centrally administered vasopressin in WKY rats on high sodium diet

75%

Zera T., Ufnal M.

Acta Neurobiologiae Experimentalis

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2005

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tom 65

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nr 2

9

Vasopressin and oxytocin release and the thyroid function

75%

Ciosek J., Drobnik J.

Journal of Physiology and Pharmacology

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2004

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tom 55

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nr 2

The aim of the present investigations was to examine the effects of the states of hypothyroidism or hyperthyroidism on vasopressin (AVP) and oxytocin (OT) release under conditions of equilibrated water metabolism as well as of osmotic stimulation, brought about by the dehydration or hypertonic saline administration. The euhydrated and simultaneously hypothyroid rats showed decreased hypothalamic AVP and OT content and somewhat higher but not significant neurohypophysial AVP content. In these animals the raised OT (but not AVP) plasma level has been observed. In hyperthyroid rats drinking tap water ad libitum the neurohypophysial AVP and OT content significantly diminished; plasma OT concentration (but not AVP) was then elevated. The state of osmotic stimulation was the reason of different response of the hypothalamo-neurohypohysial system function in hypo- or hyperthyroid rats. Significant decreases of neurohypophysial AVP and OT content were found in both hypothyroid dehydrated as well as hypothyroid hypertonic saline-treatment rats as compared with hypothyroid euhydrated ones. On the contrary, in the state of hyperthyroidism AVP content in the neurohypophysis distinctly raised in dehydrated and salt-loaded rats; in these last neurohypophysial OT content increased as well. Plasma OT (but not AVP) distinctly diminished in hyperthyroid and simultaneously dehydrated or hypertonic saline injected rats in relation to hyperthyroid control subgroup. Data from the present study suggest that: 1) altered thyroid gland function affects vasopressin and oxytocin release from the hypothalamo-neurohypophysial system in the state of equilibrated water metabolism; 2) the state of hypo- or hyperthyroidism modifies the response of AVP-ergic and OT-ergic neurons upon the osmoreceptors/osmodetectors stimulation. It may be sypposed that OT-ergic neurons display greater than AVP-ergic neurons sensitivity upon the thyroid hormone influence.

10

Thyrotropin-releasing hormone [TRH] modulates vasopressin and oxytocin release from the hypothalamo-neurohypophysial system in dehydrated rats

75%

Ciosek J., Guzek J. W., Orlowska-Majdak M.

Journal of Physiology and Pharmacology

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1993

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tom 44

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nr 3

11

The post-haemorrhagic vasopressin release into the blood

75%

Lipinska S., Forys S., Lipinska J.

Journal of Physiology and Pharmacology

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2004

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tom 55

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nr 1,1

The aim of the present study was to compare the influence of the renin-angiotensin and sympathetic system in the process of post-haemorrhagic vasopressin release. A dialysis of the venous blood from the sella turcica region was performed in male rats under anaesthesia. The animals were divided into eight experimental groups: 1) control; 2) bleeding; 3) 20 days after superior cervical ganglionectomy; 4) 20 days after superior cervical ganglionectomy and bleeding; 5) injection of captopril; 6) injection of captopril and bleeding; 7) 20 days after superior cervical ganglionectomy and injection of captopril; 8) 20 days after superior cervical ganglionectomy, injection of captopril and bleeding. The content of vasopressin in dialysates was determined by radioimmunoassay. In control rats the release of vasopressin into dialysates was constant during 180 min of the experiment. Bleeding, as well as, superior cervical ganglionectomy caused an increase in vasopressin release. Captopril did not change vasopressin release in comparison to control group. Furthermore, vasopressin release after both, bleeding and sympathetic denervation performed simultaneously was significantly abolished. We conclude that renin-angiotensin, as well as, sympathetic nervous system are involved in the increased post-haemorrhagic vasopressin release.

12

Vasopressin release from posterior pituitary lobe incubated in situ after preganglionic stimulation of the rat superior cervical ganglion

75%

Lipinska S., Orlowska-Majdak M., Traczyk W. Z.

Journal of Physiology and Pharmacology

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1992

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tom 43

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nr 4

In uretane-chloralose anaesthesia the pituitary gland was exposed by transpharyngeal approach in rats. The anterior lobe was removed and the posterior lobe was incubated in situ, that is in conditions of anatomical integrity of the hypothalamus with the posterior pituitary lobe. The 15-min samples of the medium incubating the posterior pituitary lobe in situ were collected. Vasopressin (AVP) content in the incubation medium was determined by radioimmunoassay. The stimulation of preganglionic fibers of the superior cervical ganglion (SCG) with alternate short (5 s) bursts of electric pulses with short (5 s) breaks did not change A VP release. However, stimulation of preganglionic fibres with alternate long (30 s) bursts of electric pulses with long (30 s) breaks evoked an increase in AVP release after some latency . Probably, at the hypothalamic or posterior pituitary level temporal summation should occur affecting vasopressinergic neurons or their endings and evoking AVP release.

13

Molecular docking-based test for affinities of two ligands toward vasopressin and oxytocin receptors

75%

Slusarz R., Kazmierkiewicz R., Gieldon A., Lammek B., Ciarkowski J.

Acta Biochimica Polonica

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2001

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tom 48

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nr 1

Molecular docking simulations are now fast developing area of research. In this work we describe an effective procedure of preparation of the receptor-ligand complexes. The amino-acid residues involved in ligand binding were identified and described.

14

Vasopressin release into the 3rd cerebral ventricle and into the blood after sciatic and trigeminal nerve stimulation

75%

Orlowska-Majdak M., Goraca A., Glabinski A., Traczyk W. Z.

Journal of Physiology and Pharmacology

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1994

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tom 45

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nr 2

15

Aminergic control of vasopressin secretion in the conscious rat

75%

Wells T., Forsling M. L.

Journal of Physiology and Pharmacology

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1992

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tom 43

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nr 1

The influence of aminergic pathways on basal and stimulated vasopressin (AVP) release was studied in conscious rats, the stimulus for hormone release being an intracerebroventricular (ICV) injection of 5 µl 0.85M sodium chloride. The animals were treated with either phenoxybenzamine, propranolol or haloperidol prior to administration of the central hypertonic stimulus. Phenoxybenzamine elevated basal plasma vasopressin concentrations, while propranolol and haloperidol had no effect. The secretion of АVР in response to the hypertonic stimulus was potentiated by phenoxybenzamine and haloperidol, but the effect of propranolol was equivocal. The antagonists had no effect on basal arterial pressure at the time of hypertonic saline administration or the pressor response to ICV sodium chloride.

16

Effect of NG-nitro-L-arginine on pressor action of arginine vasopressin in normotensive [WKY] and spontaneously hypertensive [SHR] rats

75%

Stys T., Szczepanska-Sadowska E.

Journal of Physiology and Pharmacology

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1994

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tom 45

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nr 2

17

Centrally applied vasopressin prevents posthemorrhagic hypotension in WKY rats

75%

Ufnal M., Zera T.

Acta Neurobiologiae Experimentalis

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2002

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tom 62

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nr 1

18

Neurokinin A and the neurohypophysial response to malatonin: in vitro studies

75%

Juszczak M.

Journal of Physiology and Pharmacology

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2002

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tom 53

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nr 4,2

The aim of this study was to investigate a possible role of neurokinin A (a member of a family of peptides known as tachykinins) in the pineal-neurohypophysial interrelationship. The effect of neurokinin A (NKA) alone or in the presence of pineal hormone - melatonin on basal and K + -stimulated vasopressin and oxytocin secretion from the hypothalamo-neurohypophysial system was studied in vitro. The present results show that NKA stimulated basal vasopressin and oxytocin release from the isolated hypothalamo-neurohypophysial system, when used at the concentration of 10-7 M/L. Melatonin diminished basal release of the neurohypophysial hormones; it also significantly inhibited the NKA-stimulated secretion of vasopressin and oxytocin. Lower concentrations of NKA did not affect the neurohypophysial hormones basal release, however, when melatonin was added to the medium enriched with NKA at the concentration of 10-9 M/L, the vasopressin secretion from the hypothalamo-neurohypophysial explants was decreased significantly. The K+ -evoked release of neurohypophysial hormones was not further modified by either NKA or melatonin. The present results confirm previous reports as to the inhibitory effect of melatonin on both vasopressin and oxytocin secretion from the hypothalamo-neurohypophysial complex in vitro. However, under present experimental conditions, the contribution of NKA in the mechanisms of pineal- neurohypophysial interrelationships has not been demonstrated.

19

Neurohormones: oxytocin, vasopressin and related peptides - structure, genes, receptors, and evolution

63%

Kochman K.

Journal of Animal and Feed Sciences

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2013

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tom 22

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nr 4

Oxytocin (OT) and vasopressin (VP), and all related hormones, consist of nine amino acids with cysteine residues in positions 1 and 6 that form a six-amino acid cyclic part, and of a C-terminal glycine in α-amidated form. These neuropeptides are classified into oxytocin and vasopressin families based on the amino acid residue at position 8. OT-like and VP-like peptides are present in every vertebrate species. These peptides are a very ancient family of hormones having representatives in diverse species of invertebrates. Invertebrates have either a vasopressin-family peptide or an oxytocin-family peptide, whereas bony fishes, the ancestors of land vertebrates, have both isotocin and vasotocin. Presently, two evolutionary structural lineages have been proposed: an isotocin-mesotocin-OT line, associated with reproductive functions, and a vasotocin-VP line participating in water homeostasis. The ancestral gene encoding the precursor protein has been present in the animal genome for a period exceeding 500 million years of evolution. The exceptionally high stability of this structure of nine-amino acid peptides during the entire process of evolution suggests very powerful selective pressure, possibly by evolution together with respective receptors and specific processing enzymes. A novel gene with a distinct function and expression appeared during evolution through duplication of an ancestral gene. The synteny and order of genes in the neurohypophysial hormone gene locus are conserved in the lamprey, elephant shark, coelacanth, and tetrapods, but disrupted in teleost fishes presumably due to the rearrangements facilitated by a whole-genome duplication event in the teleost fish ancestor.

20

Traumatic brain injury results in a concomitant increase in neocortical expression of vasopressin and its V1A receptor

63%

Pascale C. L., Szmydynger-Chodobska J., Sarri J. E., Chodobski A.

Journal of Physiology and Pharmacology. Supplement

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2006

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tom 57

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nr 11

161-167

Arginine vasopressin (AVP) has been shown to promote the disruption of the blood-brain barrier (BBB) and the formation of edema in various animal models of brain injury. However, the source(s) of this AVP have not been identified. Since the cerebral cortex was considerably affected in some of these brain injury models, we sought to determine if AVP was produced in the cerebral cortex, and, if so, whether or not this cortical AVP expression was up regulated after injury. In the present study, a controlled cortical impact model of traumatic brain injury (TBI) in rats was used, and the temporal changes in expression of AVP and its V1a receptor were analyzed by real-time reverse-transcriptase polymerase chain reaction. The expression of AVP and its V1a receptor in the ipsilateral cortex adjacent to the lesion area was significantly up regulated between 4 h and 1day post-TBI. The maximum increase in mRNA for AVP (4.3-fold) and its receptor (2.6-fold) in the ipsilateral vs. contralateral cortex was observed at 6 h post-TBI. Compared to sham-injured rats, no statistically significant changes in expression of AVP or its receptor were found in the contralateral cortex. These results suggest that the cerebral cortex is an important source of AVP in the injured brain, and the parallel increase in the expression of AVP and its cognate receptor may act to augment the actions of AVP related to promoting the disruption of the BBB and the formation of post-traumatic edema.

Ograniczanie wyników

TGLP-1 and release of vasopressin and oxytocin from the isolated rat hypothalamo-neurohypophysial system: effects of a TGLP-1 receptor agonist and antagonist

Studies on the vasopressin and oxytocin storage in the hypothalamus and neurohypophysis

Intracerebroventricular insulin affects the neurohypophysial vasopressin content in euhydrated and dehydrated rats

Effect of a prostacyclin analogue on the vasopressin and oxytocin secretion in vitro

Thyrotropin-releasing hormone modulates vasopressin and oxytocin synthesis and release from the hypothalamo-neurohypophysial system of different age male rats

Centrally applied vasopressin intensifies hypotension and bradycardia after hemorrhage in SHR rats

Galanin influences vasopressin and oxytocin release from the hypothalamo-neurohypophysial system of salt-loaded rats

Enhanced pressor response to centrally administered vasopressin in WKY rats on high sodium diet

Vasopressin and oxytocin release and the thyroid function

Thyrotropin-releasing hormone [TRH] modulates vasopressin and oxytocin release from the hypothalamo-neurohypophysial system in dehydrated rats

The post-haemorrhagic vasopressin release into the blood

Vasopressin release from posterior pituitary lobe incubated in situ after preganglionic stimulation of the rat superior cervical ganglion

Molecular docking-based test for affinities of two ligands toward vasopressin and oxytocin receptors

Vasopressin release into the 3rd cerebral ventricle and into the blood after sciatic and trigeminal nerve stimulation

Aminergic control of vasopressin secretion in the conscious rat