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)

This study examined the effects of transmural nerve stimulation, acetylcholine, adrenoceptor agonists and several peptides on the contractility of strips of human gallbladder in vitro. Acetylcholine caused concentration-related contractions of the tissues and the sensitivity to acetylcholine was similar in gallbladders with mild and severe chronic cholecystitis. Noradrenaline and adrenaline relaxed gallbladder strips, probably via beta 2-adrenoceptor stimulation. Transmural nerve stimulation always caused contractions, but in the presence of atropine inhibitory responses were demonstrable and these were antagonized by propranolol. There was no evidence of non-adrenergic inhibitory neural responses. Of the peptides tested, only cholecystokinin octapeptide (CCK-OP), gastrin, pentagastrin, substance P and caerulein caused contractions. Responses to CCK-OP, gastrin and pentagastrin were antagonized by dibutyryl cyclic GMP. Hormones which had no effect upon human gallbladder strips included motilin, secretin, bombesin, neurotensin, glucagon, vasopressin, VIP and somatostatin. Considerable differences therefore exist between human tissues and those from experimental animals with respect to the direct actions of neural and hormonal stimuli on gallbladder contractility.
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PMID:Contractility of human gallbladder muscle in vitro. 297 88

Atractyloside inhibited gluconeogenesis from dihydroxyacetone in hepatocytes from fasted rats and increased lactate synthesis. In the presence of atractyloside, lactate/pyruvate and beta-hydroxybutyrate/aceto-acetate ratios were increased and the accumulation of Fru-2,6-P2 was prevented. In the absence of atractyloside, gluconeogenesis from dihydroxyacetone was stimulated by dibutyryl-cAMP and, to a much lesser extent, by norepinephrine and vasopressin. Omission of Ca2+ increased the stimulation by norepinephrine but prevented that by vasopressin. High concentrations (greater than or equal to 40 microM) of atractyloside abolished the stimulation of gluconeogenesis by dibutyryl-cAMP but not that by norepinephrine or vasopressin. Exogenous Ca2+ was not required for hormonal stimulation in the presence of atractyloside. The stimulation by norepinephrine was inhibited by ethylene glycol bis(beta-aminoethyl ether)-N,N,N',N-tetraacetic acid or prazosin but not by propranolol. Atractyloside caused decreases of all glycolytic intermediates and an activation of pyruvate kinase. Norepinephrine partially reversed these effects. The mitochondrial and cytosolic ATP/ADP ratios were determined by digitonin fractionation of hepatocytes. Norepinephrine or vasopressin increased the cytosolic ATP/ADP in the presence of atractyloside. We suggest that the increased availability of cytosolic ATP could be responsible for the stimulation of gluconeogenesis by these hormones.
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PMID:Catecholamine and vasopressin stimulation of gluconeogenesis from dihydroxyacetone in the presence of atractyloside. 299 83

Norepinephrine and the alpha-agonist phenylephrine in concentrations of 10(-5) to 10(-3) M prompted the release of radioimmunoassayable vasopressin (up to 150 pg/min) and oxytocin (up to 20 pg/min) from intraarterially perfused explants of rat basal forebrain. Drug effects were markedly reduced or abolished in the presence of the non-specific alpha-antagonists phentolamine and phenoxybenzamine, and the specific alpha 1-antagonist prazosin. In concert with recent in vivo and in vitro electrophysiological observations, these data imply that endogenous noradrenergic pathways to magnocellular neurosecretory cells are excitatory, mediated through activation of their alpha 1-receptors, thereby enhancing the release of both vasopressin and oxytocin in the neurohypophysis.
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PMID:Alpha 1-adrenergic receptor activation releases vasopressin and oxytocin from perfused rat hypothalamic explants. 301 17

alpha 2-Adrenoceptors were first described pharmacologically ten years ago. Within three years their capacity to inhibit adenylate cyclase had been demonstrated in many tissues. They were demonstrated biochemically in the kidneys in 1981 even before any renal physiological effects of their activation were known. They predominate numerically over alpha 1-adrenoceptors in renal membranes and their density is increased in genetic forms of rat hypertension. alpha 1-Adrenoceptors normally mediate the vasoconstriction and sodium- and water-retaining effects of sympathetic neuronally released norepinephrine. Norepinephrine or epinephrine must be infused to activate alpha 2-adrenoceptors, suggesting that renal alpha 2-adrenoceptors are extrajunctional, whereas alpha 1-adrenoceptors are postjunctional. When alpha 1-adrenoceptors are chronically blocked, renal alpha 2-adrenoceptor density increases and they assume a location at postjunctional sites, the otherwise exclusive domain of alpha 1-adrenoceptors. Results from microdissection studies have established that alpha 2-adrenoceptors are present on most segments of the nephron and that their activation can suppress adenosine 3,'5'-cyclic monophosphate (cAMP) accumulation induced by most renal hormones. However, failure of alpha 2-adrenoceptor activation to suppress cAMP accumulation in some tubular segments induced by certain hormones suggests compartmentalization of adenylate cyclase regulation that is hormone-function specific. In view of the potent inhibitory effects of alpha 2-adrenoceptor stimulation on hormone activated cAMP accumulation in several discrete areas of the nephron, we suggest that alpha 2-adrenoceptors fulfill important regulatory role(s) in renal function. To date, alpha 2-adrenoceptor activation has been shown to reverse vasopressin-induced sodium and water retention, and arachidonic acid- and furosemide-induced cAMP, sodium, and water excretion in the isolated perfused kidney. Thus the effects are qualitatively and quantitatively dependent in these studies on the hormone being infused and are therefore hormone-function specific. Physiological effects of alpha 2-adrenoceptor activation of thyrocalcitonin and on parathyroid hormone-induced effects have not been studied. alpha 2-Adrenoceptor activation can inhibit renin release in some model systems and can activate a sodium-hydrogen antiporter system in proximal tubules. The physiological roles of these actions are unknown.
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PMID:Renal alpha 2-adrenoceptors and the adenylate cyclase-cAMP system: biochemical and physiological interactions. 302 68

Experiments were undertaken in the mesentery of anesthetized cats and rabbits to investigate whether the endothelium of resistance vessels mediates relaxation of arteriolar smooth muscle through the endothelium-derived relaxing factor(s) (EDRF). The microcirculation was visualized by transillumination using intravital microscopy and a Millikan camera. Pictures were obtained at a rate of 400 frames/second. Arteriolar mean diameter and surface area were computer calculated. The animals were divided in two groups. In one group of experiments, EDRF was inactivated by direct injection of hydroquinone (HQ) into the superior mesenteric artery and the second group served as control. Norepinephrine or vasopressin constricted while acetylcholine or Ca-ionophore A23187 dilated arterioles. Hydroquinone failed to inhibit arteriolar dilation in situ. The effect of HQ on the endothelium in situ was ascertained by bioassay of superior mesenteric artery strips. Our results cast doubt on the role of EDRF in the dilation of mesenteric arterioles in felines and rabbits.
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PMID:Uncertain role of endothelium-derived relaxing factor in mesenteric arterioles of cats and rabbits. 313 58

The sauna induces changes in the secretion of hormones, some similar to changes induced in any other stress situation and others characteristic of exposure to the sauna. Noradrenaline is usually the only catecholamine raised by the sauna in people accustomed to it. The secretion of the antidiuretic hormone is increased and the renin-angiotensin-aldosterone system is activated. The concentrations of the growth hormone and prolactin, in particular, secreted from the anterior pituitary are increased in the circulation. The concentration of the immunoreactive beta-endorphin in blood may also increase which may reflect the feeling of pleasure or, on the other hand, discomfort induced by the sauna. The views on the effects of the sauna on the secretion of the ACTH and cortisol are partly contradictory, probably due to differing ways of taking the sauna bath. In Finnish sauna takers the concentration of cortisol in blood is not usually increased. The changes induced by the sauna in various hormone concentrations in the circulation are, however, normalized within a couple of hours after the heat stress.
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PMID:How the sauna affects the endocrine system. 321 98

The changes in plasma levels of arginine-vasopressin (AVP) and oxytocin (OXT) of rabbits by intraventricular administration of various drugs and their effects on the release of both hormones from the isolated posterior pituitary of rats were examined. An intraventricular injection of hypertonic saline, carbachol, angiotensin II, prostaglandin E2 or histamine to a rabbit increased the concentrations of plasma AVP and OXT, whereas serotonin decreased their plasma levels. Noradrenaline increased the concentration of OXT, but not that of AVP. Dopamine did not significantly affect the plasma level of either hormone. The release of AVP and OXT from the posterior pituitary fragments of rats was stimulated by changing the osmolality of the perfusion medium in vitro. Perfusion with medium containing dopamine suppressed the release of both hormones. However, the other bioactive amines and the drugs mentioned above did not affect the release of AVP and OXT.
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PMID:A study on the release mechanism of vasopressin and oxytocin. 323 19

The blood pressure changes and behavior of vasoactive hormones after various stimuli were studied in eighteen patients with end-stage renal disease maintained on chronic hemodialysis. Group A patients (n = 9) were not subject to intra- or post-dialysis hypotensive episodes, and Group B (n = 9) frequently had such episodes. A 500 ml hypertonic saline infusion produced no change in blood pressure in either group, despite significant rise of vasopressin levels in both. Plasma renin activity levels were similar and became appropriately suppressed by the infusion in both groups, whereas norepinephrine rose significantly only in Group A, but not Group B where it was already higher at baseline. The regular dialysis session produced, as expected, a significantly more profound hypotensive effect in Group B, but was accompanied in both groups by decrease in vasopressin and increase in plasma renin activity. Norepinephrine change differed in the two groups: it decreased in Group A as expected from its capacity to be dialyzed, but rose in several hypotensive patients in Group B, indicating appropriate response to baroreceptor stimulation and leading to an unchanged average. These findings suggest that dialysis-induced hypotensive episodes are not necessarily associated with autonomic neuropathy or with abnormal patterns of vasopressor hormone response to stimuli. They also shed new light on the factors regulating vasopressin secretion under these circumstances, since they indicate that the osmoreceptor and/or sodium-sensitive receptor may be a more dominant mechanism in the regulation of vasopressin release than the volumetric mechanism responding to fluid volume changes.
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PMID:Vasopressin in end-stage renal disease: relationship to salt, catecholamines and renin activity. 330 33

The effect of clonidine (4.5 micrograms kg-1) on haemodynamics and hormonal stress responses was evaluated in 21 female patients undergoing breast surgery. The standardized general anaesthesia included diazepam as premedicant, thiopentone, enflurane, N2O, fentanyl and vecuronium. Venous plasma concentrations of noradrenaline, adrenaline, growth hormone, vasopressin, and cortisol were assayed at various times before, during and after surgery. Clonidine attenuated the sympathoadrenal response; arterial blood pressure and heart rate increases in association with intubation were lower in clonidine-premedicated patients. Noradrenaline levels were lower throughout and 3 h after surgery in the clonidine group (P less than 0.05). Adrenaline levels were lower in this group 2 min after intubation (P less than 0.05). Growth hormone, vasopressin and cortisol plasma levels were increased at the end of and after surgery, with no differences between the groups. In spite of the effect on sympathoadrenal response, clonidine did not have any significant additive anxiolytic effect. Statistically significant differences were not found as to need for postoperative analgesics.
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PMID:Oral premedication with clonidine: effects on stress responses during general anaesthesia. 343 64

Cultured rat glomerular mesangial cells (MC) were evaluated as a tool for reliable electrophysiological measurements as well as for fluorimetric determinations of intracellular Ca++. They had a resting potential similar to that observed in cultured vascular smooth muscle cells (VSMCs), in VSMCs of mouse kidney arterioles, or in glomerular--presumably mesangial--cells of kidney slices. The comparison with the other cell types was carried out in order to look for features distinguishing them from these cells, e.g., active and passive electrical membrane properties or electrical membrane responses to vasoactive pharmacological agents. In MCs, as well as in the other cell types, the average membrane potential was approx. -50 mV. The vasoconstrictor peptides angiotensin II (ANG II) and arginine-vasopressin (AVP) caused depolarizations that could be blocked by the respective specific inhibitors of these compounds. The agonist-induced depolarizations have to be attributed, at least in part, to a Ca++ inward current. Norepinephrine, if any, had only a weak action upon MCs, whereas isoproterenol either did not influence the membrane potential or hyperpolarized the cells. Other substances tested, which had no influences upon the membrane potential, were neuropeptide Y and atriopeptin 3. As to their resting electrical properties and their responses to pharmacological agents, cultured mesangial cells did not differ from glomerular, i.e., most probably mesangial, cells in the kidney slice. The difference between mesangial cells and VSMCs consists in their reaction to noradrenaline. Whereas VSMCs respond with a marked depolarization, the noradrenaline effect upon MCs in culture and in the kidney slice is either absent or very weak. Repeated passage of the cells (more than six passages) led to a gradual loss of their responsiveness to the agonists, indicating reduced receptor expression which may be interpreted as dedifferentiation. This held for both cultured MCs and VSMCs. Fluorimetric measurements using the Ca++-specific indicators quin-2 and fura-2 were performed with a purpose-developed, ultrasensitive photon-counting microspectrofluorimeter. Individual MCs as well as isolated glomeruli responded to the vasoconstrictors ANG II and AVP with an increase in Ca++-dependent fluorescence indicating that these agents indeed depolarize the cells partly via a Ca++ influx and increase cytosolic free Ca++.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The mesangial cell culture: a tool for the study of the electrophysiological and pharmacological properties of the glomerular mesangial cell. 344 61


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