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)

The effects of norepinephrine, phentalamine, oxytocin, vasopressin, several prostaglandins, and indomethacin on the spontaneous motility of isolated guinea pig cauda epididymidis were explored. Phentolamine and indomethacin reduced the isometric peak tension of spontaneous epididymal contractions. Phentolamine also depressed the frequency. Both findings suggest that catecholamines and endogenous prostaglandins are in some way regulators of the spontaneous motility of the cauda epididymidis. Norepinephrine resulted in the development of a distinct, sustained, tonic contraction without phasic activity, whereas prostaglandins E1, E2, and F2 alpha elicited a tonic increase accompanied by frequent, superimposed, phasic contractions. Both oxytocin and vasopressin comparably enhanced epididymal motility, producing contractile responses similar to those observed with prostaglandins. Since the epididymal contractions can influence the time spent by spermatozoa in passing through the ductus epididymidis, the above-mentioned compounds could play an important role in spermatozoal transport via modulation of epididymal contractile activity. In addition, such naturally occurring substances might regulate the release of sperm from the last portion of the epididymis into the ductus deferens.
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PMID:Physiologic and pharmacologic studies on the motility of isolated guinea pig cauda epididymidis. 80 41

1 The hepatic portal vein of the anesthetized dog was cannulated and perfused with blood derived from the cannulated superior mesenteric vein. 2 The portal vein was perfused at constant flow, the hepatic portal venous pressure being monitored continuously together with the inferior vena caval pressure. From these measurements, the hepatic portal venous vascular resistance was calculated. 3 Noradrenaline and adrenaline were injected intraportally in graded doses which caused dose-dependent increases in the hepatic portal vascular resistance. At all doses, adrenaline was significantly (P less than 0.05) more potent than noradrenaline. 4 Intraportal injections of vasopressin caused reductions in calculated hepatic portal venous vascular resistance in most experiments; three effects were dose-dependent. 5 No tachyphylaxis to the effects of noradrenaline, adrenaline or vasopressin was observed. 6 Intraportal injections of angiotensin caused dose-dependent increases in calculated hepatic portal vascular resistance up to 5 mug; therafter larger doses caused smaller increases in portal resistance. 7. Repeated intraportal injections of angiotensin revealed the existence of tachyphylaxis in the hapatic portal vascular bed. 8 Intraportal infusions of anagiotensin caused rises in calculated hepatic portal vascular resistance from which there was almost complete 'escape' despite the continued infusions. Infusions of noradrenaline which caused similar rises in calculated portal vascular resistance did not exhibit equivalent degrees of 'escape'. 9 The development of tachyphylaxisx explains the fact that doses of 10 and 20 mug of angiotensin injected after 5 mug doses produced smaller effects. If a much longer time interval was allowed between injections (30 min), the dose-response curve to angiotensin had a sigmoid shape. 10 These findings are discussed with respect to their possible importance in the functional status of the hepatic portal vascular bed in this species.
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PMID:The effects of intraportal injections of noradrenaline, adrenaline, vasopressin and angiotensin on the hepatic portal vascular bed of the dog: marked tachyphylaxis to angiotensin. 83 16

Norepinephrine was continuously infused for 30 minutes at a rate of 0.2 and 0.3 mug/kg/min into 3 normal human subjects, and plasma vasopressin levels, plasma osmolality, hematocrit value, blood pressure, and heart rate were determined simultaneously. In norepinephrine infusion, an elevation of mean blood pressure and a decrease in heart rate was seen, and the degree of these changes was greater with the infusion at a rate of 0.3 mug/kg/min. Plasma vasopressin levels were suppressed by the infusion, and a dose-response relationship was recognized between the infusion at rates of 0.2 mug/kg/min and 0.3 mug/kg/min, while plasma osmolality did not change, and the hematocrit value rose slightly. These results suggest that norepinephrine-induced water diuresis is related to the suppression of the vasopressin release.
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PMID:Effect of norepinephrine infusion on plasma vasopressin levels in normal human subjects. 94 39

Retinal capillary pericytes are believed to have a contractile function and to regulate retinal blood flow at the microvascular level. Membrane potential is an important control element for contractility in smooth muscle cells. In the present study, bovine retinal capillary pericytes have been grown in tissue culture and membrane potentials have been measured using glass microelectrodes. Resting potentials averaged -31 +/- 7 mV (n = 203). Relative K+ conductance was low, with a transference number for K+ of 0.16. Readdition of K+ to K(+)-depleted cells transiently hyperpolarized the membrane potential, probably by stimulating the electrogenic Na+/K+ transport. Repetitive spike-like depolarizations (action potentials) were induced by stimulating the Na+/K(+)-ATPase, by applying norepinephrine (10(-5) mol/l), and by adding 10 mmol/l Ba2+. These action potentials depended on the presence of extracellular Ca2+ and were inhibited by the Ca2+ antagonist nifedipine (10(-6) mol/l). Norepinephrine (10(-5) mol/l) depolarized the membrane by 7.4 +/- 3.5 mV (mean +/- SD, n = 49). This response was blocked by the alpha 1-antagonist prazosin (10(-5) mol/l). Histamine also led to a membrane depolarization of 8.6 +/- 2.8 mV (n = 49), which could be inhibited by the H1-antagonist diphenhydramine. Endothelin (10(-7) mol/l), vasopressin (10(-6) mol/l), and acetylcholine (10(-4) mol/l) had no major effects on membrane potential. The conclusion is that retinal capillary pericytes are excitable cells and react to several vasoactive substances.
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PMID:Membrane potentials in retinal capillary pericytes: excitability and effect of vasoactive substances. 131 66

The role of hypothalamic paraventricular adrenoceptors and angiotensin II (ANG II)-AT 1 receptors in mediating the vasopressin (AVP) release into the plasma in response to i.c.v. and local paraventricular ANG II injections was investigated in conscious chronically instrumented rats. Noradrenaline (NA) administered bilaterally into the paraventricular nucleus (PVN) dose-dependently stimulated AVP release. Bilateral PVN microinjections of the alpha 1 adrenoceptor agonists methoxamine and phenylephrine, or of the alpha2 adrenoceptor agonist clonidine, did not affect plasma AVP when given alone, but increased plasma AVP when methoxamine and clonidine were given in combination. In contrast, PVN microinjections of both the beta 1 adrenoceptor agonist dobutamine and the beta 2 adrenoceptor agonist salbutamol significantly reduced basal plasma AVP. Bilateral PVN pretreatment with the alpha 1 and alpha 2 adrenergic antagonists prazosin, idazoxan and rauwolscine, but not of the beta 1 and beta 2 adrenoceptor antagonists atenolol and ICI 118 551, significantly attenuated the i.c.v. ANG II-induced AVP release. ANG II injected bilaterally into the PVN dose-dependently increased plasma AVP. Bilateral PVN pretreatment with the specific ANG II-AT 1 receptor antagonist losartan partially inhibited the i.c.v. ANG II-induced AVP release. We conclude: 1) Beta 1 and beta 2 adrenoceptors in the PVN exert an inhibitory action on basal AVP secretion. 2) ANG II can release AVP by directly stimulating its ANG II-AT 1 receptors in the PVN. 3) PVN mediated AVP release in response to periventricular ANG II-AT 1 receptor stimulation is at least partially effected through ANG II-AT 1 receptors in the PVN impinging on alpha adrenergic terminals.
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PMID:Involvement of adrenergic and angiotensinergic receptors in the paraventricular nucleus in the angiotensin II-induced vasopressin release. 146 31

The noradrenergic innervation of vasopressin (VP)-containing neurons in the supraoptic nucleus (SON) of the rat hypothalamus was studied electron microscopically by using double-labeling immunocytochemistry combining the pre-embedding peroxidase-anti-peroxidase method with post-embedding immunocolloidal gold staining. Noradrenaline-like immunoreactive axon terminals were found to make synaptic contacts with neurophysin II-like immunoreactive neurons in the SON. This provides morphological evidence for noradrenergic control of neuronal activity of VP-containing neurons at the SON level.
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PMID:Noradrenergic innervation of vasopressin-containing neurons in the rat hypothalamic supraoptic nucleus. 150 81

It is well established that muscarinic cholinergic receptors are linked to phosphoinositide hydrolysis in brain. Previous studies of muscarinic responses used Li+ to increase inositol phosphate accumulation and suggested little or no change during aging. Li+ disrupts certain aspects of the inositol phosphate metabolism and inhibits the formation of inositol 1,3,4,5-tetrakisphosphate [Ins(1,3,4,5)P4]. Ins(1,3,4,5)P4 appears to have second messenger functions. To investigate the effects of aging on agonist stimulated Ins(1,3,4,5)P4 formation, young (6-8 months) and old (28-30 months) Fischer 344 rat cerebral cortical or hippocampal slices were challenged with various agonists known to stimulate phosphoinositide hydrolysis in brain using a recently developed assay that does not use Li+. Carbachol and quisqualate stimulated [3H]inositol trisphosphate ([3H]InsP3) and [3H]Ins(1,3,4,5)P4 formation in young and old rat cerebral cortical slices. Norepinephrine, 5-hydroxytryptamine, and vasopressin failed to stimulate [3H]Ins(1,3,4,5)P4 or [3H]InsP3 formation in either young or old rat cerebral cortical slices. In old rat cerebral cortical slices, the carbachol-stimulated [3H]Ins(1,3,4,5)P4 formation was reduced by 44%. Angiotensin II stimulated [3H]InsP3 was increased (219%) in old rats. There was no influence of aging either on the basal level or on the maximal response to carbachol or quisqualate in hippocampal slices. These studies suggest region-specific changes in phosphoinositide hydrolysis during aging.
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PMID:Decreased carbachol-stimulated inositol 1,3,4,5-tetrakisphosphate formation in senescent rat cerebral cortical slices. 150 2

Atrial stretch and paracrine hormones stimulate atrial natriuretic peptide (ANP) secretion. The potential interplay between atrial stretch and paracrine hormones was examined. Isolated superfused rat left atria paced at 4 Hz were used for study. The effects of 0, 0.5, and 1.5 g settings of initial tension on the ANP secretory response to 1 microM norepinephrine and 10 nM endothelin were examined. The peak ANP secretory responses expressed as a percent of baseline for each of the tension settings were 109 +/- 8, 132 +/- 6, and 171 +/- 10% for norepinephrine and 285 +/- 15, 294 +/- 12, and 368 +/- 19 for endothelin, respectively. The effects of 0.5 microM norepinephrine, 1 nM endothelin, and 100 nM vasopressin on stretch-stimulated secretion were examined. Norepinephrine and endothelin increased ANP secretion 144 +/- 16 and 136 +/- 2% above baseline, respectively. Vasopressin did not increase ANP secretion. Norepinephrine and vasopressin did not significantly influence the ANP secretory response to stretch. In contrast, endothelin increased the response to stretch by 33% (P less than 0.035). We conclude 1) the greater the degree of atrial stretch, the greater is the response to norepinephrine and endothelin; 2) endothelin enhances the secretory response to stretch; and 3) norepinephrine and vasopressin do not affect stretch-stimulated release. These results predict a greater ANP secretory response to hormonal stimulation in vivo in volume-expanded states.
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PMID:Interaction between stretch and hormonally stimulated atrial natriuretic peptide secretion. 153 Nov 4

A comprehensive study of monoamine transmitter and metabolite concentrations measured by HPLC was undertaken in female (vasopressin-deficient) Brattleboro rats as compared to Long Evans rats. Noradrenaline was significantly increased in 8 out of 13 dissected brain regions, whereas concentrations of the metabolite 3-methoxy-4-hydroxyphenylglycol were not altered. The increases were not restricted to areas which are normally innervated by vasopressin-containing neurons. Serotonin was increased in 6 and dopamine in 4 regions and this was accompanied in some areas by increases in the metabolites 5-hydroxyindolacetic acid and dihydroxyphenylacetic acid. Only in the striatum, cerebellum, and the medulla-pons no changes could be detected in any of the compounds of interest. These results show that the long term absence of vasopressin in Brattleboro rats appears to be associated with increases in monoamine transmitter contents and decreased metabolite/transmitter ratios. The regional distribution of these changes does not bear any relationship to the regional distribution of vasopressin cell bodies or nerve endings.
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PMID:Widespread alterations in central noradrenaline, dopamine, and serotonin systems in the Brattleboro rat not related to the local absence of vasopressin. 169 74

Studies were conducted to clarify the effects of noradrenaline on oleate metabolism in isolated hepatocytes from fed rats. Noradrenaline caused an inhibition of ketogenesis from oleate along with a stimulation of glucose release through alpha 1-adrenergic receptors. Anti-ketogenic action of noradrenaline was confirmed by the suppression of the formation of radioactive acid-soluble products from [1-14C]oleate in response to this agent. Noradrenaline increased the conversion of [1-14C]oleate into 14CO2 but failed to affect [1-14C]oleate esterification. When hepatocytes were incubated in a medium containing 1 mM EGTA but no Ca2+, the effects of noradrenaline on oleate oxidation were negated. On the other hand, noradrenaline-induced increase in glucose release remained unchanged even in the absence of Ca2+ in the incubation medium. Decrease in ketogenesis and increase in glucose release produced by vasopressin was completely abolished by calcium depletion. Noradrenaline caused a significant increase in cAMP levels in both the presence and absence of Ca2+, although the effect was more marked in the latter. Vasopressin did not affect it. The noradrenaline-induced increase in cAMP and glucose release in the absence of Ca2+ was also mediated by alpha 1-adrenergic receptors. These data are discussed and it is suggested that alpha 1-adrenergic agonists may control hepatic ketogenesis and glycogenolysis through two separate signal transduction mechanisms, i.e., a calcium-mobilizing system which is common with vasopressin, and a cAMP generation system which vasopressin lacks.
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PMID:Alpha 1-adrenergic regulation of ketogenesis in isolated rat hepatocytes. 184 21


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