Plasma arginine vasopressin during neck suction in upright sitting man

1987 ◽  
Vol 114 (2) ◽  
pp. 243-248 ◽  
Author(s):  
P. Norsk ◽  
F. Bonde-Petersen ◽  
J. Warberg
Keyword(s):  
Arterial Pressure ◽  
Arginine Vasopressin ◽  
Venous Pressure ◽  
Haemoglobin Concentration ◽  
Plasma Osmolality ◽  
Systolic Arterial Pressure ◽  
Plasma Sodium ◽  
Fluid Restriction ◽  
Vasopressin Secretion ◽  
Plasma Arginine

Abstract. In order to examine the influence of carotid baroreceptor stimulation on arginine vasopressin secretion, 8 normal healthy males were subjected to static neck suction of −3.3 kPa for 20 min in the upright sitting position after overnight food and fluid restriction. The plasma concentration of arginine vasopressin did not change significantly during neck suction. However, in 3 subjects the termination of neck suction induced large increases in plasma arginine vasopressin from 1.8 to 63.7 ng/l, from 0.7 to 34.3 ng/l and from 2.1 to 19.0 ng/l, respectively. Two subjects experienced symptoms such as nausea and paleness during neck suction. Systolic arterial pressure increased slightly but significantly during neck suction from 15.3 ± 0.3 to 15.7 ± 0.4 kPa (N = 7, P < 0.05), whereas mean arterial pressure, diastolic arterial pressure, central venous pressure, heart rate, plasma osmolality, plasma sodium and potassium were unchanged. Haemoglobin concentration in blood and haematocrit increased significantly during and after neck suction, whereas plasma volume decreased. We conclude that neck suction with a negative pressure of 3.3 kPa in upright sitting man does not significantly affect plasma arginine vasopressin. However, termination of the stimulation induces large increases in some subjects. This may be explained by a direct effect on the vagus nerve or by a selective deloading of carotid baroreceptors.

Thirst and vasopressin release in the dog: an osmoreceptor or sodium receptor mechanism?

1980 ◽  
Vol 238 (5) ◽  
pp. R333-R339 ◽  
Author(s):  
T. N. Thrasher ◽  
C. J. Brown ◽  
L. C. Keil ◽  
D. J. Ramsay
Keyword(s):  
Plasma Osmolality ◽  
Sodium Concentration ◽  
Plasma Sodium ◽  
Nacl Solution ◽  
Elevated Plasma ◽  
Vasopressin Release ◽  
Hypertonic Glucose ◽  
Hypertonic Solutions ◽  
Vasopressin Secretion ◽  
Plasma Arginine

The effects of intravenous infusion of hypertonic NaCl, sucrose, glucose, urea, or isotonic NaCl solution on thirst and plasma arginine vasopressin concentration (AVP) were studied in five conscious dogs. The changes in osmolality and sodium concentration of plasma and cerebrospinal fluid (CSF) were measured at the threshold of drinking, or after 45 min if no drinking occurred. Hypertonic NaCl and sucrose stimulated drinking in all dogs and significantly elevated plasma AVP. Equally hypertonic glucose, urea, or isotonic NaCl failed to stimulate any drinking or vasopressin secretion. All hypertonic solutions caused significant and similar increases in the osmolality and sodium concentration of CSF. Plasma osmolality was increased by the hypertonic solutions. Plasma sodium was increased by hypertonic NaCl, decreased by sucrose and glucose, and not changed by urea. Isotonic NaCl had no effect on either plasma or CSF composition. These data are not consistent with either a sodium or an osmoreceptor mechanism located within the blood-brain barrier (BBB) or with a peripheral sodium receptor mechanism. An intracranial osmoreceptor located on the blood side of the BBB is proposed to explain these results.

Regulation of vasopressin secretion in a patient with chronic hypernatraemia

1985 ◽  
Vol 110 (3) ◽  
pp. 346-351 ◽  
Author(s):  
Simon Smitz ◽  
Jean-Jacques Legros
Keyword(s):  
Hypertonic Saline ◽  
Arginine Vasopressin ◽  
Plasma Osmolality ◽  
Concomitant Increase ◽  
Specific Radioimmunoassay ◽  
Vasopressin Secretion ◽  
Plasma Arginine ◽  
The Brain ◽  
Unrestricted Diet ◽  
Hypertonic Saline Infusion

Abstract. A patient with the chronic hypernatraemia syndrome is described. Using a sensitive and specific radioimmunoassay, the plasma arginine-vasopressin (AVP) level was measured under various conditions. With an unrestricted diet, the plasma AVP level was inappropriately low for the degree of plasma hyperosmolality (0.9 pmol/l and 302 mOsm/kg, respectively). After chronic water loading, plasma osmolality was 271 mOsm/kg, plasma AVP level 1.5 pmol/l, and the urine remained hypertonic with respect to the plasma. During hypertonic saline infusion, plasma osmolality increased from 271 to 294 mOsm/kg without a concomitant increase in the plasma AVP concentration. After sc injection of apomorphine and after haemodynamic stimulation, the plasma AVP concentration increased from 0.8 to 36 pmol/l and from 1.2 to 6.3 pmol/I, respectively. These data demonstrate a selective deficiency in the osmoregulation of the AVP secretion. The observed neuroendocrine abnormalities may be linked to a congenital malformation of the brain.

Hyponatraemia in quadriplegic patients

1988 ◽  
Vol 75 (4) ◽  
pp. 441-444 ◽  
Author(s):  
David J. Leehey ◽  
Alicia A. Picache ◽  
Gary L. Robertson
Keyword(s):  
Arginine Vasopressin ◽  
Fluid Intake ◽  
Plasma Osmolality ◽  
Free Water ◽  
Plasma Sodium ◽  
Free Water Clearance ◽  
Water Excretion ◽  
Water Load ◽  
Daily Urine ◽  
Plasma Arginine

1. Studies were performed in five hyponatraemic (plasma sodium 129 ±1.6 mmol/l; plasma osmolality 268 ±3.0 mosmol/kg) quadriplegic patients in order to elucidate its aetiology. Five age- and sex-matched healthy subjects served as controls. 2. Daily urine volumes were high (4454 ± 624 ml) in the quadriplegic patients secondary to habitually increased fluid intake. 3. All quadriplegic patients had suppressed plasma arginine vasopressin levels (< 0.8 pmol/l) and were able to form dilute urine after a water load (20 ml/kg). However, free water clearance and the ability to excrete the water load were frequently impaired, and these defects were associated with reductions in both osmolar clearance and delivery of filtrate to the distal diluting sites of the nephron. 4. During hypertonic saline (5%, w/v, NaCl) infusion, plasma arginine vasopressin rose progressively before plasma osmolality reached the normal range, consistent with a resetting of the osmostat. 5. We conclude that hyponatraemia in quadriplegic patients is related to an intrarenal defect in water excretion and resetting of the osmostat coupled with increased fluid intake.

Osmoregulation in pseudopregnant and prolactin-treated rats: comparison with normal gestation

1988 ◽  
Vol 254 (3) ◽  
pp. R478-R484 ◽  
Author(s):  
W. M. Barron ◽  
M. D. Lindheimer
Keyword(s):  
Arginine Vasopressin ◽  
Plasma Osmolality ◽  
Plasma Sodium ◽  
Minimal Effect ◽  
Sprague Dawley ◽  
Pregnant Rats ◽  
Sprague Dawley Rats ◽  
Plasma Arginine ◽  
Normal Gestation

Osmoregulation was studied throughout rodent pregnancy focusing on the importance of the fetoplacental unit and prolactin in the observed alterations. Plasma osmolality (Posmol) and plasma sodium (PNa), similar in 8-day gravid and virgin Sprague-Dawley rats, decreased significantly by gestational day 10, reaching a nadir 8-10 mosmol/kg and 3-5 meq/l, respectively, below virgin levels by day 14 (both P less than 0.001). Despite this, plasma arginine vasopressin (PAVP) was measurable and similar in all pregnant and virgin groups. Osmotic thresholds for arginine vasopressin (AVP) secretion, similar in 8-day gravid and virgin rats, decreased 7.7 and 10.7 mosmol/kg in 12- and 14-day pregnant rats, respectively (both P less than 0.001). In contrast, Posmol decreased less than 2 mosmol/kg in 12- to 14-day pseudopregnant animals. When pseudopregnancy was prolonged to 18 days by prior hysterectomy, Posmol was only 2.6 mosmol/kg below that of cycling, hysterectomized controls. In other studies 14 days of hyperprolactinemia evoked by estradiol or treatment with ovine or rat prolactin had minimal effect on Posmol. We conclude that parallel decrements in Posmol and osmotic thresholds for AVP release occur during early rodent pregnancy, alterations that cannot be explained by gestational increases in circulating prolactin. In addition, the failure of pseudopregnancy. to mimic the hypotonicity of gestation suggests an important role for the fetoplacental unit in the osmoregulatory changes of rat pregnancy.

Arginine vasopressin, circulation, and kidney during graded water immersion in humans

1986 ◽  
Vol 61 (2) ◽  
pp. 565-574 ◽  
Author(s):  
P. Norsk ◽  
F. Bonde-Petersen ◽  
J. Warberg
Keyword(s):  
Arginine Vasopressin ◽  
Water Immersion ◽  
Venous Pressure ◽  
Free Water ◽  
Systolic Arterial Pressure ◽  
Free Water Clearance ◽  
Plasma Arginine ◽  
Normal Males ◽  
Solute Excretion ◽  
Rebreathing Method

Ten normal males rested sitting upright at an air temperature of 28 degrees C for 5.5 h (control, C) and underwent 4 h of graded water immersion (WI) to the umbilicus (UI), to the chest (CI), and to the neck (NI), respectively (water temperature = 34.5 degrees C), on different experimental days. Plasma arginine vasopressin (PAVP) was suppressed during WI compared with C and maximally so during NI. However, there was no change in PAVP comparing CI with UI even though central venous pressure (CVP) increased. CVP increased during CI and NI compared with C but was unchanged during UI, whereas cardiac output (rebreathing method), stroke volume, and plasma volume increased to approximately the same level during all three steps of WI compared with C. Heart rate and total peripheral vascular resistance decreased during UI, CI, and NI. Systolic arterial pressure (SAP) and pulse pressure (PP) were increased gradually from prestudy related to the degree of WI. Also diuresis, natriuresis, kaliuresis, osmotic excretion, and clearance were increased gradually compared with C, whereas free water clearance (CH2O) gradually decreased. There were weak negative but statistically significant correlations between PAVP and CVP and between changes in PAVP from prestudy and corresponding changes in SAP and PP. Furthermore, a statistically significant and negative correlation between CH2O and natriuresis could be established. We conclude that graded immersion gradually increases central blood volume and decreases PAVP. However, not only cardiopulmonary mechanoreceptors but also arterial baroreceptors may play a role in AVP suppression during WI in humans. In hydropenic subjects the suppression of PAVP during WI is apparently not effective in counteracting the decrease in CH2O induced by increased solute excretion.

Prompt recovery of plasma arginine vasopressin in diabetic coma after intravenous infusion of a small dose of insulin and a large amount of fluid

1990 ◽  
Vol 122 (4) ◽  
pp. 455-461 ◽  
Author(s):  
San-e Ishikawa ◽  
Toshikazu Saito ◽  
Koji Okada ◽  
Shoichiro Nagasaka ◽  
Takeshi Kuzuya
Keyword(s):  
Blood Volume ◽  
Serum Protein ◽  
Arginine Vasopressin ◽  
Small Dose ◽  
Plasma Osmolality ◽  
Diabetic Coma ◽  
Diabetic Patients ◽  
Volume Depletion ◽  
Circulating Blood Volume ◽  
Plasma Arginine

Abstract. 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 < 0.01), serum protein (r = 0.487, p < 0.01), Posm (r = 0.388, p < 0.01), and blood glucose (r = 0.582, p < 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 <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.

Altered osmotic thresholds for vasopressin secretion and thirst in human pregnancy

1984 ◽  
Vol 246 (1) ◽  
pp. F105-F109 ◽  
Author(s):  
J. M. Davison ◽  
E. A. Gilmore ◽  
J. Durr ◽  
G. L. Robertson ◽  
M. D. Lindheimer
Keyword(s):  
Plasma Osmolality ◽  
Late Pregnancy ◽  
Base Line ◽  
Urinary Volume ◽  
Human Pregnancy ◽  
Slow Infusion ◽  
Vasopressin Secretion ◽  
The Subject ◽  
The Mean ◽  
Plasma Arginine

Osmoregulation was studied in eight women during late pregnancy and again 8-10 wk postpartum. Base-line plasma osmolality (Posmol) was significantly lower during (280.9 +/- 2.1 mosmol/kg, SD) than after (289.4 +/- 2.1 mosmol/kg) pregnancy yet 24-h urinary volume and plasma arginine vasopressin (PAVP) measured in vasopressinase-inactivated blood was similar in both groups (pregnancy, 1.39 +/- 0.56 pg/ml; postpartum, 1.25 +/- 0.62 pg/ml). After 12 h of dehydration PAVP rose similarly and significantly both during (2.25 +/- 0.81 pg/ml) and after (2.89 +/- 1.19 pg/ml) gestation, and Uosmol was similar on both occasions (pregnancy, 779 +/- 121 mosmol/kg; postpartum, 784 +/- 102 mosmol/kg). When Posmol was increased by the slow infusion of 5% saline PAVP increased as soon as body tonicity did both during and after pregnancy. PAVP correlated significantly with Posmol in each subject (range of r, 0.75-0.99) and the mean regression lines [pregnancy, PAVP = 0.32 (Posmol; -279), r = 0.79; postpartum, PAVP = 0.38 (Posmol, -285), r = 0.86] demonstrated that the apparent osmotic threshold for AVP secretion was 6 mosmol/kg lower during than after gestation. Similarly the Posmol at which the subject experienced a conscious desire to drink was lower in pregnant (287 +/- 1.6 mosmol/kg) compared with postpartum subjects (298 +/- 2.0 mosmol/kg; P less than 0.001). These data demonstrate decreased osmotic thresholds for AVP release and thirst during human pregnancy and explain why gravidas can maintain their new lower Posmol within narrow limits.

Normotensive sodium loading in normal man: regulation of renin secretion during β-receptor blockade

2009 ◽  
Vol 296 (2) ◽  
pp. R436-R445 ◽  
Author(s):  
Simon Mølstrøm ◽  
Nils H. Larsen ◽  
Jane A. Simonsen ◽  
Remon Washington ◽  
Peter Bie
Keyword(s):  
Arterial Pressure ◽  
Sodium Excretion ◽  
Sodium Intake ◽  
Venous Pressure ◽  
Macula Densa ◽  
Renin Secretion ◽  
Sodium Reabsorption ◽  
Plasma Sodium ◽  
Adrenergic Blockade ◽  
Saline Loading

Saline administration may change renin-angiotensin-aldosterone system (RAAS) activity and sodium excretion at constant mean arterial pressure (MAP). We hypothesized that such responses are elicited mainly by renal sympathetic nerve activity by β1-receptors (β1-RSNA), and tested the hypothesis by studying RAAS and renal excretion during slow saline loading at constant plasma sodium concentration (Na+ loading; 12 μmol Na+·kg−1·min−1 for 4 h). Normal subjects were studied on low-sodium intake with and without β1-adrenergic blockade by metoprolol. Metoprolol per se reduced RAAS activity as expected. Na+ loading decreased plasma renin concentration (PRC) by one-third, plasma ANG II by one-half, and plasma aldosterone by two-thirds (all P < 0.05); surprisingly, these changes were found without, as well as during, acute metoprolol administration. Concomitantly, sodium excretion increased indistinguishably with and without metoprolol (16 ± 2 to 71 ± 14 μmol/min; 13 ± 2 to 55 ± 13 μmol/min, respectively). Na+ loading did not increase plasma atrial natriuretic peptide, glomerular filtration rate (GFR by 51Cr-EDTA), MAP, or cardiac output (CO by impedance cardiography), but increased central venous pressure (CVP) by ∼2.0 mmHg ( P < 0.05). During Na+ loading, sodium excretion increased with CVP at an average slope of 7 μmol·min−1·mmHg−1. Concomitantly, plasma vasopressin decreased by 30–40% ( P < 0.05). In conclusion, β1-adrenoceptor blockade affects neither the acute saline-mediated deactivation of RAAS nor the associated natriuretic response, and the RAAS response to modest saline loading seems independent of changes in MAP, CO, GFR, β1-mediated effects of norepinephrine, and ANP. Unexpectedly, the results do not allow assessment of the relative importance of RAAS-dependent and -independent regulation of renal sodium excretion. The results are compatible with the notion that at constant arterial pressure, a volume receptor elicited reduction in RSNA via receptors other than β1-adrenoceptors, decreases renal tubular sodium reabsorption proximal to the macula densa leading to increased NaCl concentration at the macula densa, and subsequent inhibition of renin secretion.

Distension of the pulmonary vein – atrial junctions and plasma vasopressin in the chloralose-anaesthetized dog

1983 ◽  
Vol 61 (8) ◽  
pp. 905-910 ◽  
Author(s):  
N. Wilson ◽  
J. R. Ledsome
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Pulmonary Vein ◽  
Arginine Vasopressin ◽  
Left Atrial ◽  
Vagus Nerves ◽  
Plasma Vasopressin ◽  
Plasma Arginine ◽  
Atrial Receptors ◽  
Anaesthetized Dog

The effects of localized distension of the pulmonary vein–left atrial junctions on plasma arginine vasopressin (AVP) have been examined in chloralose anaesthetized dogs. Pulmonary vein distension caused an increase in heart rate and a decrease in plasma AVP concentration. Cooling the vagosympathetic nerves to 10 °C caused an increase in arterial pressure and plasma AVP concentration and prevented the changes in heart rate and plasma AVP concentration caused by pulmonary vein distension. Cooling the vagus nerves to 16 °C did not change heart rate, arterial pressure, or plasma AVP concentration but significantly reduced the changes in heart rate and plasma AVP concentration caused by pulmonary vein distension. Propranolol (0.5 mg/kg) decreased heart rate and prevented the increase in heart rate associated with pulmonary vein distension but did not abolish the decrease in plasma AVP concentration. It is concluded that distension of the pulmonary vein – left atrial junctions causes a decrease in plasma AVP concentration by stimulating atrial receptors with myelinated afferent fibres. The decrease in plasma AVP concentration is not secondary to the reflex changes in heart rate caused by pulmonary vein distension.

Dependent effect of drinking volume on vasopressin but not atrial peptide in humans

1989 ◽  
Vol 257 (4) ◽  
pp. R762-R764 ◽  
Author(s):  
T. D. Williams ◽  
J. R. Seckl ◽  
S. L. Lightman
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Atrial Natriuretic Peptide ◽  
Hormone Secretion ◽  
Plasma Osmolality ◽  
Reflex Inhibition ◽  
Analog Scale ◽  
Dependent Effect ◽  
Plasma Arginine

The act of drinking causes a fall in plasma arginine vasopressin (AVP) concentration that precedes changes in plasma osmolality. To investigate the specificity of this drinking stimulus on hormone secretion, six volunteers (5 male, 1 female, aged 22-39 yr) were water deprived for 36 h and then drank 15 ml/kg water at 10-12 degrees C using 15-20 swallowing actions/min over 3.5 +/- 0.5 min (mean +/- SE). This caused a fall in plasma AVP from 4.5 +/- 0.7 to 3.2 +/- 0.5 pmol/l (P less than 0.05) and in thirst (by 5.7 +/- 0.6 on a 10-cm linear analog scale) (P less than 0.05) 5 min after drinking. No significant changes occurred in mean arterial pressure, heart rate, or plasma atrial natriuretic peptide (ANP) concentration. A second study was undertaken to determine whether the reflex inhibition of AVP secretion is activated simply by the act of swallowing regardless of the volume of liquid consumed. The six volunteers were water deprived for 36 h and then sipped and swallowed 1 ml/kg water at 10-12 degrees C using 15-20 swallowing actions/min over 3.0 +/- 0.1 min. There was no change in plasma AVP concentration, although thirst was reduced by 2.3 +/- 0.6 (P less than 0.05) at 5 min. Plasma AVP 10 min after sipping and swallowing (4.2 +/- 0.8 pmol/l) was significantly greater than at 10 min after drinking 15 ml/kg (2.8 +/- 0.5 pmol/l) (P less than 0.05) despite the fact that plasma osmolality at this stage was similar in both studies. We conclude that the drinking-mediated reflex inhibition of AVP secretion in humans is dependent on swallowing an adequate volume and is not accompanied by changes in hemodynamics or in plasma ANP concentration.

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