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Query: UNIPROT:P01185 (
vasopressin
)
23,126
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
1. Experiments were carried out to test whether neosurugatoxin (NSTX) which blocks autonomic ganglia also acts centrally, like hexamethonium, on nicotinic cholinoceptors involved in the neural control of release of
vasopressin
and oxytocin from the neurohypophysis. 2. In the water-loaded rat under ethanol
anaesthesia
, nicotine 100 micrograms i.v. produced a pressor and an antidiuretic response accompanied by an increase in the urinary excretion of
vasopressin
and of oxytocin-like radioimmunoreactivity (OLRI). This indicates release of both
vasopressin
and oxytocin. 3. Under conditions in which tachyphylaxis was avoided, NSTX, 80 ng i.c.v., caused a prolonged inhibition of the release of both hormones by nicotine. 4. NSTX i.c.v. caused some reduction in the pressor response to nicotine. It is suggested that this response involves both central and peripheral stimulation of the sympathetic nervous system and that the central component is blocked by neosurugatoxin. 5. Muscarine, 40 ng i.c.v., produced a pressor and an antidiuretic response with increased urinary excretion of
vasopressin
and OLRI. All these effects were blocked by atropine but were not inhibited by NSTX. 6. Sodium nitroprusside (SN), 200 micrograms i.v., and hypertonic saline (HS; 1.54 M NaCl solution) 4 microliters i.c.v., both produced antidiuretic responses accompanied by increased urinary excretion of
vasopressin
and OLRI. The ratio of the excretion of
vasopressin
to that of OLRI was 5.1 +/- 1.3 (mean +/- s.e.: n = 8) for SN and 1.2 +/- 0.24 (mean +/- s.e.: n = 6) for HS.NSTX 80 ng i.c.v., caused a significant reduction in the antidiuretic response to the hypotension induced with SN: the increased urinary excretion of
vasopressin
was also significantly reduced but not that of OLRI. NSTX had no effect on the response to HS.7. We conclude that NSTX acts centrally on nicotinic cholinoceptors to block the release of
vasopressin
and oxytocin by nicotine and the release of
vasopressin
, but not that of oxytocin, by hypotension. It does not inhibit the release of either hormone by a central osmotic stimulus.
...
PMID:The effect of neosurugatoxin on the release of neurohypophysial hormones by nicotine, hypotension and an osmotic stimulus in the rat. 150 51
Desmopressin acetate (DDAVP) is a synthetic analogue of
vasopressin
used to promote hemostasis and reduce postoperative blood loss. Desmopressin acetate can cause hypotension in humans. Our study evaluated the hemodynamics of rapid administration of DDAVP into the isolated hindlimb in live rats and assessed this response after pretreatment with various antagonists. Thirty male Sprague-Dawley rats (350-450 g) were given intraperitoneal pentobarbital
anesthesia
(50 mg/kg). Perfusion was set at a rate that gave a control mean hindlimb perfusion pressure (HPP) of 100-120 mm Hg. Rats were assigned to five groups (N = 5, each group), with each rat serving as its own control. As a control, saline solution (in volumes equivalent to those used for the antagonists) was injected into the hindlimb preparation before the agonist injections. Each group received both the clinical preparation of DDAVP (i.e., with preservative) and a laboratory preparation of DDAVP in doses of 0.3-3 ng. Group 1 was tested before and after injection of saline solution control; group 2, before and after propranolol (0.5 mg/kg); group 3, before and after meclofenamate (1.5 mg/kg), a cyclooxygenase inhibitor; group 4, before and after nitroarginine (5 mg/kg) an inhibitor of nitric oxide synthesis; and group 5, before and after atropine sulfate (1 mg/kg). Chlorobutanol (25-75 micrograms), the preservative in the clinical preparation of DDAVP, was tested for changes in HPP in five rats similarly prepared. Systemic mean arterial pressure remained constant during the study. The HPP decreased with increasing doses of the clinical preparation of DDAVP, compared with saline solution controls, whereas no change occurred with the laboratory preparation of DDAVP.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Effect of desmopressin acetate on hindlimb perfusion pressure in rats: what is the mechanism? 151 Feb 63
Water-electrolyte homeostasis and its basic regulatory hormones have been studied in 36 patients with neurosurgical brain pathology during surgical interventions performed under balanced
anesthesia
(sodium hydroxybutyrate combined with NLA drugs). The study has revealed 3 types of reactions in hormones regulating water-electrolyte homeostasis: type I--a decrease in
vasopressin
(VP) concentration and renin-angiotensin-aldosterone system (RAAS) activity; type II--VP increase and RAAS activation; type III--an increase in VP content and RAAS disbalance. It has been shown that type I reaction is accompanied by marked osmotic disturbances. The impact of sodium hydroxybutyrate on RAAS is manifested in aldosterone secretion suppression.
...
PMID:[Regulation of the water-electrolyte balance during neurosurgical operations with balanced anesthesia using sodium oxybutyrate]. 152 47
50 patients undergoing elective total hip replacement under epidural
anesthesia
and dextran infusion were given two doses of the
vasopressin
analogue desmopressin 0.3 micrograms/kg BW or placebo in a double-blinded randomized prospective study. Intraoperative blood loss and drainage loss did not differ significantly between groups, but desmopressin reduced the mean total blood loss (calculated from hemoglobin decrease and blood transfusions) by 310 mL (P less than 0.05).
...
PMID:Effects of desmopressin on blood loss in hip arthroplasty. Controlled study in 50 patients. 152 84
Human atria through release of atrial natriuretic peptide play an important role in extracellular fluid homeostasis. This study investigates the perioperative role of atrial natriuretic peptide, renin, angiotensin, aldosterone, and
vasopressin
in patient response to cardiopulmonary bypass after coronary artery bypass operations. Serum levels of these hormones were measured, along with hemodynamic profiles, urine output, and urine electrolytes, before induction of
anesthesia
, after discontinuation of cardiopulmonary bypass, 1 hour postoperatively, and 3 hours postoperatively. Serum levels of atrial natriuretic peptide were found to be significantly elevated immediately after discontinuation of cardiopulmonary bypass. These elevations did not correspond temporally to elevated central venous pressure or tachycardia. Significant natriuresis and diuresis were observed during the first postoperative hour. This diuresis failed to correspond temporally with alterations noted in serum levels of atrial natriuretic peptide, renin, angiotensin, aldosterone, and
vasopressin
. The mechanism responsible for the increases in serum atrial natriuretic peptide and the postoperative natriuresis and diuresis after cardiopulmonary bypass remain unknown.
...
PMID:Atrial natriuretic peptide may not play a role in diuresis and natriuresis after cardiac operations. 153 91
The influence of blood sampling,
anesthesia
and surgery on plasma
vasopressin
concentration was assessed in rats. Mean plasma concentration in conscious, chronically catheterized rats was 1.4 +/- 0.1 pg/ml (n = 6). This value remained constant over repeated plasma samplings in the same animals. On the other hand, decapitation increased the plasma
vasopressin
concentration to 6.0 +/- 2.4 (in pg/ml) (n = 6), inactin
anesthesia
to 2.9 +/- 0.6 (n = 6),
anesthesia
and femoral cannulation to 13.3 +/- 5.8 (n = 6) and surgery for renal micropuncture to 81.3 +/- 35.0 (n = 6). It is concluded that the level of circulating plasma
vasopressin
is highly dependent on the sampling technique and is closely related to the extent of surgery.
...
PMID:Effects of blood sampling, anesthesia and surgery on plasma vasopressin concentration in rats. 154 58
The hemodynamic effects of separate and combined intravenous administration of the
vasopressin
(AVP) V1-receptor antagonist SK&F 100273 (10 micrograms/kg) and the angiotensin I converting enzyme inhibitor captopril (20 mg + 1 mg/h) were studied in 12 sheep during stable halothane
anesthesia
(1.5% end-tidal conc.). The separate blockade of either V1-receptors or angiotensin II (ANG II) synthesis induced a small (7-10%), but significant, fall in mean systemic arterial pressure (MSAP), whereas the combined treatment caused a 30% reduction in blood pressure. The changes in systemic vascular resistance paralleled those of the MSAP. Consequently, the cardiac output was largely unaffected by the interference with AVP effects and/or ANG II synthesis. The halothane
anesthesia
effectively increased the plasma levels of AVP and ANG II, and plasma renin activity without any relation to changes in MSAP. When either the AVP effects or ANG II synthesis were blocked separately, there was a slight tendency for a compensatory increase of the unimpeded hormonal system. It is concluded that halothane
anesthesia
increases the plasma levels of AVP and ANG II in sheep, and that the maintenance of the arterial pressure is dependent on the concurrent vasopressor effects of the two hormones in this situation.
...
PMID:Hemodynamic effects of vasopressin antagonism and angiotensin I converting enzyme inhibition during halothane anesthesia in sheep. 154 32
Several recent reports have suggested that pressor hormones may be released during and after carotid endarterectomy and that release of these factors may be associated with postoperative hypertension and other postoperative morbidity. We measured
vasopressin
, adrenocorticotropic hormone, and cortisol in jugular venous blood during carotid endarterectomy under general
anesthesia
in 43 patients with routine carotid shunting. Jugular venous
vasopressin
increased significantly after the second period of carotid occlusion for shunt removal and remained increased at closure. Vasopressin did not change during the initial carotid occlusion for shunt placement or during the endarterectomy itself, and neither ACTH nor cortisol changed at any sample time. Greater resting
vasopressin
and cortisol and larger responses of
vasopressin
were observed in patients receiving phenylephrine to correct intraoperative hypotension. There were no correlations between postoperative hypertension or postoperative complications and intraoperative hormone values. These results suggest (1) basal intraoperative
vasopressin
values reflect the blood volume of the patient, (2) increased
vasopressin
was not related to postoperative morbidity, and (3) intraoperative increases in pressor hormones are most likely physiologic responses to specific stimuli such as hypovolemia or hypotension rather than pathologic phenomena. We speculate that the increase of
vasopressin
after the second carotid occlusion and reperfusion of the brain may be due to the action of humoral factors released into the carotid circulation from the endarterectomy site.
...
PMID:Jugular venous vasopressin increases during carotid endarterectomy after cerebral reperfusion. 161 7
The colchicine-induced accumulation of
vasopressin
(AVP) and oxytocin (OXT) has recently been applied to estimate the synthesis and turnover rates for these neuropeptides in whole rat hypothalamus. In the present studies, this pharmacologic procedure has been examined as a potential method for estimating hypothalamic somatostatin (SRIF) synthesis rate, and evaluated further for its utility in estimating nonapeptide synthesis in individual hypothalamic nuclei. Adult male rats received a single injection of colchicine (8 micrograms) into the third ventricle under pentobarbital
anesthesia
. Twenty-four hr later, immunoreactive (IR) levels of AVP and OXT increased considerably, as previously noted. Hypothalamic IR-SRIF levels, however, were unaffected. The absolute increases in IR-AVP and IR-OXT were greatest in the supraoptic nucleus (SON), with smaller increments in the para/periventricular hypothalamus (PVH) and the median eminence (ME). IR-SRIF levels showed no changes in the PVH or the ME. As a test, the method was applied to the detection of changes in AVP synthesis in diabetic rats. The colchicine procedure reported increases in AVP synthesis in both the SON and PVH in diabetic animals, a result compatible with that obtained previously for whole hypothalamus using radiolabeled procedures. Together, the results indicate that the colchicine procedure is useful in detecting changes in the syntheses of some (AVP and OXT) but not all (SRIF) neuropeptides, and that when applicable, the method is sufficiently sensitive to detect changes in small hypothalamic regions. The method may prove useful in estimating changes in peptide synthesis analogous to that used for serotonin and dopamine; e.g., 5-hydroxytryptophan and dopa accumulation following inhibition of aromatic L-amino acid decarboxylase.
...
PMID:Colchicine-induced increases in immunoreactive neuropeptide levels in hypothalamus: use as an index of biosynthesis. 167 40
It has been hypothesized that a decreased activity of vagal afferents might contribute to the activation of neurohumoral systems in congestive heart failure. Therefore, we studied the effects of vagal nerve blockade by local
anesthesia
on neurohormones in six conscious dogs before and after induction of heart failure by rapid right ventricular pacing (250 beats/min, 10 days). In healthy dogs, vagal blockade significantly increased plasma
vasopressin
levels (from 1.5 +/- .6 to 13.7 +/- 10.5 pg/ml, p less than 0.02), without significantly affecting plasma catecholamines and renin. After 10 days of pacing, mean arterial pressure and cardiac output were decreased, right atrial and pulmonary arterial pressures and plasma levels of norepinephrine, dopamine, and atrial natriuretic peptide were increased. In this state, vagal blockade significantly increased plasma renin activity (from 1.52 +/- .43 to 3.18 +/- .54 ngAI/ml/h, p less than 0.02) and plasma
vasopressin
(from 4.2 +/- 3.3 to 89.1 +/- 54.9 pg/ml, p less than 0.02), this increase being significantly higher than in healthy dogs. We conclude that in these dogs with low cardiac output state, which resembles early heart failure, vagal afferent activity is increased and effectively suppresses renin and
vasopressin
. This does not exclude the possibility that in later stages of heart failure vagal afferent dysfunction may develop, resulting in neurohumoral disinhibition.
...
PMID:Effects of vagal blockade on neurohumoral systems in conscious dogs with heart failure. 169 88
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