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)

1. The effect of noradrenaline as well as of vasopressin and angiotensin II to increase oxygen uptake and perfusion pressure by the isolated perfused rat hindlimb were completely inhibited by the vasodilators, nitroprusside (0.5 mM), nifedipine (2.5 microM) and isoprenaline (50 nM). 2. Oxygen uptake due to sciatic nerve stimulation of skeletal muscle contraction was not inhibited by 0.5 mM nitroprusside but was found to increase further that produced by a maximum dose of either noradrenaline or angiotensin II. 3. Analysis of high energy phosphates in samples of freeze-clamped hindlimb muscle showed no difference before and after vasoconstrictor addition or with muscle sampled in vivo. 4. It is concluded that norepinephrine mediated increase in oxygen uptake by the perfused rat hindlimb results from its vasoconstrictor action.
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PMID:Inhibition by vasodilators of noradrenaline and vasoconstrictor-mediated, but not skeletal muscle contraction-induced oxygen uptake in the perfused rat hindlimb; implications for non-shivering thermogenesis in muscle tissue. 229 85

The capsaicinoid spice principles capsaicin and dihydrocapsaicin were shown to be thermogenic in the isolated rat hindlimb perfused with constant flow. Both principles elicited similar maximal increases in oxygen consumption (VO2) and perfusion pressure. For capsaicin, the mean maximal increase in VO2 was 1.39 +/- 0.28 mumol/g h or 23 per cent with a perfusion pressure increase of 15.8 +/- 2.8 mmHg, or 54.5 per cent. Dihydrocapsaicin increased VO2 by 1.13 +/- 0.24 or 20 per cent and a perfusion pressure rise of 14.2 +/- 5.0 mmHg or 49 per cent. Above 0.8 microM of either capsaicinoid there was inhibition of oxygen consumption after transient stimulation. Concurrent infusion of the adrenergic antagonists prazosin (alpha 1) and propranolol (beta) had little or no effect on the actions of either capsaicin or dihydrocapsaicin, nor did division of the somatic nerves to the hindlimb. These results indicate a local site of action of these principles in the hindlimb not mediated by a secondary release of catecholamines. Increases in both VO2 and pressure were significantly blocked by the vasodilator nitroprusside. This is in agreement with our previous findings that nitroprusside can block the effects of angiotensin, vasopressin and flow-induced increases in VO2 and perfusion pressure in the perfused hindlimb. The present findings suggest that capsaicin and dihydrocapsaicin can be thermogenic in the rat and that the mechanism of action directly involves vasoconstriction in some manner. We have previously suggested that there might be significant direct smooth muscle vascular consumption of oxygen during sustained vasoconstriction. The findings with capsaicin and dihydrocapsaicin are consistent with this hypothesis.
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PMID:Capsaicin and dihydrocapsaicin stimulate oxygen consumption in the perfused rat hindlimb. 234 Dec 30

The effect of hydration status on plasma vasopressin release was studied in six healthy volunteers undergoing a 15-min bicycle ergometer exercise. The hydration states were dehydration, produced by a 14-h abstinence from fluids, euhydration, and hyperhydration caused by drinking 20 ml kg-1 water 2 h before the exercise. The exercise load was individually adjusted to 70% of maximal oxygen uptake. Exercise resulted in a significant increase in plasma vasopressin only during euhydration, in spite of the marked increase in plasma osmolality in all hydration states. The vasopressin concentrations during hyperhydration were significantly lower than during euhydration. Plasma volume and serum sodium were significantly affected by the exercise. The highest responses were obtained in euhydration and the lowest in hyperhydration. On this basis, the body's drive towards normal homeostasis and to the best ability to respond to the challenges of the environment is rational.
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PMID:The effect of hydration status on plasma vasopressin release during physical exercise in man. 235 44

Blood pressure is usually well maintained during epidural or spinal anesthesia even in the presence of extensive sympathetic blockade. The authors investigated whether hormonal systems support arterial pressure and how the circulation copes with a hypoxic challenge when activation of the sympathetic nervous system is selectively impaired by neural blockade. Accordingly, the effects of high epidural anesthesia alone and combined with hypoxia were evaluated in seven awake trained dogs. On different days, either bupivacaine 0.5% (8-12 ml) or saline (placebo) were randomly injected epidurally and the effects evaluated on cardiovascular (arterial pressure, heart rate) and respiratory (blood gases, oxygen consumption) variables, as well as on hormone plasma concentrations (vasopressin, norepinephrine, epinephrine, renin) during both normoxia and hypoxia. During epidural anesthesia alone, vasopressin increased tenfold (1.7 pg/ml +/- 1.0 SD to 16.8 +/- 13.8, P less than 0.05), norepinephrine decreased (90 pg/ml +/- 31 to 61 +/- 28, P less than 0.05) while epinephrine and renin concentrations remained unchanged. Mean arterial and pulse pressure decreased by 13 mmHg and 23 mmHg (P less than 0.05), respectively. In dogs without sympathetic blockade (saline group), hypoxemia (PaO2: 31 +/- 4 mmHg) evoked an increase in mean blood pressure by 37 mmHg +/- 8 and heart rate by 50 beats per min +/- 17. In contrast, in the presence of sympathetic blockade but with a similar degree of hypoxemia, blood pressure failed to increase (+ 1 mmHg +/- 14) and heart rate rose by only 15 beats per min +/- 11. These differences between groups were statistically significant (P less than 0.001). Hypoxemia induced a similar hypocarbia (PaCO2:25 mmHg) in both groups, indicating that the ventilatory response to hypoxemia was preserved after epidural blockade. During hypoxemia vasopressin concentrations increased 35-fold to 64 pg/ml +/- 38 (P less than 0.0001) compared to base line only during epidural anesthesia, but not after epidural saline (2 pg/ml +/- 2), while other hormones showed no significant differences. The authors conclude that high epidural anesthesia in awake unsedated dogs: 1) almost completely abolishes the normal cardiovascular response to hypoxemia while promoting vasopressin secretion; 2) preserves the ventilatory response to hypoxemia; and 3) is associated with increased vasopressin concentrations, most likely to compensate for decreased cardiac filling and/or arterial blood pressure when sympathoadrenal responses are impaired. Thus, the changes in cardiovascular vital signs in response to severe hypoxemia are markedly blunted when spinal sympathetic outflow is selectively eliminated by epidural anesthesia.
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PMID:Sympathetic blockade by epidural anesthesia attenuates the cardiovascular response to severe hypoxemia. 200 Oct 46

The hypothesis that withdrawal of increased sympathetic activity may be beneficial in heart failure was tested by administration of the centrally acting adrenergic inhibitor methyldopa. Fourteen subjects with chronic, stable New York Heart Association Functional Class 2 or 3 heart failure receiving digitalis and diuretics were randomized to methyldopa (n = 8) 500-1000 mg daily or placebo (n = 6). Clinical, hemodynamic, neurohumoral, and platelet alpha 2-receptor effects were studied after chronic (3 weeks) administration. Sympathetic inhibition did not alter symptom status or exercise duration but reduced plasma norepinephrine concentration during exercise and permitted the same level of exercise to be attained at a lower pressure-rate product, indicating reduced myocardial oxygen consumption. Left ventricular ejection fraction and stroke volume tended to increase, and systemic vascular resistance tended to decrease during exercise after methyldopa administration, suggesting enhanced vasodilation. Upright plasma renin activity increased from 8.2 +/- 2.2 to 13.3 +/- 3.0 ng/nl/h (p = 0.03) after methyldopa, but plasma antidiuretic hormone concentration changed insignificantly. In a subset of patients, platelet alpha 2-receptor density and affinity were unaltered. Renal function was also unchanged. Thus, sympathetic inhibition induced by methyldopa in selected patients with chronic, stable heart failure does not worsen symptom status or exercise performance, and may produce a beneficial effect by withdrawal of excess sympathetic activity with reduction of plasma norepinephrine levels.
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PMID:Sympathetic inhibition with methyldopa in heart failure. 242 85

Effects of the active oxygen on the extrusion mechanism of once-increased cytoplasmic Ca2+, which causes various physiological phenomena, were investigated using different kinds of culture cells. First we found that, in response to stimulation with vitamin K (VK), various culture cells showed a decrease in cytoplasmic Ca2+ concentration. On the presumption that this phenomenon might be related to the oxidizing action of VK, we performed the same experiments using oxidizing agents such as H2O2 or KO2. They also showed a decrease in cytoplasmic Ca2+ concentration. Furthermore, they suppressed the increase of cytoplasmic Ca2+ by vasopressin. It would be inferred from these results that the active oxygen may act upon some site of the cellular signal transduction system of cell membrane to lower the cytoplasmic Ca2+ level.
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PMID:[Effect of active oxygen on cytoplasmic Ca2+ sequestration mechanism]. 251 16

The factors associated with the exercise-induced increase in plasma atrial natriuretic peptide (ANP) have not been clearly established. Thus the purpose of the study was to further document the stimulus for the exercise-induced release of ANP and to examine the role of ANP in the control of hydromineral balance during exercise. Eight healthy male volunteers (25.1 +/- 4.5 yr) were submitted to a graded cycling exercise in both the upright and supine positions. Venous blood was sampled at rest and at the end of each 5-min work load at 40, 60, and 80% maximal oxygen uptake (Vo2max), at maximal exercise, and during recovery through an indwelling catheter for the determination of plasma vasopressin, aldosterone, catecholamines, plasma renin activity, and ANP concentrations. Results indicate a significant increase in ANP (pg/ml) from rest to maximal exercise in the upright position [rest, 21.9 +/- 10.2; 40%, 24.7 +/- 12.6; 60%, 32.4 +/- 17*; 80%, 47.8 +/- 27.7*; 100% Vo2max, 65.9 +/- 34.5* (*P less than or equal to 0.05)]. Supine concentrations were significantly higher than upright at 40 (37.9 +/- 15.2), 60 (54.0 +/- 18.8), and 80% Vo2max (68.9 +/- 16.6). Plasma ANP during maximal exercise was similar in both positions. Plasma vasopressin, aldosterone, renin activity, and catecholamines increased with increasing exercise intensity in both positions, although lower values were systematically observed in the supine position. The association of higher plasma ANP and blunted plasma vasopressin, plasma renin activity, and norepinephrine concentrations during supine exercise suggests that ANP may exert modulatory effects on the control of the hydromineral hormonal system during exercise.
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PMID:Plasma atrial natriuretic peptide during brief upright and supine exercise in humans. 252 14

Effects of surgical intervention on plasma levels of antidiuretic hormone (ADH) and alpha-human atrial natriuretic polypeptide (alpha-hANP) under sevoflurane-nitrous oxide-oxygen anesthesia were evaluated in 24 patients, ranged in ages from 15 to 65, who underwent non-abdominal surgery (orthopedic surgery) or abdominal surgery (gastrointestinal or gynecological surgery). Anesthesia was induced and maintained with sevoflurane, nitrous oxide and oxygen. Succinylcholine was administered to facilitate tracheal intubation and pancuronium was given during abdominal surgery when needed. Lactated Ringer's solution was administered intravenously throughout the procedures. Neither plasma ADH nor alpha-hANP levels changed significantly during sevoflurane anesthesia alone for 20 min. Plasma ADH levels were unchanged during surgery in patients who underwent non-abdominal surgery, but they tended to increase although insignificantly after the recovery from anesthesia. On the contrary, plasma ADH levels increased significantly during surgery and in the recovery room in patients who underwent abdominal surgery. Plasma alpha-hANP levels were unchanged during surgery and in the recovery room in patients who underwent non-abdominal or abdominal surgery. The authors' findings suggest that ADH secretion was significantly stimulated with abdominal intervention but not with orthopedic one, furthermore neither anesthesia nor surgical stress induced any influence on plasma alpha-hANP levels.
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PMID:[Effects of surgical intervention on plasma levels of antidiuretic hormone and alpha-human atrial natriuretic polypeptide under sevoflurane anesthesia]. 253 Mar 70

The effects of inadequate expansion of maternal blood volume on uterine blood flow, fetal oxygen levels and vasoactive mediators during the third trimester were studied in 8 pregnant sheep. Results were compared to those obtained during 15 normal pregnancies. Prevention of the normal (20 ml/day) increase in maternal plasma volume was achieved by repeated haemorrhage and injections of furosemide. These treatments also reduced the rise in blood flow to the pregnant uterine horn that normally occurs during this period of gestation: at term flow was only 508 +/- 61 (SEM) compared to 838 +/- 83 ml/min in the control group (P greater than 0.01). This reduction in uterine blood flow caused a gradual fall in fetal PaO2, and rise in fetal levels of plasma renin activity, vasopressin, catecholamines and angiotensin II without change in pHa or base excess. Four to 5 days prior to delivery, the difference from control in PaO2 was -3.9 +/- 0.5 mmHg, plasma renin activity +2.9 +/- 1.7 ng/ml.h, vasopressin +4.2 +/- 1.1 pg/ml, catecholamines +957 +/- 145.3 pg/ml and angiotensin II +243 +/- 108.2 pg/ml. Furthermore, the fall in PaO2 and rise in vasoactive mediators that normally occur 3-5 days prior to the onset of labour was either absent (PaO2 and plasma renin activity) or blunted. Thus when expansion of blood volume during pregnancy is inadequate, blood flow to the uterus is adversely affected. This leads to various degrees of chronic fetal hypoxaemia and stimulation of vasoactive mediator systems. However, the normal stimulation of vasoactive mediator systems that occurs 3-5 days before delivery appears to be blunted. Experimental prevention of blood volume expansion during pregnancy produces an excellent model for the study of chronic mild fetal hypoxaemia.
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PMID:Prevention of the normal expansion of maternal plasma volume: a model for chronic fetal hypoxaemia. 269 56

The biochemical abnormalities associated with heart failure include dysfunction of contractile proteins, functional impairment of energy-linked enzymes and disruption of cell membrane structure. The haemodynamic impairment resulting from cardiac dysfunction activates several neurohormonal systems, notably the renin-angiotensin-aldosterone system, sympatho-adrenal system and vasopressin release, whilst clinically important factors include an enlarged heart, increased systolic wall stress and an increased myocardial oxygen demand. An inverse relationship exists between systolic wall stress (afterload) and contractile function in heart failure. Moreover the increased systolic wall stress that occurs as a result of reduced cardiac output raises myocardial oxygen consumption, causing cardiac function to deteriorate still further. Diastolic abnormalities play an important role in hypertrophic disorders, in ventricular dilatation and in cases of myocardial ischaemia. The therapeutic objectives are therefore to decrease heart size, to reduce wall stress and oxygen demand, and to enhance diastolic distensibility.
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PMID:Contractile, haemodynamic and neurohormonal abnormalities in heart failure. 280 88


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