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. In water-loaded rats under ethanol anaesthesia, the injection of 2-4 microliters 1.54M NaCl solution (hypertonic saline:HS) into a lateral cerebral ventricle (i.c.v.) produced an antidiuretic and a pressor response, together with increased urinary excretion of vasopressin and 'oxytocin-like radioimmunoreactivity' (OLRI). In lactating rats HS also produced a milk-ejection response which was shown to be due to the release of oxytocin. 2. The injection of 20-40 micrograms gamma-aminobutyric acid (GABA) or 40-80 ng muscimol i.c.v. 2 min before HS inhibited the antidiuretic, pressor and milk-ejection responses and reduced the urinary excretion of vasopressin and OLRI. 3. The pressor response to HS was abolished by a ganglion blocking agent but it was not reduced by a vasopressin antagonist. After the antagonist, the antidiuretic response to HS was abolished and the pressor response was accompanied by a diuresis both of which were blocked by muscimol. 4. The threshold dose of HS for an antidiuretic response was 4-8 times higher on injection into the cisterna magna (i.cist.) than when injected i.c.v. GABA, i.v. or i.cist, did not inhibit the response to HS i.c.v. 5. The results confirm other evidence that, in the rat, in contrast some other species, an osmotic stimulus causes release of both vasopressin and oxytocin. This release is blocked by GABA and muscimol. These drugs and HS act at a site reached not from the subarachnoid space but from the cerebral ventricles, probably the hypothalamus. The pressor response to HS under the experimental conditions used is due entirely to central sympathetic stimulation and this effect, as well as the release of vasopressin and oxytocin, is blocked by muscimol.
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PMID:Central inhibition by gamma-aminobutyric acid and muscimol of the release of vasopressin and oxytocin by an osmotic stimulus in the rat. 233 82

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

In a search for factors contributing to the sustained blood pressure (BP) elevation in acutely volume-loaded animals, dextran dissolved in lactated Ringer's solution (20 ml/kg) was infused into 34 mongrel dogs over a period of 1 hour under pentobarbital anesthesia and changes in hemodynamic and humoral variables were monitored during its infusion and for 3 hours after its infusion. BP elevation during volume loading (from 114 +/- 3 to 128 +/- 3 [SEM] mm Hg) was attributed to an increase in cardiac output. After volume loading, some dogs maintained BP elevation whereas others did not. The former group showed an increase in total peripheral resistance, demonstrating a transformation of cardiac output to total peripheral resistance as a responsible factor in maintenance of the elevated BP. The plasma levels of norepinephrine, vasopressin, and plasma renin activity were not elevated, indicating that these vasoactive factors were not responsible for elevation of the BP or total peripheral resistance. The changes in the hematocrit, atrial natriuretic factor, urine volume, and urinary sodium excretion were identical in the two groups, and natriuresis was not prominent when total peripheral resistance was high. Pressor responses to norepinephrine and angiotensin II were potentiated 3 hours after stopping infusion in both groups, but this potentiation was not correlated with the increase in total peripheral resistance or mean BP. Thus, acute volume expansion produced resistance-dependent hypertension following the initial volume-dependent hypertension. It is unlikely that a vascular sensitizing natriuretic factor plays a role in the resistance-dependent BP elevation. The mechanism and physiological importance of hypersensitivity to vasoactive substances remain to be elucidated.
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PMID:Vasoconstriction and hypersensitivity to vasoactive substances after acute volume expansion in dogs. 245 68

Desmopressin (DDAVP), a synthetic vasopressin, temporarily corrects bleeding abnormalities associated with mild hemophilia A, von Willebrand disease, and disorders of platelet function. The side effects of DDAVP are considered benign although most of its use has been in adults and older children. We report four children under the age of 2 years who became hyponatremic after intravenous DDAVP administration (0.3 microgram/kg). Three of them developed grand mal seizures. A review of the literature and these cases indicate that associated risk factors for hyponatremia after DDAVP administration include stress, surgery, anesthesia and narcotics (endogenous release of antidiuretic hormone), vomiting (loss of Na+), liver disease (hindered metabolism of DDAVP), renal tubular acidosis (chronically low serum Na+), multiple doses of DDAVP, and overhydration with hyponatremic fluids. DDAVP is not a benign drug in this age group and shows a serious potential for hyponatremia and seizures. Fluid restriction, avoidance of hyponatremic solutions, and close monitoring of serum electrolytes and urine output for at least 15-20 hr after the administration of DDAVP, when used in children under the age of 2 years, is warranted.
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PMID:Hyponatremia and seizures in young children given DDAVP. 250 Aug 51

Both oxytocin (OXY) and arginine vasopressin (AVP) enhance the effects of corticotropin-releasing factor on ACTH release by the pituitary. One of these, AVP, plays a role in the control of fluid balance and responses to hypoxemic stress in the fetal sheep. To determine the possibility that OXY also participates in fetal neuroendocrine events, OXY-containing neuronal structures must first be demonstrated within the fetal endocrine hypothalamus. OXY-immunoreactive elements were examined in fetal sheep hypothalami late in gestation and compared to AVP-containing structures using immunocytochemical procedures. Six fetal sheep ranging from 126 to 144 days gestational age were delivered via cesarian section from timed pregnant Rambouillet-Columbia ewes and killed by an overdose of anesthesia. The fetal head was perfused via bilateral carotid catheters and processed for immunocytochemical localization of OXY or AVP using the avidin-biotin complex procedure. At all fetal ages examined, OXY- and AVP-containing neurons were found within the paraventricular nuclei (PVN), supraoptic nuclei (SON) and accessory magnocellular hypothalamic nuclei. OXY-containing neurons were found principally in the SON and PVN. They were generally less numerous and less intensely stained than the AVP neurons. In the SON, they concentrated along the dorsal borders of the nucleus above the AVP neurons. In PVN, clusters of OXY cells were located along the dorsal and lateral borders of the nucleus surrounding the AVP neurons; in the periventricular division, they were intermingled with the AVP neurons. Small numbers of OXY axons were located in the external zone of the median eminence; whereas most OXY axons extended into the hypothalamo-neurohypophyseal tract and posterior lobe of the pituitary. A few of the OXY axons in the pituitary stalk were diverted to the pars intermedia. Likewise, some of the OXY fibers from the external zone of the median eminence entered the pars tuberalis but were rarely found in the distal lobe of the pituitary. In contrast, AVP axons richly innervated the external zone of the median eminence, and neural lobe. Like OXY, AVP axons from the median eminence and the pituitary stalk sent projections to the adenohypophysis. AVP fibers in the pars distalis frequently contacted corticotropes and were more numerous than OXY fibers in this region. These data provide anatomical evidence that OXY and AVP may directly regulate the fetal adenohypophysis. Of these two neuropeptides, AVP predominates anatomically.
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PMID:Neuropeptide cells and fibers in the hypothalamus and pituitary of the fetal sheep: comparison of oxytocin and arginine vasopressin. 251 63

The use of buprenorphine-diazepam-N2O (60%)-O2 anesthesia in open heart surgery was investigated. The authors examined the hemodynamic changes produced and the response of stress hormones. Twenty adult patients with atrial septal defects undergoing surgical correction were studied in two groups of 10, receiving either 6 micrograms/kg of buprenorphine (B6) or 12 micrograms/kg of buprenorphine (B12) for the induction of anesthesia. Both groups received a subsequent dose of 6 micrograms/kg of buprenorphine with the commencement of extracorporeal circulation (ECC). With surgery, mean arterial pressure showed a transient increase in both groups and thereafter was stable. Heart rate in the B6 group was increased from the onset of surgery to the day after, while the B12 group showed no significant change. Filling pressures showed no change in either group. Plasma catecholamine concentrations in the B6 group, in contrast to the B12 group, increased significantly from midoperation to after completion of the operation (ECC 10 minutes, B6 group v B12 group: plasma norepinephrine 616 +/- 231 v 195 +/- 38 pg/mL, plasma epinephrine 1385 +/- 392 v 572 +/- 132 pg/mL, P less than 0.05). Plasma ADH levels in both groups rose with the commencement of surgery, reaching a peak at ECC 10 minutes (B6 group 88.1 +/- 8.4 v B12 group 124.4 +/- 27.2 pg/mL). However, in contrast to plasma catecholamines, the antidiuretic hormone (ADH) levels in the B12 group remained higher until the first postoperative day. Therefore, patients who received the larger dose of buprenorphine had better control of hemodynamics and catecholamines, but a greater elevation of plasma ADH levels.
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PMID:Variations in hemodynamic and stress hormonal responses in open heart surgery with buprenorphine/diazepam anesthesia. 252 Sep 12

Cardiovascular and hormonal responses to aortic cross-clamping (ACC) and declamping (ADC) were studied in 20 patients undergoing reconstructive aortic surgery anesthetized with fentanyl and droperidol. Ten of the patients served as a control group, and 10 patients were treated with oral captopril (25 mg the day before operation and 25 mg one hour before anesthesia) to prevent intraoperative and postoperative hypertension. After the induction of anesthesia in the captopril group, hypotension was seen in four patients and bradycardia in three patients. In both groups, the most important changes in hemodynamics after the ACC were an increase in systemic vascular resistance and decreases in cardiac and stroke index. After the ADC, the cardiac index (CI) improved nearly to the level before the ACC. The urine output during anesthesia was 46 +/- 5 mL/h in the control group and 73 +/- 11 mL/h (P less than 0.05) in the captopril group. Postoperatively, patients in both groups were hypertensive and tachycardic. In the control group, plasma renin activity rose significantly during the ACC, indicating activation of the renin-angiotensin system (RAS). In both groups, significant increases in plasma vasopressin (PAVP), epinephrine, and norepinephrine were also observed before the ACC and during the postoperative period. The results suggest that oral captopril increases the risk of hypotension and bradycardia after induction of anesthesia, and does not prevent postoperative hypertension.
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PMID:Hemodynamic and hormonal changes in patients pretreated with captopril for surgery of the abdominal aorta. 252 Sep 15

The effects of rapid atrial pacing on central hemodynamics, plasma hormones, and renal function were investigated in eight control and nine cardiac-denervated dogs under chloralose anesthesia. Pacing at approximately 250 ppm for 60 min caused similar increases in pulmonary wedge and right atrial pressures, systemic vascular resistance, and plasma atrial natriuretic peptide (ANP) in both groups. In control dogs, pacing produced a fall in both plasma vasopressin (AVP) and plasma renin activity (PRA) and a rise in urine flow rate associated with an increase in free water but not sodium clearance. In contrast, in cardiac-denervated dogs, both plasma AVP and PRA increased during pacing; urine flow rate did not change, and marked sodium retention occurred. This study supports the concept that the increase in urine flow during rapid atrial pacing is mediated by inhibition of renin and AVP secretion through intact cardiac nerves. The secretion of ANP is unaffected by cardiac denervation. The natriuretic and vasodilator actions of high plasma ANP concentrations during rapid atrial pacing can be inhibited either by neurally mediated cardiorenal effects in normal animals or by stimulation of the renin-angiotensin system after cardiac denervation.
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PMID:Atrial natriuretic peptide response to rapid atrial pacing in cardiac-denervated dogs. 252 92

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 cardiovascular effects of althesin (ALT) and urethan-chloralose (UC) anesthesia were compared in conscious, chronically instrumented rats. Althesin had no effect on arterial pressure or base-line resistance in the renal, superior mesenteric, and hindquarters vasculatures but increased heart rate. In contrast, UC decreased arterial pressure, heart rate, and mesenteric resistance. Although UC attenuated depressor responses to nitroglycerin, neither anesthetic significantly altered regional vascular reactivity to intravenous phenylephrine and nitroglycerin. The cardiac chronotropic baroreflex was examined by comparing the slope of the curves relating maximal changes (delta) in heart rate (pulse interval) that occurred at the point coinciding in time with the maximal changes in mean arterial pressure produced by phenylephrine and nitroglycerin. Neither anesthetic significantly altered the baroreflex slope (delta pulse interval/delta mean arterial pressure) for pressor and depressor stimuli. Both anesthetics attenuated the sympathoexcitatory response to cerebroventricular angiotensin II, although ALT had less of a depressive effect (pressor response during ALT and UC = 65 and 30%, respectively, of conscious). Plasma renin activity (PRA) and the hemodynamic response to peripheral angiotensin-receptor antagonism were significantly increased (PRA by almost 6-fold) during UC, whereas ALT was without effect. Similarly, UC but not ALT induced vasopressin-dependent vascular tone. Ganglionic blockade indicated that peripheral neurogenic tone was not altered by ALT anesthesia. These data suggest that althesin produces fewer hemodynamic disturbances than urethan-chloralose and largely maintains cardiovascular regulation intact.
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PMID:Effects of althesin and urethan-chloralose on neurohumoral cardiovascular regulation. 256 59


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