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)

dl-Propranolol (0.8-1.6 mg/kg - h for 1 h) produced a transient two- to three-fold increase in sodium excretion in nondiuretic rats infused with Pitressin and aldosterone and in water diuretic rats. Sodium excretion increased more in rats depleted of renin by chronic Doca and salt administration than in rats maintained on a low salt diet. An angiotensin inhibitor (1,sarcosine-8,valine angiotensin II) decreased sodium excretion. Therefore the natriuresis was not mediated by antidiuretic hormone, aldosterone, or renin-angiotensin. d-Propranolol did not produce a natriuresis. Prior treatment with phenoxybenzamine did not prevent the natriuretic response but chlorisondamine pretreatment did. The natriuresis is produced by beta blockade and requires post ganglionic nerve function but is independent of alpha receptors. dl-Propranolol decreased heart rate and cardiac output but systemic pressure did not fall and renal blood flow increased. This suggests a dopamine-mediated renal vasodilation and natriuresis. Haloperidol and pimozide, both dopamine blocking agents with minimal beta blocking effects, prevented the natriuretic response. We conclude that propranolol may increase sodium excretion directly by blocking beta receptors in the distal nephron and indirectly by dopamine-mediated renal vasodilation.
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PMID:Propranolol induces acute natriuresis by beta blockade and dopaminergic stimulation. 1 Oct 39

The action of prostacyclin (PGI2) on arterial pressure, heart rate, plasma concentration of angiotensin II and vasopressin was studied in groups of normal, renal hypertensive and DOC hypertensive rats. PGI2 was given by continuous iv. infusion at successive doses of 0.25, 0.5 and 1.0 microgram/kg x min, each rate for one hour. Arterial pressure was reduced to normal or below normal in the hypertensive rats, though the fall of blood pressure was greatest in the DOC hypertensive animals. Mean arterial pressure at the end of infusion was 89 mm Hg for normal rats, 87 mm Hg for renal hypertensive rats and 69 mm Hg for DOC hypertensive rats. Diastolic pressure fell more than systolic pressure suggesting a vasodilator mechanism. Heart rate was reduced significantly at the end of the infusion in the three groups of rats. Prostacyclin was also infused for 3 hours at a constant rate of 0.5 microgram/kg x min. The arterial pressure lowering effect was maintained throughout the infusion period.
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PMID:The vasodepressor action of prostacyclin (PGI2) and its effect on plasma angiotensin II and vasopressin in unanaesthetized normotensive and hypertensive rats. 39 17

Studies on the vasopressor role of the antidiuretic hormone arginine-vasopressin (AVP) in DOC hypertension, in two-kidney Goldblatt hypertension, and in spontaneous hypertension of rats, and during acute blood pressure elevation after intracerebroventricular injection of angiotensin II and in glycerol-induced acute renal failure of rats are reviewed. For the measurement of plasma AVP a radioimmunoassay has been developed. For this assay, a series of criteria has been met which allows the conclusion that, in plasma of rats, the antibody measures AVP only. For the blockade of vasopressor effects of AVP a specific antiserum has been used. On the basis of a series of control studies it has been concluded, but not proven that the antiserum lowers blood pressure exclusively by blockade of AVP. It could be shown that in the various animal models of hypertension and of acute blood pressure elevation AVP exerts systemic vasoconstriction when its plasma concentrations are elevated. In those models where the renin-angiotensin system played no role in blood pressure control, the height of blood pressure was closely related to the plasma AVP concentrations. When this relationship was compared with that obtained after the i.v. infusion or injection of AVP, a marked shift to the left became apparent. Hence, sensitization to the vasopressor effect of AVP had occurred, the factor of sensitization amounting to more than 1,000. It is concluded that AVP is not only an antidiuretic hormone but also a vasopressor hormone, and that any systemic vasopressor effect of AVP requires a mechanism of sensitization.
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PMID:Neurohypophyseal vasopressor principle: vasopressor hormone as well as antidiuretic hormone? 73 54

Atrial natriuretic factor (ANF) is widely distributed in the preoptic area and the hypothalamus, it is present there both in cell bodies and nerve terminals. Effect of experimental alterations in the salt and water balance was examined on preoptic-hypothalamic ANF levels measured in ten microdissected nuclei. Immunohistochemical analysis was also performed to confirm radioimmunological results. Following interventions were performed in adult male rats: adrenalectomy (5 days), daily 0.9% NaCl, aldosterone (5 micrograms/100 g) and dexamethasone (2 micrograms/ml drinking water) treatments in both intact and adrenalectomized groups, and in rats with diabetes insipidus (Brattleboro rats) and DOC-salt hypertension. Although no appreciable alterations were observed in the intensity of ANF-like immunoreactivity in sections of the preoptic-hypothalamic region, ANF levels altered markedly in the periventricular structures (organum vasculosum laminae terminalis, preoptic and periventricular nuclei). Little or no changes were measured in ANF levels of other hypothalamic nuclei (except the perifornical nucleus). Adrenalectomy depleted ANF levels which were restored by NaCl drinking. Aldosterone elevated ANF concentrations both in intact and adrenalectomized animals while dexamethasone treatment was without any significant effect on ANF levels in the periventricular preoptic nucleus. Diabetes insipidus or DOC-salt hypertension had little or no effect on ANF levels in this brain area. Unchanged ANF concentrations were also measured in the vasopressin-containing supraoptic nucleus following adrenalectomy or in diabetes insipidus rats.
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PMID:Atrial natriuretic factor in central nervous system regulatory mechanisms: effect of experimental alterations in water and salt homeostasis and blood pressure. 214 14

Following our previous report that development of DOC-salt hypertension is attenuated in female rats, we have now determined the effects of gonadectomy on the pathogenesis of this model of hypertension. Male and female rats were gonadectomized at age three weeks, and the DOC-salt protocol was initiated two weeks later and continued for three weeks. In intact rats, hypertension developed more rapidly and to a higher level in males than in females. By contrast, in gonadectomized rats, there was no sex difference in blood pressure because the development of hypertension was attenuated in males and exacerbated in females. None of these differences could be attributed to differences in either saline consumption or vasopressin release since no differences were found among the groups for either variable. Although the underlying mechanisms are uncertain, our results clearly show that the gonadal hormones affect the development of DOC-salt hypertension in the rat.
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PMID:Gonadectomy abolishes the sexual dimorphism in DOC-salt hypertension in the rat. 280 61

The effect that several substances may have on ANF release by atrial slices and on its tissular content was investigated. alpha- and beta-adrenergic and cholinergic agonists, vasopressin, met-enkephaline, dexamethasone and DOC, in concentration ranging from 10(-4) to 10(-8) M, were added into the incubation media and incubated 1 and 4 hours. No changes were observed in ANF concentration either in the media or in its tissular concentration as measured by a specific radioimmunoassay. When intact rats were previously treated with DEXA, DOC or DEXA + DOC and their atria incubated "in vitro", an increase in the release of ANF was observed in the Dexa-treated group only, but all treated groups had higher tissular ANF concentration. It is concluded that neither alpha- or beta-adrenergic, nor cholinergic agonists or vasopressin and met-enkephaline stimulate ANF release "in vitro". On the other hand steroids may regulate ANF release and synthesis in the intact rat. It seems likely that the ANF released into the media corresponds to a short peptide.
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PMID:Mechanisms of release of atrial natriuretic factor. I. Effect of several agonists and steroids on its release by atrial minces. 293 80

A Golgi-Cox study was undertaken to determine whether enhanced electrical activity was associated with any morphological changes in the dendrites of the magnocellular neurones in the hypothalamic supraoptic nucleus. Brattleboro rats, animals dehydrated by administration of 2% sodium chloride solution instead of drinking water and animals given 1% sodium chloride solution and deoxycortone to induce vasopressin-dependent hypertension were compared with controls. In each of the stimulated groups, the cell bodies were hypertrophied implying that the stimuli were effective. Dendritic span (the area of a triangle drawn round, and containing the entire Golgi-stained dendritic tree) was significantly increased (p less than 0.01) in Brattleboro rats but was decreased by sodium chloride-induced dehydration (p less than 0.01). Deoxycortone treatment reversed the reduction induced by dehydration. Hippocampal cells showed no significant differences. Thus, the cells of the magnocellular system rapidly alter their morphology when stimulated but the changes are more complex than a simple hypertrophy associated with enhanced activity.
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PMID:Stimulus-related changes in the dendrites of magnocellular neurones. 340 52

To investigate the possible role of vasopressin (VP) in the maintenance of DOC-salt hypertension the effect of two VP pressor antagonists on mean arterial pressure and the pressor responsiveness to exogenous VP were studied in conscious, freely moving rats with malignant DOC-salt hypertension. Intravenous injections of either 20 micrograms/kg of dP Tyr(Me)AVP or 10 micrograms/kg of d(CH2)5Tyr(Me)AVP had no significant effect on mean arterial pressure and heart rate, although both antagonists almost completely abolished the pressor response to VP. Furthermore, the animals with DOC-salt hypertension exhibited decreased pressor responsiveness to exogenous VP. The present findings strongly suggest that VP is not essential as a pressor hormone for maintaining blood pressure in malignant DOC-salt hypertension.
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PMID:Evidence against a vasopressor role of ADH in malignant DOC-salt hypertension. 384 Oct 34

1. The responses of the mean arterial pressure to (-)-noradrenaline, tyramine, angiotensin II-val(5)-amide, vasopressin and rat renin have been contrasted in renal hypertensive and in salt plus desoxycorticosterone hypertensive rats. The responses were measured in rats both unanaesthetized and rats anaesthetized with pentobarbitone.2. Responses of unanaesthetized, ganglion blocked renal hypertensive rats to noradrenaline, tyramine and vasopressin markedly exceeded, and to angiotensin II and renin were markedly smaller than, those of unanaesthetized ganglion blocked salt + DOC hypertensive animals. Responses to angiotensin and to renin were apparently enhanced in the latter animals.3. Hydrochlorothiazide and frusemide markedly reduced mean arterial pressure in salt + DOC hypertensive rats before and after ganglionic blockade.4. Neither diuretic caused significant reduction in the mean arterial pressures of unanaesthetized, renal hypertensive rats in the absence of ganglionic blockade: frusemide did so in anaesthetized and unanaesthetized rats after ganglionic blockade.5. Whereas the diuretics did not affect the responses of the renal hypertensive rats to pressor agents, frusemide and to a lesser extent hydrochlorothiazide tended to depress the responses to pressor agents in salt induced hypertension.6. Hydrochlorothiazide did not influence mean arterial pressure in unanaesthetized rats with neurogenic hypertension.
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PMID:Responses of mean arterial pressure to pressor agents and diuretics in renal hypertensive and salt hypertensive rats. 432 21

The effects of various hormones on the urinary excretion of kallikrein and esterase A2 were studied in rats. Chronic treatment with antidiuretic hormone had no effect on the excretion of either enzyme. Deoxycorticosterone treatment or a low sodium diet stimulated urinary kallikrein excretion (as is well known), but had no effect on urinary esterase A2. Dexamethasone markedly suppressed the excretion of both kallikrein and esterase A2 and increased the excretion of proteins (inhibitors) that bind to each of these enzymes. It is likely that the suppressive effect of glucocorticoid on urinary kallikrein and esterase A2 activities is due to the increase in urinary binding proteins. There is also a strong correlation between the excretion of kallikrein and esterase A2 in normal untreated rats. Such a correlation might arise from a common effect of glucocorticoid-influenced inhibitors on both enzymes.
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PMID:Hormonal effects on kallikrein, esterase A2, and their inhibitors in rat urine. 619 92


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