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)

A method was devised for the perfusion of the cerebral ventricles in conscious rats. Using this method a basal secretion rate of 15 +/- 3 pg of immunoreactive angiotensin II per min was calculated. This material was suggested to be of extrarenal origin. In comparison to findings in normal Long-Evans rats, pressor responses to intraventricular perfusions of angiotensin II were reduced in rats heterozygous for hypothalamic diabetes insipidus and virtually absent in rats homozygous for the hypothalamic deficiency whether they were treated with vasopressin or not. The pressor response to intraventricular angiotensin II is suggested to be related to the release of vasopressin.
Endocrinology 1976 Sep
PMID:Pressor action of centrally perfused angiotensin II in rats with hereditary hypothalamic diabetes insipidus. 95 71

Neurohypophyseal dispersions and fractions enriched for neurosecretosomes and pituicytes were prepared from rats subjected to 6 days of water deprivation and 9-10 days of lactation as stimuli of the hypothalamo-neurohypophyseal system (HNS). After water deprivation the content of the fractions changed in such a way that the neurosecretosomes, and to a lesser extent also the pituicytes, accumulated at a lower density within the gradient used for separation. Stimulation by means of lactation did not show such changes when a comparison was made with dioestrus. Microchemical and histochemical tests for acid phosphatase showed that most of the activity in the controls was present in the neurosecretosomes. A rough calculation, which takes into account the different yields for the dispersion elements, showed a rather equal distribution for acid phosphatase activity between axonal and pituicytic compartments of the intact neurohypophysis. The known acid phosphatase activity response of the neural lobe after HNS stimulation, which was also detectable in the dispersion, resulted histochemically in an increased staining intensity for both neurosecretosomes and pituicytes, but with microassay it was distributed along a gradient similar to oxytocin. It was therefore concluded that this lysosomal enzyme response within the neurophypophysis is preferentially localized in the neurohypophysis is preferentially localized in the neurosecretory axons.
Brain Res 1976 Sep 17
PMID:Acid phosphatase in rat neurohypophyseal dispersions and its fractions enriched for neurosecretosomes and pituicytes after water deprivation and lactation. 96 51

The effects of infusions of PGE1 (30 ng/kg min-1) into the lateral cerebral ventricle were studied in the conscious, hydrated goat. The infusions caused release of antidiuretic hormone and increased renal sodium excretion. When PGE1 was infused together with hypertonic NaCl these effects became markedly enhanced and the infusion also induced drinking and a rise in the arterial blood pressure. Much weaker effects were obtained by the infusion of the hypertonic NaCl alone. This sodium-PGE1 interaction is discussed in relation to previously observed, central sodium-angiotensin II interaction. A more pronounced drinking effect was obtained in response to the intraventricular infusion of PGE1 + angiotensin II, than to the infusion of either substance separately. The PGE1 administered into the lateral cerebral ventricle did not induce any febrile response.
Acta Physiol Scand 1976 Sep
PMID:Influence of prostaglandin E1 on cerebral mechanisms involved in the control of fluid balance. 97 Jan 60

Unanesthetized dogs were infused with heterologous (hog) renin at 0.33 Goldblatt U/kg per h for 2 h, once normally hydrated and once after 48 h of dehydration. Dehydration increased the average plasma osmolality from 306 to 322 mosmol/kg, the plasma renin activity (PRA) from 0.5 to 1.4 ng/ml per h, and the plasma antidiuretic hormone (ADH) concentration from 1.7 to 3.7 muU/ml, although the latter was not statistically significant. Renin infusion resulted in approximately the same average PRA, about 10 ng/ml per h, in both states of hydration. Mean arterial blood pressure increased during renin infusion in both states of hydration, although the increase was greater when the dogs were normally hydrated. There was no apparent effect of renin infusion on plasma ADH concentration when the dogs were normally hydrated, but in the dehydrated state renin infusion was accompanied by an increase from 3.7 to 6.3 muU/ml in plasma ADH concentrations after 80 min of infusion. There were no apparent changes in plasma osmolality or sodium or potassium concentrations due to the renin infusions; however, plasma osmolality and potassium concentration decreased during the course of the experiment. The results suggest a possible role for the renin-angiotensin system of renin released by the kidney in the control of ADH during dehydration. The metabolic clearance rate of the hog renin was 37 ml/min-kg.
Am J Physiol 1976 Sep
PMID:Effect of dehydration on stimulation of ADH release by heterologous renin infusions in conscious dogs. 97 Apr 47

1 The influence of potassium loading on the renal excretion of sodium, potassium and solute during high rate vasopressin administration has been investigated in sheep. 2 Adrenalectomized sheep were infused with 0.43 M KCl at 2 ml/min for 2-2.5 hours. Coincident with the rise in plasma potassium concentration, the urinary excretion of sodium, potassium, solute and water was increased as was the reabsorption of solute-free water. The rates of urinary excretion of sodium and potassium, osmolal clearance (COsm) and solute-free water reabsorption (TcH2O) for the first 50 min of potassium infusion were each found to be linearly related to the plasma potassium concentration. 3 After 50 min an infusion of vasopressin at 1 or 4 mu/min was superimposed on the potassium infusion for a period of 30 minutes. The administration of vasopressin was consistently associated with further augmentation of potassium excretion and clearance, of osmolal clearance and of solute-free water reabsorption to values above those anticipated from the pre-vasopressin regression lines for these parameters. Urinary sodium showed a coincident depression in the rate of excretion and clearance during the same period. 4 Thirty to fifty minutes after the cessation of vasopressin infusion the potassium and sodium excretions had returnied to values which approximated the pre-vasopressin relations between plasma potassium and the urinary excretions of these ions. 5 Both rates of vasopressin infusion were equally effective in increasing the potassium clearance. Any differences in clearance between the two rates of vasopressin administration were not statistically significant. 6 The large increments in potassium excretion (averaging greater than 40%) were interpreted as indicating that, when vasopressin is present at high concentrations, the distal tubule is one site of action of the hormone in the nephron of sheep.
Br J Pharmacol 1976 Sep
PMID:The effect of high rates of vasopressin administration on renal potassium and sodium excretion during potassium loading in the sheep. 97 79

Recent data on various environmental stressors and blood hormone patterns are presented for lactating cattle. Known stressor effects of such factors as environmental temperature, air pollution, and noise on the plasma thyroxine, growth hormone, cortisol, prolactin, progesterone, luteinzing hormone, epinephrine, and norepinephrine of lactating cattle are discussed. Information on stressor effects is lacking on glucagon, insulin, vasopressin, calcitonin, oxytocin, thyrotrophic hormone, follicle stimulating hormone, melatonin, parathyroid hormone, and estrogens in the lactating cow. The importance of evaluating both the effect of environmental stressor and of production or lactation intensity is emphasized in the overall interpretation of changes in hormone of plasma. The short and long term environmental heat effects on thyroxine, cortisol, and growth hormone are clear with initial increased due to acute stressors and a decline of amounts in plasma after prolonged exposure to stressors. The relationship of amounts in plasma of these hormones to milk production appears to be related directly for cortisol, growth hormone, and prolactin with an inverse relationship with thyroxine. Epinephrine and norepinephrine seem to be elevated with prolonged environmental heat stress. However, the influence of intensity of lactation has not been measured. Hormones in plasma as they relate to stressor effects and milk production are important as potential indicators of the physiological state of a cow and reflect the physiological compensations a cow undergoes at various lactation intensities and/or stress exposure.
J Dairy Sci 1976 Sep
PMID:Effects of environmental and other stressors on blood hormone patterns in lactating animals. 98 81

1. The rat hypothalamus (containing the supra-optic nuclei, paraventricular nuclei, median eminence and proximal pituitary stalk) has been incubated in vitro and shown to be capable of releasing the neurohypophysial hormones, oxytocin and arginine vasopressin, at a steady basal rate about one twentieth that of the rat neural lobe superfused in vitro. 2. The hypothalamus and neural lobe in vitro released both hormones in a similar arginine vasopressin/oxytocin ratio of about 1-2:1. However, when release was expressed relative to tissue hormone content, the hypothalamus was shown to release about three times as much arginine vasopressin and six times as much oxytocin as the neural lobe. 3. Dopamine in a concentration range of 10(-3)-10(-9)M caused graded increases in hormone release from the hypothalamus in vitro to a maximum fivefold increase over preceding basal levels. The demonstration that apomorphine also stimulated hormone release whereas noradrenaline was relatively ineffective suggested that a specific dopamine receptor was involved. A separate cholinergic component in the release process was indicated by the finding that acetylcholine stimulated release to a maximum fivefold increase in concentrations of 10(-3)-10(-9)M. 4. The fact that the isolated hypothalamus can be stimulated by dopamine and acetylcholine to release increased amount of oxytocin and arginine vasopressin raises the question of the origin and fate of the hormones released in this way. The possibility that they could be released into the hypophysial portal circulation from median eminence to affect the anterior lobe of the pituitary is discussed. 5. In similar doses, both dopamine and noradrenaline injected into the lateral cerebral ventricles of the brain of the anaesthetized, hydrated, lactating rat caused the release of arginine vasopressin and oxytocin. Apomorphine release both hormones but at a higher dose level and to less effect than the catecholamines. 6. The hormone release induced in vivo by dopamine could be prevented by the prior administration of haloperidol or phentolamine and these antagonists were equally effective in blocking the hormone release due to noradrenaline. The involvement of a specific dopamine receptor was more clearly implicated by the use of pimozide which completely inhibited the hormone release due to dopamine and apomorphine but not that due to noradrenaline. 7. It is suggested that the release of neurohypophysial hormones can be stimulated via a dopaminergic nervous pathway in addition to a cholinergic one. The possibility that the osmoreceptor mechanism for the release of antidiuretic hormone from the neural lobe of the pituitary may involve such a dopaminergic pathway is discussed.
J Physiol 1976 Sep
PMID:The effect of dopamine on neurohypophysial hormone release in vivo and from the rat neural lobe and hypothalamus in vitro. 98 83

Injection of posterior pituitary powder induces an intense mitotic stimulation in the zona glomerulosa of the adrenal gland of young rats. This effect is much more pronounced in females than in males. It is maximal at two days treatment. Longer periods result in a hypertrophied zona glomerulosa and lower mitotic activity. A search for the hormone responsible for the stimulation shows that vasopressin, and to a lesser extent oxytocin, are mitogenic. ACTH, alpha-MSH, beta-MSH and the pineal hormones have no effect. Renin (but not angiotensin) induces a significant stimulation. It is concluded that vasopressin exerts a potent influence on the glomerulosa. This is in contrast with the prevalent view that the glomerulosa is little affected by the hypophysis.
Cell Tissue Res 1976 Sep 06
PMID:Adrenal glomerulosa mitotic stimulation by posterior pituitary hormones. 99 Dec 6

Females from two inbred strains of chickens, one normal and one having hereditary diabetes insipidus, were treated with five levels (2.5, 1.0, 0.5, 0.25, and 0.1 units) of Schwartz-Mann (Grade A, 100 units/mg.) arginine vasotocin via ic. injections at 2-hr. intervals. Paired sibs, one normal and one having diabetes insipidus (di), from an F2 population were used in one experiment to compare responses at the level of 2.5 units. Only di females were used for the remaining four levels of treatment. Water intake was determined every two hours and calculated as a percentage of water (ml.)/body wt. Results show that hereditary diabetes insipidus in chickens is arginine vasotocin-sensitive at the 0.5 unit and higher levels. The genetic defect appears to affect the quantity of antidiuretic hormone produced.
Poult Sci 1976 Sep
PMID:Influence of arginine vasotocin on a genetically determined excessive appetite for water in chickens. 99 8

Basic physiology and pathophysiological mechanisms of renal concentrating ability and its defects are discussed. Normal urinary concentration depends on the concerted action of a variety of factors. Consequently, many different causes may underly the symptom of polyuria. Clinical tests of concentrating ability (water deprivation, pitressin test) are of diagnostic importance in diabetes insipidus and polydipsia, but have little practical value in the work-up for chronic renal disease. A critical analysis of maximal concentrating capacity (TcH2O) during induced osmotic diuresis is conducted. It is inferred that the height and shape of the normal TcH2O curve results basically from two physiological processes: It is raised by increasing NaCL transport out of the medullary parts of the ascending limbs of Henle's loops and lowered by influx of hypotonic tubular urine into the collecting ducts. Preponderance of hypotonic influx may result in hypotonic final urine in the absence of tubular functional abnormalitiy. It is not appropriate, therefore, to classify renal concentrating defects according to the shape and height of the TcH2O curve. A synopsis and short description of the known renal concentrating defects is given. They are classified into hereditary, metabolic, diuretic-induced, and toxic disturbances, as well as those seen in renal disease of various etiology. Each defect is discussed in terms of the underlying pathophysiological mechanism as far as currently understood. The most important mechanisms are either disturbed NaCL transport in the ascending limb of Henle's loop, or antidiuretic hormone (ADH) dependent or ADH independent decrease in water permeability of the enddistal convolutions and collecting ducts, or osmotic diuresis.
Schweiz Med Wochenschr 1976 Sep 11
PMID:[Diagnosis and pathophysiology of renal concentration disorders]. 100 42


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