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Biomedical subjects

G L Robertson

Publications and source records attributed to G L Robertson.

At least 91 records · Page 5Linked to original sources
PubMed1981

Vasopressin function in familial cranial diabetes insipidus.

A family suffering from cranial diabetes insipidus, that extends over 4 generations, is described. Inheritance of polyuria was autosomal dominant. Vasopressin function was studied in members of the last 2 generations, 4 of whom had polyuria. Osmoregulation of vasopressin secretion was assessed by infusion of hypertonic saline. Plasma vasopressin remained undetectable in one patient, while 2 others had very blunted vasopressin responses to osmotic stimulation. Three non-osmotic stimuli were applied. Controlled hypotension produced by trimetaphan infusion and insulin-induced hypoglycaemia did not increase plasma vasopressin but apomorphine-induced nausea caused a minimal rise in plasma vasopressin to 0.7 pg/ml. Polyuria and thirst resolved with antidiuretic therapy in all patients studied. Congenital absence of vasopressin as in Brattleboro rats is unlikely to account for diabetes insipidus in this disorder since small increases in vasopressin have been demonstrated in these patients. In view of previous post-mortem findings, familial cranial diabetes insipidus is most likely to be due to degeneration of vasopressin-synthesizing neurones.

Adult↗
PubMed1981

Increased thirst and plasma arginine vasopressin levels during 2-deoxy-D-glucose-induced glucoprivation in humans.

Insulin-induced hypoglycemia by unknown mechanism(s) increases plasma arginine vasopressin (AVP) levels in humans. Mechanisms for increased AVP levels during central nervous system glucoprivation were investigated by administering 20-min i.v. infusions of 2-deoxy-d-glucose (50 mg/kg), a competitive inhibitor of glucose utilization, or normal saline (sham), to 24 normal volunteers. Some of the infusions were administered in combination with neuropharmacological blocking agents (placebo). The behavioral, physiological, metabolic, and hormonal correlates of 2-deoxy-d-glucose (2DG)-induced gluco-privation and AVP secretion were studied in a group (n = 5) pretreated for 1 wk with either mazindol (1 mg per os three times per day), a potent norepinephrine and dopamine-reuptake blocker, or placebo. A second group (n = 5) received either propranolol (3 mg/3 min followed by 80 mug/min) or normal saline infusion before and during 2DG administration. With 2DG alone, plasma AVP levels increased from 1.3+/-0.3 pg/ml at base line to a peak of 4.5+/-1.4 pg/ml at 60 min and remained elevated for 150 min. From 30 to 180 min after 2DG administration, the 2DG-infused volunteers increased their water intake in comparison with sham-infused volunteers. Marked increases in epinephrine and slight increases in norepinephrine were associated with increases in plasma glucose and renin activity and decreases in plasma potassium. Plasma sodium and osmolality increased transiently and mean arterial pressure (MAP) fell. These changes, however, were small and inconstant and could not account for the observed increases in thirst and AVP levels. Pretreatment with mazindol prevented the decrease in MAP and the increase in plasma renin activity (PRA) following 2DG infusions without modifying increased thirst, water intake, or AVP responses to glucoprivation. Pretreatment with propranolol effectively blocked beta-adrenoreceptors as evidenced by increased MAP and plasma epinephrine, and abolition of the RPA increases during 2DG-induced glycoprivation, but did not suppress AVP and thirst responses. A cervical cord-sectioned patient lacking descending sympathetic out-flow had a potentiated thirst response to 2DG-induced glucoprivation in the absence of increases in sodium, catecholamines, and PRA. Thus 2DG administration activates mechanisms for increased thirst and AVP which are unrelated to changes in peripheral catecholamines, MAP, PRA, and osmolality.

Arginine Vasopressin↗
PubMed1981

Arginine vasopressin response to insulin-induced hypoglycemia in man.

Insulin-induced hypoglycemia causes an increase in plasma vasopressin concentration in man and rat. To assess the mechanism by which this occurs, the effect of hypoglycemia was studied in healthy adults. After insulin injection, a 7-fold rise in plasma immunoreactive arginine vasopressin to 8.2 +/- 3.6 pg/ml was observed in 10 normal subjects. This was associated with a rise in plasma sodium of 2 meq/liter, but no significant change in mean arterial pressure or hematocrit was observed. The significance of the plasma sodium rise was assessed by observing the vasopressin response to hypoglycemia in a patient shown previously to have a selective loss of the vasopressin response to osmotic stimulation. His plasma vasopressin rose from 1.6 to 12.5 pg/ml with no fall in blood pressure or volume. beta-Adrenergic blockade with propranolol before repeat insulin-induced hypoglycemia did not reduce the vasopressin response (peak plasma vasopressin, 8.1 +/- 1.7 pg/ml), despite suppression of PRA. Linear regression analysis showed that the rise in plasma vasopressin and the percentage decline in plasma glucose correlated significantly (r = 0.57, P less than 0.001). In conclusion, hypoglycemia releases vasopressin nonosmotically by a mechanism that appears to be independent of factors currently known to effect vasopressin secretion.

Adult↗
PubMed1981

DDAVP treatment of diabetes insipidus during pregnancy and the post-partum period.

A 23 year old woman with diabetes insipidus who had previously been treated with pitressin, pituitary snuff and chlorpropamide, was treated with DDAVP during pregnancy. DDAVP concentrations immunoassayed as vasopressin were determined in maternal serum and breast milk. Oxytocin antibodies were also determined in maternal serum.

Adult↗
PubMed1981

Vasopressin secretion in primary polydipsia and cranial diabetes insipidus.

Vasopressin secretion was studied in a group of 18 patients with polydipsia (urine volume greater than 21/24 h) in whom nephrogenic diabetes insipidus had been excluded. Osmoregulation of vasopressin release was defined by hypertonic saline infusion, and three independent non-osmotic tests of vasopressin release were also applied. A wide spectrum of abnormalities in vasopressin secretion was observed. Four patients seem to have primary polydipsia, since they showed a normal response to osmotic stimulation, but non-osmotic vasopressin release was subnormal in two. The remaining 14 patients had cranial diabetes insipidus, as judged by subnormal or absent vasoprsssin responses to hypertonic saline infusion. Of these 14, five had undetectable vasopressin during osmotic stimulation, but each mounted a response to the non-osmotic stimuli; three of these had familial polyuria. Three further patients appeared to have isolated osmoreceptor defects, showing normal responses to non-osmotic stimuli but none to osmotic stress. Four patients with partial cranial diabetes insipidus, as judged by subnormal vasopressin response to osmotic stimuli, seemed to have normal osmoreceptor function but deficient vasopressin release. There was no correlation between the degree of vasopressin response to osmotic stimuli and the three non-osmotic tests of vasopressin release, and in particular vasopressin release should not replace osmotic tests to define cranial diabetes insipidus.

Adult↗
PubMed1980

Role of vasopressin in the impaired water excretion of glucocorticoid deficiency.

The mechanism whereby glucocorticoid deficiency impairs renal water excretion was studied in the conscious mineralocorticoid-replaced, adrenalectomized rat. Control animals received physiologic replacement with prednisolone, and experimental animals were deprived of glucocorticoid hormone for either 1 or 14 days. The control animals excreted 95 +/- 1.9% of an acute water load (30 ml/kg) in 3 hours, a value significantly higher than the volume excreted by animals deprived fo glucocorticoid hormone for 1 day (70.0 +/- 3.6%, P less than 0.01) and 14 days (40.0 +/- 3.9%, P less than 0.01). Following the acute water load, plasma vasopressin levels, as measured by radioimmunoassay, was 1.08 pg/ml in the control rats, a value significantly lower than values obtained after the water load in rats deprived of glucocorticoid hormone for 1 day (2.5 +/- 0.2 pg/ml, P less than 0.01) and 14 days (2.4 +/- 0.3 pg/ml, P less than 0.01). To further examine the effect of plasma vasopressin in the impaired water excretion of glucocorticoid deficiency, we performed studied in Brattleboro rats with central diabetes insipidus. In these animals with absence of vasopressin, a defect in water excretion was observed after 14 days, but no 1 day, of glucocorticoid deficiency. In Sprague-Dawley rats, the impaired water excretion after 14 days of glucocorticoid deficiency was associated with a significantly lower cardiac index (209 +/- 14 vs. 291 +/- 11 ml/min/kg, P less than 0.01) and renal blood flow (3.8 +/- 0.3 vs. 5.7 +/- 0.2 ml/min/g, P less than 0.01) than that observed after 1 day of glucocorticoid deficiency. In diabetes insipidus rats, after 14 days of glucocorticoid deficiency, the percentage of an acute water load excreted (121 +/- 7% vs. 158.7 +/- 7.0%, P less than 0.01) was lower than that observed after 1 day of glucocorticoid deficiency. In summary, the present results indicate that glucocorticoid deficiency impairs renal water excretion by both vasopressin-dependent and vasopressin-independent mechanisms. The vasopressin-dependent renal mechanism is associated with a marked decrease in both systemic and renal hemodynamics.

Adrenalectomy↗
PubMed1980

Plasma vasopressin response to hypertonic saline infusion to assess posterior pituitary function.

Hypertonic saline was infused into 11 volunteers to osmotically stimulate vasopressin secretion. A strong positive correlation between plasma arginine vasopressin (PAVP) and plasma osmolality (Pos) was obtained, defined by the function PAVP=0.63 (Pos-284), r=+0.80, P<0.001. The sensitivity of vasopressin secretion to osmotic stimulation was represented by the slope of the expression and the theoretical threshold of vasopressin release by the abscissal intercept. Plasma osmolality at the onset of thirst was 298.5±1.1 mmol/kg. Application of hypertonic saline infusion to 10 polyuric patients clearly separated those with normal osmoregulation of vasopressin secretion from those with cranial diabetes insipidus.

Adult↗
PubMed1980

Vasopressin response to 2-deoxy-D-glucose in the rat.

The effect of 2-deoxyglucose (2DG) upon plasma arginine vasopressin (AVP), measured by a specific and sensitive RIA, has been studied in unanesthetized male Sprague-Dawley rats. Injection of the drug ip at a dose of 100 mg/kg BW caused a 10-fold rise in plasma AVP to 23.4 +/- 4.9 pg/ml (mean +/- SD). This effect was associated with a rise in plasmas osmolality to 301.8 +/- 3.9 mosmol/kg, but this change was accounted for totally by a rise in plasma glucose to 17.3 +/- 3.0 mM and in plasma urea to 3.4 +/- 0.4 mM. The only effective solute, plasma sodium, fell to 135.0 +/- 0.8 mM. Idiogenic osmoles did not change. Blood volume was reduced by about 5%, while PRA and mean arterial pressure did not change. Thus, the rise in plasma AVP caused by 2DG was not mediated by osmotic or hemodynamic stimuli. Treatment with propranolol (2.5 mg/kg BW) 15 min before 2DG completely abolished the AVP response. These results indicate that 2DG stimulates AVP release by a primary mechanism different from that which mediates the effect of insulin-induced hypoglycemia on AVP.

Animals↗
PubMed1980

Rat vasopressin response to insulin-induced hypoglycemia.

The effect of insulin-induced hypoglycemia upon plasma arginine vasopressin measured by a specific and sensitive RIA has been studied in unanesthetized male Sprague-Dawley rats. Hypoglycemia caused a 5-fold rise in plasma arginine vasopressin to a maximum of 28.0 +/- 9.1 pg/ml (mean +/- SD). This response was associated with a 2% fall in plasma osmolality, a rise in plasma sodium of less than 1%, a 10% fall in estimated blood volume, and no significant change in mean arterial blood pressure. PRA was increased 5-fold by hypoglycemia. However, beta-adrenergic blockade with propranolol completely prevented the renin response without altering the rise in vasopressin. In contrast, water loading abolished and hypertonic saline loading enhanced the effect of hypoglycemia on plasma vasopressin. We conclude that insulin-induced hypoglycemia stimulates vasopressin secretion by some as yet unrecognized primary mechanism whose responsiveness can be altered by changes in osmolality.

Animals↗
PubMed1980

Evidence in man that cigarette smoking induces vasopressin release via an airway-specific mechanism.

The plasma vasopressin response to intravenous nicotine (2 mg) and smoking cigarettes of high (1.2 mg) and low (0.6 mg) nicotine content was studied in healthy young subjects with a history of cigarette smoking. Nicotine administered intravenously had no effect on plasma vasopressin. There was a statistically significant increase in plasma vasopressin after both the low and high content cigarettes, with the high content cigarettes resulting in a significantly greater increase. All three interventions resulted in transient increases in blood pressure and pulse of similar magnitude. These studies indicate that cigarette smoking-induced vasopressin release is not mediated via an action of circulating nicotine, and suggest the presence of an airway-specific mechanism for vasopressin release.

Adult↗
PubMed1979

Influence of the emetic reflex on vasopressin release in man.

The mechanisms underlying the frequent association of nausea and vomiting with elevations of plasma vasopressin(PAVP) were studied in man and rat. After oral water loads (N = 16), plasma osmolality fell in all human subjects and was associated with a decline in PAVP in 14 asymptomatic human subjects. In 2 human subjects, nausea occurred and was associated with increases in PAVP, without changes in blood pressure. During ethanol infusion (N = 28), PAVP was suppressed unless nausea supervened. In 4 nauseated human subjects, PAVP escaped from ethanol inhibition and rose to levels 10 times basal, despite the absence of hemodynamic changes. Apomorphine, a potent dopamine agonist and emetic agent, was administered to human volunteers in doses of 7 to 24 microgram/kg. There was no increase in PAVP in 3 human subjects who remained asymptomatic (7 to 16 microgram/kg). Ten human subjects experienced nausea after 16 microgram/kg, which was followed shortly by marked increases in PAVP. Emesis occurred in 5 human subjects given 16 to 24 microgram/kg, and was followed by PAVP levels similar to those seen with nausea alone. In 7 human subjects from the nausea group, the repeat study (16 microgram/kg) after pretreatment with dopamine antagonist (haloperidol, N = 4; fluphenazine, N = 3) resulted in complete blockage of apomorphine-induced AVP release. In rats, which lack an emetic reflex, apomorphine doses of 200 microgram/kg induced only slight increases in PAVP when compared to the response to 16 microgram/kg in man. These studies indicate that stimulation of the emetic reflex results in AVP-release in man. Nausea-mediated AVP release supervenes over concomitant osmolar or pharmacologic (ethanol) inhibition.

Alcohols↗