Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of furosemide on plasma renin, vasopressin (AVP), and aldosterone concentrations was studied in 10 control and 6 nephrectomized lambs during the 1st 2 wk of life. In a separate study in 10 newborn lambs, 1-sarcosine-8-alanine-angiotensin II (saralasin acetate, 5 mug/kg per min) was infused alone for 40 min, after which furosemide 2 mg/kg i.v. was injected in association with continuing saralasin acetate infusion. Plasma renin activity increased from a mean (+/-SEM) of 21.3+/-3.4 ng/ml per h in the 10 control lambs to 39.4+/-8.2 ng/ml per h at 8 min (P < 0.001) and remained high through 120 min after furosemide. Plasma AVP and aldosterone concentrations increased from respective mean values of 2.1+/-0.4 muU/ml and 12.8+/-2.5 ng/dl to 9.8+/-2.0 muU/ml (P < 0.01) and 23.0+/-7.7 ng/dl (P < 0.05) at 35 min and 13.8+/-2.1 muU/ml and 23.0+/-4.4 ng/dl at 65 min after furosemide (each P < 0.01). There was an insignificant AVP response in the 10 lambs treated with angiotensin inhibitor: from a mean base line of 4.7+/-0.9 to 8.3+/-2.0 muU/ml at 35 min, and 7.4+/-2.0 muU/ml at 65 min after furosemide. There was no increase in AVP in the anephric lambs. The mean increment AVP response from base line in the newborn lambs without saralasin, Delta 10.8+/-2.0 muU/ml, was greater than in the lambs with saralasin, Delta4.0+/-1.9 (P < 0.05), and greater than in the anephric lambs, Delta3.3+/-2.1 muU/ml (P < 0.05). The mean blood pressure fell 6 mm Hg in the 10 control lambs (P < 0.05), 7 mm Hg in the anephric lambs (P < 0.05), and 16 mm Hg in the lambs treated with angiotensin inhibitor (P < 0.05) by 35 min after furosemide. However, the changes in plasma AVP were not related to the fall in blood pressure. These data support the view that the observed AVP response to furosemide in the newborn lamb was mediated through the renin-angiotensin system.
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PMID:Endogenous angiotensin stimulation of vasopressin in the newborn lamb. 42 54

The effect of pain on plasma AVP concentration in man has previously been studied only during major surgery with general anaesthesia. Plasma AVP concentration (pAVP) and plasma osmolality (pOsm) were measured in thirty-six patients seen in a surgical emergency department complaining of pain and in fifty-one control subjects. No significant difference in pOsm was found, but pAVP was significantly higher in the emergency room patients in pain (M +/- SEM = 4.94 +/- 0.98 pmol/1 compared to 2.31 +/- 0.32 pmol/1 in control subjects, P less than 0.01). In the control subjects, age was found to have a low but significant inverse correlation with pAVP (r = 0.37, P less than 0.01). Chronic smoking was associated with significant elevation of pAVP (3.81 +/- 0.99 pmol/1 in smokers vs. 1.89 +/- 0.28 pmol/1 in non-smokers, P less than 0.02). Neither smoking nor age could account for the difference in pAVP between the pain and control groups. Thus, pain is a non-osmolar factor capable of elevating AVP in conscious man.
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PMID:The effect of pain on plasma arginine vasopressin concentrations in man. 63 Jul 25

1. Oxytocin receptors in the uterus of the brushtail possum (T. vulpecula) were characterized by radioreceptor assay and compared with those of the sheep and rat uterus. 2. A single oxytocin binding site was found with an affinity (Kd) and receptor concentration (Ro) of 3.0 +/- 0.8 nmol/l and 200 +/- 60 fmol/mg protein, respectively (SEM; n = 5). The receptor was stable at -20 degrees C; divalent ions were required for optimum binding. 3. Competitive displacement curves with related peptides showed the following order of specificity: vasotocin greater than oxytocin greater than mesotocin = arginine-vasopressin = [Thr4, Gly7]-oxytocin greater than lysine-vasopressin = isotocin much greater than [d(CH2)5, D-Phe2, Ile4, Ala9-NH2]-AVP. 4. It was concluded that oxytocin receptors in the possum have similar characteristics to those of placental mammals.
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PMID:Uterine oxytocin receptors in an Australian marsupial, the brushtail possum, Trichosurus vulpecula. 196 6

Ipecacuanha syrup induces emesis by an early peripheral (gastric irritant) action and a later central effect at the chemoreceptor trigger zone (CTZ). We have studied the responses of plasma AVP, ACTH and ACTH-precursors to early and late ipecacuanha-induced nausea in nine healthy male subjects. Symptom severity was assessed using a linear analogue scale. All subjects reported 'early' nausea (N1) with a latency of 16 +/- 2 min (mean +/- SEM) and eight subjects vomited. Six subjects experienced recurrent nausea (N2) (latency 106 +/- 10.4 min) of whom five also vomited. The interval between the cessation of N1 and the onset of N2 was 55 +/- 10.8 min (range 25-80 min). The severity of nausea at the onset of N1 or N2 was similar but the AVP and ACTH responses were highly variable. Thus, while mean plasma AVP concentrations increased during both symptom periods, in three subjects during N1 and in three subjects during N2 plasma AVP concentrations did not rise above the normal range, despite marked symptoms. No clear pattern of AVP response to distinguish early peripheral from late central ipecacuanha-induced emesis was demonstrated. Whilst mean plasma ACTH concentrations increased during both N1 and N2 there were no changes in mean plasma ACTH-precursor concentrations. Analysis of pooled data for N1 and N2 demonstrated direct correlations between the nausea score and the peak incremental plasma responses of either AVP or ACTH and, despite the variability, peak incremental concentrations of AVP and of ACTH were also correlated. The data indicate that there is no difference in the AVP responses to peripherally or centrally stimulated ipecacuanha-induced nausea.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The responses of arginine vasopressin and adrenocorticotrophin to nausea induced by ipecacuanha. 198 63

We studied the changes in plasma arginine vasopressin in 5 patients with diabetic ketoacidosis and one patient with non-ketotic hyperosmolar coma who had marked hyperglycemia (36.6 +/- 4.6 mmol/l, mean +/- SEM) and dehydration. Plasma osmolality (Posm) was 342.2 +/- 11.4 mOsm/kg H2O, and hematocrit, serum protein, and blood urea nitrogen were also elevated at hospitalization. Circulating blood volume was decreased by approximately 21% as compared with that on day 7. Plasma AVP level was increased to 8.5 +/- 1.6 pmol/l at hospitalization. When hyperglycemia was improved by iv infusion of a small dose of insulin plus fluid administration, plasma AVP level promptly decreased to 2.4 +/- 0.4 pmol/l within six hours. When plasma AVP level had normalized, Posm was still as high as 305 mOsm/kg H2O, but the loss of circulating blood volume was only 4.2% of the control state. Plasma AVP level was positively correlated with change in hematocrit (plasma AVP = 3.58 + 0.45.hematocrit, r = 0.468, p less than 0.01), serum protein (r = 0.487, p less than 0.01), Posm (r = 0.388, p less than 0.01), and blood glucose (r = 0.582, p less than 0.01). Plasma AVP level was negatively correlated with the change in circulating blood volume (plasma AVP = 3.6 - 0.14.change in circulating blood volume, r = -0.469, p less than 0.01). These results indicate that both non-osmotic and osmotic stimuli are involved in the mechanism for AVP release in patients with diabetic coma, and that the non-osmotic control of AVP may contribute to circulating homeostasis, protecting against severe blood volume depletion in diabetic patients suffering from hyperglycemia and dehydration.
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PMID:Prompt recovery of plasma arginine vasopressin in diabetic coma after intravenous infusion of a small dose of insulin and a large amount of fluid. 211 Apr 10

In seven healthy male volunteers we investigated changes in plasma atrial natriuretic factor [( ANF]), arginine vasopressin [( AVP]) and plasma volume (PV) during supine immersion. Twenty minutes head-out water immersion in a supine position in a thermo-neutral water bath attenuated the increase in PV induced by 20 min in a supine position in air, but increased the mean plasma [ANF] from 32.0 pg.ml-1, SEM 5.1 to 53.3 pg.ml-1, SEM 3.6 and decreased the mean plasma [AVP] from 1.4 pg.ml-1, SEM 0.1 to 0.9 pg.ml-1, SEM 0.04. Simultaneously, diuresis and natriuresis increased markedly. During a 20-min control period in the supine posture without immersion, PV, plasma [ANF] and [AVP] remained unaffected while diuresis and natriuresis did not increase to the same extent. These data suggest that an increase in the central blood volume induced by a weak external hydrostatic pressure during supine immersion triggered the changes in plasma [ANF] and [AVP] and that the increase was probably due to a shift of blood volume from peripheral to central vessels. The changes in plasma [ANF] contributed to the changes in natriuresis.
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PMID:The role of posture on the changes in plasma atrial natriuretic factor and arginine vasopressin levels during immersion. 214 37

Vasopressin (AVP) was infused into four healthy human volunteers to explore by Doppler ultrasound the vasoconstrictive action of AVP on the internal carotid (ICA) and the medial cerebral artery (MCA, transcranial Doppler technique). Although AVP levels rose to 74.2 pg/ml (+/- 13 pg, SEM) no significant changes of flow velocity were observed in the ICA as well as the MCA. There was no effect on the pulsatility index of the MCA velocity profile indicating that peripheral vascular resistance remained unchanged during AVP infusion. These results do not support an effect of AVP at high physiological levels on the vascular diameters of the ICA, MCA and cerebral arteriolar system in humans.
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PMID:Failure to demonstrate a vasoconstrictive effect of vasopressin on the internal carotid and middle cerebral arteries: a transcranial ultrasound Doppler study. 295 90

In order to assess the effects of centrally administered atrial natriuretic peptide (ANP) on renal water and electrolytes handling, arterial blood pressure, plasma vasopressin, renin activity, aldosterone, and ANP concentrations, synthetic alpha-human ANP (alpha-hANP) was administered intracerebroventricularly at a dose of 2.6 pmol.kg-1.min-1 for 30 min in pentobarbital-anaesthetized dogs (N = 6). In the control study (N = 6), artificial cerebrospinal fluid was infused. Intracerebroventricular administration of alpha-hANP increased significantly urine flow from 178 +/- 37 to 303 +/- 43 microliter/min (mean +/- SEM), sodium excretion from 27.3 +/- 8.9 to 54.4 +/- 10.5, mumol/min, potassium excretion from 16.1 +/- 3.7 to 24.0 +/- 5.1 mumol/min, and osmolar and negative free water clearances, accompanied by a significant rise in renal blood flow from 77.0 +/- 14.6 to 94.9 +/- 16.9 ml/min. Whereas glomerular filtration rate fell significantly, blood pressure and heart rate did not change. Plasma ANP, aldosterone, and PRA did not change significantly during the experiment, but plasma AVP were slightly but significantly decreased from 52 +/- 11 to 34 +/- 6 nmol/l. On the other hand, these parameters showed no changes in the control study, except a significant fall in glomerular filtration rate and a significant rise in PRA. Thus, it has been confirmed that ANP centrally brings about diuresis, natriuresis, and kaliuresis via some unknown mechanisms independent of the release of these hormones.
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PMID:Effects of centrally administered atrial natriuretic peptide on renal functions. 295 80

The effects of atrial natriuretic peptide (ANP) on mean arterial blood pressure, heart rate, plasma renin activity, aldosterone, cortisol, norepinephrine, epinephrine and arginine vasopressin were studied in 6 anuric subjects receiving regular hemodialysis. An iv bolus injection of 8 nmol of ANP followed by infusion at 32 pmol.kg-1.min-1 for 1 h in the pre- and posthemodialysis period was performed. Basal plasma ANP was higher before than after hemodialysis. ANP administration produced a reduction in mean arterial blood pressure accompanied by an elevation of norepinephrine and of plasma renin activity (from 2.49 +/- 0.52 to 3.39 +/- 0.85 nmol.1-1.h-1 predialysis and from 2.78 +/- 0.71 to 3.15 +/- 0.86 nmol.l-1.h-1 postdialysis, respectively, mean +/- SEM; P less than 0.05). Plasma aldosterone and cortisol were significantly decreased. Plasma epinephrine and AVP remained unchanged. These hemodynamic and hormonal changes were similar in the pre- and the postdialysis period. These results suggest that 1) ANP causes a fall in mean arterial blood pressure, which in turn induces reflex tachycardia and activation of the sympathetic nervous system without diuresis; 2) the activated sympathetic nervous system as reflected in elevation of plasma norepinephrine may increase plasma renin activity; 3) reduced plasma aldosterone is not influenced by enhancement of the renin-angiotensin system; therefore, 4) reduction of plasma aldosterone as well as cortisol is probably due to direct action of ANP, and finally 5) AVP had no direct relation with ANP administration.
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PMID:Hormonal responses to synthetic atrial natriuretic peptide in patients on regular hemodialysis. 297 50

The goal of this study was to examine humoral mechanisms that regulate blood flow to the choroid plexus. We determined the effects of arginine vasopressin on blood flow (microspheres) to the choroid plexus in anesthetized and awake rabbits. In anesthetized rabbits, blood flow to the choroid plexus was 342 +/- 31 (mean +/- SEM) ml/min/100 g under control conditions. Intravenous infusion of vasopressin at 4 and 40 mU/kg increased plasma vasopressin levels from 11 +/- 1 to 55 +/- 15 and 441 +/- 120 pg/ml, respectively, and blood flow to the choroid plexus decreased by 48 +/- 6% and 70 +/- 4%. Cerebral blood flow was not affected by infusion of vasopressin. Similar responses to infusion of vasopressin were observed in awake rabbits. The V1 antagonist [d(CH2)5Tyr(Me)AVP] (10 micrograms/kg i.v.) had no effect on resting blood flow, but abolished the effect of vasopressin on blood flow to the choroid plexus. Vasoconstrictor responses of the choroid plexus to intravenous infusion of phenylephrine were not attenuated by the V1 antagonist. Thus, circulating vasopressin, at plasma levels that are observed under physiological and pathophysiological conditions, has marked effects on blood flow to the choroid plexus. These effects appear to be mediated through a V1 receptor. We speculate that vasopressin may play an important role in regulation of blood flow to the choroid plexus and perhaps in the regulation of cerebrospinal fluid production.
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PMID:Humoral regulation of blood flow to choroid plexus: role of arginine vasopressin. 339 58


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