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 rapid method for isolating highly purified rat liver plasma membrane vesicles using isotonic medium and Percoll self-forming gradient centrifugation is described. The vesicles were characterized by enzyme markers and electron microscopy. The method also yielded a fraction rich in nuclei. The vesicles transported Ca2+ in an ATP-dependent manner and this was enhanced by oxalate. The Vmax for Ca2+ uptake was 0.65 +/- 0.08 nmol/mg X min, which was approximately 18-fold higher than for other liver plasma membrane preparations, and the Km for Ca2+ was 5.2 +/- 0.4 nM. Calcium uptake was inhibited by 40-50% in vesicles isolated from rat livers perfused for 3 min with 10(-7)M vasopressin. The half-maximally effective concentration of vasopressin was 5 X 10(-10)M which correlates with that for raising cytosolic Ca2+ and phosphorylase a. Inhibition was not significant in vesicles from livers perfused with vasopressin for only 1 min, indicating that inhibition of the Ca2+ pump may not be involved in the rise in cytosolic Ca2+ observed at 1-2 s with this hormone. Epinephrine (10(-5)M) and angiotensin II (10(-7)M) inhibited Ca2+ uptake by 31 +/- 10 and 26 +/- 5%, respectively, at 3 min. Glucagon (10(-7)M) had no effect. It is proposed that the inhibitory action of the Ca2+-dependent hormones on the plasma membrane Ca2+ pump plays an important role in the actions of these hormones by prolonging the elevation in cytosolic Ca2+.
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PMID:Vasopressin-, angiotensin II-, and alpha 1-adrenergic-induced inhibition of Ca2+ transport by rat liver plasma membrane vesicles. 669 8

Adrenaline (through alpha 1-adrenoceptors), vasopressin and angiotensin II stimulate mitochondrial glutaminase activity. This stimulation probably contributes to the ureogenic effect of these hormones. The activity of the enzyme is sensitive to Ca2+ depletion. A role of Ca2+ in hormonal modulation of glutaminase activity is suggested.
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PMID:Hormonal stimulation of mitochondrial glutaminase. Effects of vasopressin, angiotensin II, adrenaline and glucagon. 687 Aug 14

The effect of pulsatile flow during cardiopulmonary bypass on the hormonal stress response was studied in 26 patients. Thirteen had routine and 13 had pulsatile bypass with an average pulse pressure of 30 mm Hg. Plasma vasopressin levels were significantly elevated during bypass in both groups, but were lower with pulsation (66 +/- 11 vs 36.3 pg/ml, p less than 0.05). Epinephrine levels increased in both groups during bypass, but were higher after bypass (1179 +/- 448 vs 713 +/- 140 pg/ml, p less than 0.05) and in the recovery room (1428 +/- 428 vs 699 +/- 155 pg/ml, p less than 0.05) in the nonpulsatile group. The same response was noted in the norepinephrine levels (924 +/- 225 vs 465 +/- 90 pg/ml, p less than 0.05; 1015 +/- 491 vs 717 +/- 112 pg/ml, p less than 0.05). There were no significant changes in renin activity in either group, but the increase after cardiopulmonary bypass was greater in the nonpulsatile group (2.0 +/- 0.7 vs 1.36 +/- 0.4 ng/ml/hr, NS). These data suggest that pulsatile flow significantly attenuates the vasopressin and catecholamine stress response to cardiopulmonary bypass. This may explain the increased flow requirements and better tissue perfusion and organ function and the decreased incidence of postoperative hypertension after bypass using pulsatile flow.
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PMID:Attenuation of the stress response to cardiopulmonary bypass by the addition of pulsatile flow. 702 45

Osmotic control for vasopressin release has been recognized for several years. Further understanding of factors affecting the sensitivity and threshold of ADH release has been advanced by the technological development of a sensitive radioimmunoassay. Evidence suggesting that ADH secretion is also mediated by nonosmotic stimuli involving a separate anatomic pathway from the hypothalamic osmoreceptor has been well documented. Experimental results suggest that the parasympathetic afferent pathways from both "high" and "low" pressure receptors constitute the most important nonosmotic pathways for ADH release. Factors such as hypoxia, altered hemodynamic states, alpha- and beta-adrenergic stimuli, nicotine, adrenal insufficiency, and advanced hypothyroidism are likely examples which activate this nonosmotic pathway. Clarification of the exact interrelationship between the osmotic and nonosmotic release of ADH needs further examination, particularly in the area of central neurotransmitters. However, available information allows for the proposal of a model of this interaction and its clinical implications which may explain many cases of "reset osmostat." Recent available data also provide support for ADH playing a role in the maintenance of blood pressure under certain circumstances. Like other potent vasoconstrictors, preliminary evidence suggests that ADH requires transcellular calcium influx for its vascular effects. Adrenal, thyroid, and edematous disorders have all been shown to be associated with abnormal water excretion. The results of recent studies indicate that these abnormal physiological states have impaired water excretion as a result of both nonosmolar factors stimulating ADH release and intrarenal factors, including diminished glomerular filtration rate or increased proximal tubule reabsorption which lead to decreased distal fluid delivery to the diluting segment of the nephron. Verney's original studies demonstrating the osmoreceptor regulation of ADH release remain a milestone in renal physiology. In the past decade, considerable new information about nonosmotic regulation of ADH has led to further understanding of renal water regulation in health and disease; nevertheless, many of these answers have only stimulated the imagination to ponder even more questions.
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PMID:The physiology of vasopressin release and the pathogenesis of impaired water excretion in adrenal, thyroid, and edematous disorders. 724 4

The effects of adrenaline (A) upon waterdiuresis were studied in conscious, hydrated goats, provided with a permanent cannula into the 3rd ventricle. Adrenaline induced a reduction in urinary volume and in free water clearance and a rise in the osmolality of the urine. These effects were dose-dependent and significant. A biphasic Cl-excretion pattern, consisting op of an initial fall below control level and a subsequent increase was observed. Na+ and K+ excretion rates were reduced. Central pretreatment with phentolamine completely antagonized the antidiuretic action of A. Propranolol, atropine and hexamethonium were ineffective. Alpha-adrenoceptors might be involved in vasopressin release.
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PMID:Antidiuretic effects of intracerebroventricular infusion of adrenaline in conscious goats. 727 75

The mechanisms by which elevated levels of vasopressin (ADH) in man and animals cause serious myocardial dysfunction, evidenced by arrhythmias, reduction in cardiac output and coronary blood flow, are not settled. Experiments were conducted in 16 isolated working left ventricles to examine their metabolic and hemodynamic responses to the infusion of vasopressin and the combination of vasopressin and epinephrine. Contractile performance was evaluated by analysis of positive dP/dt, contractile element velocities, and ventricular work-curves using stroke work/end-diastolic pressure. Relaxation parameters, including negative dP/dt and the early diastolic relaxation time constant, were also studied. Coronary blood flow was reduced 22% or less by vasopressin while cardiac output was maintained at a constant level. Myocardial oxygen consumption, lactate and potassium balances were determined from arterial and coronary sinus concentrations. Vasopressin produced myocardial dysfunction indicated by decrements in contractile and relaxation indices, without evidence of global ischemia. Epinephrine restored the mechanical performance to normal without significant change in coronary blood flow, myocardial oxygen consumption, or lactate and potassium balance.
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PMID:Mechanisms of impaired cardiac function by vasopressin. 736 15

Segments of colon were denervated, vascularly isolated, and autoperfused at normal arterial pressure in the anesthetized dog. Norepinephrine, vasopressin, isoproterenol, and histamine were infused i.a. in graded doses. Norepinephrine and vasopressin reduced colonic blood flow and increased the arteriovenous oxygen difference; oxygen uptake by the colon fell, and the capillary filtration coefficient (Kf,c) was reduced. Isoproterenol and histamine increased colonic blood flow and reduced the arteriovenous oxygen difference; oxygen uptake by the colon did not change significantly. The Kf,c increased with isoproterenol, but changes due to histamine were more variable. Vasoconstrictor drugs tend to reduce, and vasodilators tend to increase oxygen uptake by the colon; the effects of altered blood flow are, however, alleviated by changes in colonic oxygen extraction, such that moderate drug-induced changes in blood flow (-25 to +50%) are not associated with appreciable (less than or approximately 10%) changes in oxygen uptake.
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PMID:Effects of norepinephrine, vasopressin, isoproterenol, and histamine on blood flow, oxygen uptake, and capillary filtration coefficient in the colon of the anesthetized dog. 737 72

1. Urine flow and compositions were determined in normally hydrated, waterloaded and hypotonic saline infused hens under various ambient temperatures (Ta). 2. At Ta 29 and 32 degrees C normal urine flow was reduced and osmolality increased; at Ta 0 and -5 degrees C urine flow increased and osmolality decreased. 3. In hydrated hens at Ta 32 degrees C antidiuresis occurred within 10 min and persisted for 2 hr without any significant change in rectal temperature (Tr). 4. At Ta 40 degrees C there was no antidiuresis but a tendency for urine flow to increase; Tr also rose. The antidiuresis shown by water-restricted hens at Ta 20 degrees C was abolished at Ta 40 degrees C. 5. An antidiuresis, similar to that seen at Ta 32 degrees C, could be produced at Ta 20 degrees C by moderate haemorrhage, exposure to infra-red heating or by vasopressin or vasotocin. Adrenaline and noradrenaline provoked a diuresis. 6. Hypothalamic heating failed to elicit an antidiuresis but hypothalamic cooling increased urine flow at Ta 20 degrees C and abolished the antidiuretic response at Ta 32 degrees C. 7. It is concluded that the antidiuresis seen at warm ambient temperatures is caused by the release of antidiuretic hormone possibly as a response to a rise in skin temperature.
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PMID:The effects of ambient temperature on urinary flow and composition in the fowl. 744 41

Hypertonic saline solution appears to be an attractive method of volume expansion. In 45 patients undergoing elective aorto-coronary bypass grafting, endocrinologic and circulatory responses to volume loading with hypertonic saline solution prepared in low molecular weight (MW) hydroxyethyl starch (HES) solution (72 g/L NaCl, HES concentration: 6%; MW: 200,000 D; degree of substitution [DS]: 0.5) (HS-HES) was compared randomly to patients who had received low molecular weight HES solution (LMW-HES). A group of patients without volume loading served as a control. Volume was infused to double the low pulmonary capillary wedge pressure (PCWP < 5 mmHg) after induction of anesthesia. Plasma levels of atrial natriuretic peptide (ANP), endothelin, vasopressin, and catecholamines were measured before, during, and after cardiopulmonary bypass (CPB) until the first postoperative day. In addition to systemic circulatory changes, capillary skin blood flow was measured by laser Doppler flowmetry. ANP plasma concentration increased in both volume groups (HS-HES: +79%; HES: +32%), whereas it decreased in the control (-20%). Infusion of HS-HES resulted in an increase in plasma endothelin concentration before and after CPB (from 3 to 6 pg/mL). Five hours after CPB, both treatment groups had higher endothelin plasma concentrations than the control patients (P < 0.05). Epinephrine and norepinephrine plasma levels increased most markedly in the control patients and were highest in the postbypass period in these patients. CI increased most after infusion of HS-HES (+65%) (P < 0.05). In the postbypass period, CI remained significantly higher in both volume groups than in the controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Volume loading with hypertonic saline solution: endocrinologic and circulatory responses. 752 Feb 97

In this comparative study, we carried out liposuction on 20 patients randomly divided in two groups to find an alternative medication to epinephrine that would not result in secondary effects at the cardiovascular level but would offer a similar vasoconstricting capacity. Also, a variation of the wet technique is described that decreases blood loss secondary to liposuction. The area to undergo liposuction is infiltrated with a cannula of our own design. Epinephrine is not used as a vasoconstrictor but rather L-ornithine 8-vasopressin at a concentration of 0.01 IU/ml chilled saline. With this new technique, the amount of blood removed is minimal, even in the case of extraction of large volumes of fat.
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PMID:Effect of L-ornithine 8-vasopressin on blood loss during liposuction. 766 38


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