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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Resting and stimulated free calcium concentrations have been measured in platelets loaded with the fluorescent probe quin2 from 30 patients with essential hypertension and from 30 age-matched controls. 2. Cytosolic free calcium concentrations were 94.6 +/- 2.7 (mean +/- SEM) in the hypertensive group and 91.7 +/- 2.8 nmol/l in the normotensive group, the difference was not significant. 3. Arginine vasopressin caused a transient increase in platelet free calcium concentration in all subjects. In the presence of extracellular calcium the increase was significantly higher in the control subjects than in the hypertensive patients (P = 0.005). In the absence of extracellular calcium, arginine vasopressin caused much smaller increases, and there was then no difference between the responses of the two groups. 4. Platelet free calcium concentrations were measured again in 13 patients after 8 weeks treatment with either verapamil (n = 6) or atenolol (n = 7). The reductions in systolic pressure after drug treatment were correlated with the changes in cytosolic free calcium concentrations (r = 0.75, P less than 0.01).
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PMID:Platelet cytosolic free calcium in essential hypertension: responses to vasopressin. 276 58

Insulin-induced hypoglycemia is a potent stress stimulating ACTH release, but the factors responsible for this ACTH secretion are not known. In this study, several ACTH-stimulating factors, such as CRH, arginine vasopressin (AVP), epinephrine (E), norepinephrine (NE), and dopamine, in addition to ACTH, cortisol, and glucose, were simultaneously measured in plasma before and 15, 30, 60, 90, and 120 min after iv administration of 0.1 U/kg BW regular insulin to seven normal subjects. Insulin administration resulted in significant rises in the mean plasma ACTH level from 4.6 +/- 1.1 (+/- SEM) to 21.6 +/- 4.8 pmol/L at 30 min (P less than 0.01) and in plasma cortisol from 330 +/- 60 to 720 +/- 50 nmol/L at 60 min (P less than 0.01). These increases were preceded by a 41.0 +/- 1.9% (P less than 0.001) fall in blood glucose levels. The mean plasma CRH level rose significantly from 1.0 +/- 0.1 to 1.2 +/- 0.1 pmol/L (P less than 0.01) at 30 min and remained elevated until 120 min. In addition, concomitant and significant rises in plasma AVP levels (basal, 1.5 +/- 0.01; peak, 4.5 +/- 1.1 pmol/L at 30 min; P less than 0.01), E (basal, less than 50; peak, 640 +/- 130 pmol/L at 30 min; P less than 0.01), and NE (basal, 0.07 +/- 0.01; peak, 0.17 +/- 0.03 nmol/L at 60 min; P less than 0.05), but not dopamine, also occurred. These results suggest that multiple ACTH-releasing factors, such as CRH, AVP, E, and NE, are involved in ACTH secretion induced by insulin-induced hypoglycemia in man.
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PMID:Hormonal responses to insulin-induced hypoglycemia in man. 282 51

A chronic fetal sheep preparation was developed to measure, without interruption in utero, urethral and urachal urine output to the amniotic and allantoic sacs, respectively. Fetal urethral, urachal and total urine output was measured during a 5 day post-operative period, in late gestation. Total fetal urine output increased from day 1 to a volume of 1216 +/- 115 ml/day (SEM) on day 5 post-operative. Urachal urine output increased significantly from 12 ml/day on day 1 to 467 ml/day on day 5 (P less than 0.05). Fetal arterial blood gases, pH and immunoreactive ACTH, cortisol and immunoreactive arginine vasopressin concentrations were stable throughout the 5-day recovery period. Fetal urachal urine output to the allantoic cavity and total fetal urine output appears to require 4-5 days to stabilize post-operatively. Fetal urine is a major source of amniotic and allantoic fluid in late gestation and the volume of these sacs may be influenced, in part, by the distribution of urethral and urachal urine output.
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PMID:Urethral and urachal urine output to the amniotic and allantoic sacs in fetal sheep. 284 19

To determine the effect of clonidine, an alpha 2-adrenergic agonist, on atrial natriuretic factor (ANF) release during water deprivation, plasma immunoreactive ANF (IR-ANF) arginine vasopressin, diuresis and natriuresis were measured in rats which had been deprived of water for 24 and 48 hr after intravenous (IV) administration of 50 micrograms clonidine. In normally-hydrated rats clonidine produced a marked elevation of plasma IR-ANF from 40.5 +/- 4.6 pg/ml to 1064 +/- 22 pg/ml (mean +/- SEM) and sodium excretion from 73.3 +/- 6.8 microEq to 723.4 +/- 62.3 microEq. Clonidine evoked an increase in plasma IR-ANF from 16.6 +/- 5.9 pg/ml to 229.5 +/- 60 pg/ml (mean +/- SEM) after 24 hr water deprivation and from 13.6 +/- 7.4 pg/ml to 104.8 +/- 21 pg/ml (mean +/- SEM) after 48 hr water deprivation. Clonidine did not induce any significant changes in vasopressin levels. During 24 hr and 48 hr water deprivation vasopressin rose from 3.1 +/- 0.3 pg/ml to 7.3 +/- 1.3 pg/ml and 8.4 +/- 0.6 pg/ml (mean +/- SEM), respectively. In normally-hydrated rats clonidine produced a marked diuresis and natriuresis. These effects and urinary cGMP excretion were significantly inhibited by anti-ANF antibodies. Clonidine caused a significant increase in urine output in 24 hr water-deprived rats but the response was markedly lower than that seen in normally-hydrated rats. In conclusion, clonidine stimulates ANF release both in normally-hydrated and water-deprived rats. The diuretic effect of clonidine appears to be related to ANF release but not to inhibition of vasopressin.
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PMID:Clonidine stimulates atrial natriuretic factor (ANF) release in water-deprived rats. 285 43

Apomorphine, a centrally-acting emetic, was administered subcutaneously (50 micrograms/kg) to nine normal subjects (four male, five female; aged 22-36 years) and four patients with idiopathic diabetes insipidus (DI) (one male, three female; aged 24-49 years). In the normal subjects this stimulus caused nausea (and vomiting in seven of nine) with a latency of 9.5 +/- 0.9 min which was followed by a large increase in plasma arginine vasopressin (AVP) concentration (from 0.9 +/- 0.2 pmol/l to 249 +/- 104 pmol/l at 15 min after the onset of symptoms; mean +/- SEM, P less than 0.01). There was a small but significant increase in plasma oxytocin (OXT) concentration (from 1.6 +/- 0.4 pmol/l to 6.2 +/- 3.4 pmol/l; P less than 0.05). Mean arterial pressure (MAP) fell slightly (from 87 +/- 1.9 mm Hg to 71 +/- 4.4 mm Hg; P less than 0.05) 15 min after the onset of nausea; there was no change in blood haematocrit or plasma osmolality and sodium concentration. In the DI patients apomorphine produced nausea (with vomiting in three of four) with a latency of 10.0 +/- 1.4 min but failed to cause an increase in either plasma AVP or OXT. In the DI patients the fall in MAP did not reach statistical significance (83 +/- 4 mm Hg to 71 +/- 11 mm Hg); there was also no change in haematocrit, osmolality or sodium concentration. Ipecacuanha, an emetic with both peripheral and central actions, was administered orally to seven normal subjects (three male, four female; aged 22-36 years) six of whom also underwent apomorphine tests.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Responses of plasma oxytocin and arginine vasopressin to nausea induced by apomorphine and ipecacuanha. 290 23

We have investigated the role of adrenal steroids and the opiates in regulating arginine vasopressin (AVP) secretion into the pituitary stalk blood of the rat. The portal plasma concentration of AVP in urethane-anesthetized male rats was 532 +/- 68 pg/ml (mean +/- SEM), while the peripheral plasma AVP concentration in intact urethane-anesthetized rats was 20.7 +/- 5.7 pg/ml. Column chromatography on Sephadex G-25 of an extract of a pool of portal plasma revealed that the material being assayed comigrated with synthetic AVP. Bilateral adrenalectomy (ADX) 5 days before the collection of portal blood elevated portal plasma AVP concentrations approximately 6-fold (655 +/- 124 pg/ml in controls vs. 4090 +/- 504 pg/ml in adrenalectomized animals). Dexamethasone administration (15 micrograms/kg X day) for 5 days prevented the ADX-induced increase in portal plasma AVP concentrations without significantly changing portal plasma AVP concentrations in intact rats. Portal plasma concentrations of beta-endorphin were not changed by ADX or dexamethasone treatment. The iv infusion of morphine sulfate (3 mg/kg) dramatically decreased the concentration of AVP in the portal plasma of the rat (501 +/- 101 pg/ml before morphine vs. 185 +/- 50 pg/ml after morphine). The inhibitory effect of morphine was reversed by naltrexone (1.0 mg/kg), whereas naltrexone alone did not alter AVP secretion. Morphine administration also decreased systemic plasma AVP concentrations in urethane-anesthetized rats (27.1 +/- 6.6 pg/ml in controls vs. 3.3 +/- 1.3 pg/ml in morphine-treated rats). Naltrexone treatment reversed this effect. These results suggest that AVP secretion into pituitary stalk blood is under the inhibitory influence of the adrenal steroids, and the increased concentration of AVP found in portal blood may be partially responsible for the elevated levels of ACTH after ADX. Furthermore, morphine-induced activation of the pituitary-adrenal axis is apparently independent of hypothalamic AVP secretion.
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PMID:The concentration of arginine vasopressin in pituitary stalk plasma of the rat after adrenalectomy or morphine. 293 37

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

We studied, in normal volunteers, the effects of 1 hour of hypoxia on the concentration of angiotensin-converting enzyme and bradykinins, along with previously measured parameters of renal and endocrine function. Ten men, 18 to 42 years of age, undergoing water diuresis, breathed a low-oxygen mixture (five breathed 10.5% O2 and five 12% O2); all breathed 21% O2 on a control day. Measurements included mean blood pressure and heart rate every 2 to 3 minutes; plasma levels of renin activity, aldosterone, arginine vasopressin, norepinephrine, and bradykinin, and angiotensin-converting enzyme activity, before and at the end of gas breathing; and urine volume (UV), creatinine, Na+, and bradykinin concentration. Arterial blood gases and effective renal plasma flow were determined at the end of gas breathing only. Mean values +/- SEM for arterial blood gases with low O2 were pH 7.39 +/- 0.02, PO2 46 +/- 2 torr, PCO2 39 +/- 2 torr (12% O2) and 7.48 +/- 0.01, 35 +/- 1 torr, 33 +/- 1 torr (10.5% O2). Responses were otherwise identical in both groups, and data were combined for analysis. With hypoxia, heart rate and effective renal plasma flow increased significantly, P less than 0.005; no changes occurred in Uv, urine Na+ concentration, glomerular filtration rate, plasma or urine bradykinin concentration, serum angiotensin-converting enzyme activity, plasma renin activity, plasma aldosterone concentration, plasma arginine vasopressin concentration, or plasma norepinephrine concentration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal and hormonal responses to acute hypoxia in normal individuals. 298 95

A cytochemical assay has been developed to measure human plasma arginine vasopressin. It is based on the stimulation of Na+-K+, ATPase activity located in the outer medulla of the rat kidney, and is capable of detecting very low plasma arginine vasopressin concentrations, limit of detection 0.01 pmol/l. Specificity for vasopressin stimulation of the enzyme is conferred on the assay by the use of specific vasopressin antiserum. Index of precision of the assay is 0.21. Degradation of arginine vasopressin in plasma in inhibited by phenanthroline. Samples may be stored up to 8 weeks at -70 degrees C. Intra- and inter-assay coefficients of variation were 22% (n = 8) and 104% (n = 12), respectively. A sustained water load in eight healthy male adults caused a fall in plasma osmolality from a basal of 286.5 +/- 2.0 (mean +/- SEM) to 279.2 +/- 2.4 mmol/kg after the load (P less than 0.001), which was associated with a reduction in urine osmolality from 867 +/- 54 to 69 +/- 3 mmol/kg. Plasma immunoreactive arginine vasopressin fell from 1.3 +/- 0.3 pmol/l to become undetectable (less than 0.3 pmol/l), but plasma cytochemical arginine vasopressin decreased from 0.96 +/- 0.14 to 0.07 +/- 0.02 pmol/l. There was a curvilinear relationship between plasma osmolality and plasma cytochemical arginine vasopressin, which militated against the concept of an osmotic threshold for vasopressin release.
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PMID:Development of a cytochemical assay for plasma vasopressin: application to studies on water loading normal man. 301 8

Osmoregulation of vasopressin release and thirst was studied in the mid-follicular and mid-luteal phases of the menstrual cycle of five patients with cyclical oedema defined by peripheral oedema and weight gain (greater than 3.0 kg) manifest in two consecutive luteal phases. Results are compared to those already obtained in eight healthy women. In the patients, basal plasma osmolality in the mid-luteal phase was significantly lower than in the mid-follicular periods (patients, 283 +/- 1, 287 +/- 1 mOsmol/kg, respectively, mean +/- SEM, P less than 0.05; controls, 282 +/- 1, 286 +/- 1 mOsmol/kg, respectively, P less than 0.05). Plasma osmolality (pOsm) and plasma arginine vasopressin (pAVP) were measured during hypertonic (850 mmol/l) saline infusion in both phases of the cycle; linear regression analyses of these data gave the following mean regression equations, (i) mid-follicular, pAVP = 0.55 (pOsm - 285), r = 0.94 and (ii) mid-luteal, pAVP = 0.42 (pOsm - 281), r = 0.93. The abscissal intercept was significantly different (P less than 0.025). Osmotic threshold for severe thirst onset was lower in the mid-luteal phase compared to the mid-follicular value (296 +/- 1, 299 +/- 1 mOsmol/kg, respectively, P less than 0.01). Basal data and results of thirst onset and theoretical threshold for vasopressin release in response to osmotic stimulation obtained in the patients were similar to healthy control women. We conclude that osmoregulation in cyclical oedema is normal.
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PMID:Osmoregulation of vasopressin secretion and thirst in cyclical oedema. 325 60


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