Inhibition of plasma vasopressin after drinking in dehydrated humans

1984 ◽  
Vol 247 (6) ◽  
pp. R968-R971 ◽  
Author(s):  
G. Geelen ◽  
L. C. Keil ◽  
S. E. Kravik ◽  
C. E. Wade ◽  
T. N. Thrasher ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Volume ◽  
Arginine Vasopressin ◽  
Tap Water ◽  
Renin Activity ◽  
Plasma Vasopressin ◽  
Rapid Fall ◽  
Before And After ◽  
Plasma Arginine

To study the effects of nonosmotic and nonvolumetric factors that may influence secretion of vasopressin, serum Na+, K+, and osmolality (Osm), hemoglobin, hematocrit, plasma arginine vasopressin (AVP), aldosterone (PA), and renin activity (PRA) were measured in five men and three women (26–50 yr, 73 +/- 4 kg) before and after 24 h of mild dehydration (food but no fluid) and seven times during the 1st h after rehydration with 10 ml/kg of tap water (17.5 +/- 0.5 degrees C) consumed in 105 s (range 35-240 s). Dehydration increased mean serum Na+ 3.7 +/- 0.7 meq/l (P less than 0.05), osmolality 9.1 +/- 1.1 mosmol/kg (P less than 0.05), and AVP from a hydrated level of 1.7 +/- 0.2 to 3.3 +/- 0.5 pg/ml (delta = 1.6 pg/ml, P less than 0.05). After rehydration AVP fell to 2.4 +/- 0.3 pg/ml (P less than 0.05) within 3 min and reached the water-replete level of 1.8 +/- 0.3 pg/ml 9 min after drinking started. Serum Na+ and Osm did not change until 30–60 min after drinking. No significant changes occurred in PRA, hemogloblin, hematocrit, or calculated delta in plasma volume, but PA increased from 11.1 +/- 1.5 ng/dl after dehydration to 15.6 +/- 2.6 ng/dl (P less than 0.05) between 30 and 60 min after drinking. The rapid fall in plasma AVP after rehydration took place in the absence of the expected changes in the primary regulators of plasma AVP (i.e., osmolality and plasma volume), with no change in blood pressure. The results suggest that oropharyngeal factors, alone or combined with gastric stimuli, are implicated.

Plasma vasopressin and renin activity in women exposed to bed rest and +Gz acceleration

1976 ◽  
Vol 40 (6) ◽  
pp. 911-914 ◽  
Author(s):  
L. C. Keil ◽  
S. Ellis
Keyword(s):  
Plasma Renin Activity ◽  
Arginine Vasopressin ◽  
Plasma Renin ◽  
Bed Rest ◽  
Significant Rise ◽  
Renin Activity ◽  
Marked Rise ◽  
Plasma Vasopressin ◽  
Before And After ◽  
Plasma Arginine

To study the effect of prolonged recumbency on plasma vasopressin and renin activity, eight women (23–34 yr) were subjected to 17 days of absolute bed rest. The +3 Gz tolerance of the subjects was tested before and after 14 days of bed rest. From day 2 and through day 17 of bed rest, plasma arginine vasopressin (AVP) levels were reduced 33%. Plasma renin activity (PRA) increased 91% (P less than 0.05) above ambulatory control values from days 10 through 15 of bed rest. When compared to precentrifuge values, exposure to +3 Gz prior to bed rest provoked a 20-fold rise (P less than 0.05) in mean plasma AVP but resulted in only a slight increase in PRA. After bed rest, acceleration increased plasma AVP 7-fold (P less than 0.02); however, the magnitude of this increase was less than the post +3Gz value obtained prior to bed rest. After bed rest, no significant rise was noted in PRA following +3 Gz. This study demonstrates that prolonged bed rest leads to a significant rise in the PRA of female subjects, while exposure to +Gz acceleration provokes a marked rise in plasma AVP.

Menstrual status and plasma vasopressin, renin activity, and aldosterone exercise responses

1989 ◽  
Vol 67 (2) ◽  
pp. 736-743 ◽  
Author(s):  
M. J. De Souza ◽  
C. M. Maresh ◽  
M. S. Maguire ◽  
W. J. Kraemer ◽  
G. Flora-Ginter ◽  
...  
Keyword(s):  
Follicular Phase ◽  
Renin Activity ◽  
Cycle Phase ◽  
Menstrual Phase ◽  
Menstrual Status ◽  
Plasma Vasopressin ◽  
Before And After ◽  
Early Follicular Phase ◽  
Plasma Arginine ◽  
Midluteal Phase

The effects of menstrual cycle phase (early follicular vs. midluteal) and menstrual status (eumenorrhea vs. amenorrhea) on plasma arginine vasopressin (AVP), renin activity (PRA), and aldosterone (ALDO) were studied before and after 40 min of submaximal running (80% maximal O2 uptake). Eumenorrheic runners were studied in the early follicular and midluteal phases determined by urinary luteinizing hormone and progesterone and plasma estradiol and progesterone assays; amenorrheic runners were studied once. Menstrual phase was associated with no significant differences in preexercise plasma AVP or PRA, but ALDO levels were significantly higher during the midluteal phase than the early follicular phase. Plasma AVP and PRA were significantly elevated at 4 min after the 40-min run in the eumenorrheic runners during both menstrual phases and returned to preexercise levels by 40 min after exercise. Plasma ALDO responses at 4 and 40 min after exercise were higher in the midluteal phase than the early follicular phase. Menstrual status was associated with no significant differences in preexercise AVP or PRA; however, ALDO levels were significantly higher in the amenorrheic runners. After exercise, responses in the amenorrheic runners were comparable with the eumenorrheic runners during the early follicular phase. Thus, submaximal exercise elicits significant increases in plasma AVP and PRA independent of menstrual phase and status. However, plasma ALDO is significantly elevated during the midluteal phase, exercise results in a greater response during this menstrual phase, and amenorrheic runners have elevated resting levels of ALDO.

The Effect of the Methionine Enkephalin Analogue DAMME on the Vasopressin Response to Tilt in Man

1980 ◽  
Vol 59 (6) ◽  
pp. 501-503 ◽  
Author(s):  
S. L. Lightman ◽  
Mary L. Forsling
Keyword(s):  
Blood Pressure ◽  
Pulse Rate ◽  
Plasma Volume ◽  
Arginine Vasopressin ◽  
Pressure Pulse ◽  
Volume Changes ◽  
Methionine Enkephalin ◽  
Head Up Tilt ◽  
Plasma Arginine

1. Infusion of the methionine enkephalin analogue DAMME (Sandoz) inhibits the rise in plasma arginine vasopressin after a 65° head-up tilt. 2. DAMME does not significantly affect the blood pressure, pulse rate or plasma volume changes produced by tilt.

The Response of Arginine Vasopressin and Plasma Renin to Postural Change in Normal Man, with Observations on Syncope

1976 ◽  
Vol 51 (3) ◽  
pp. 267-274 ◽  
Author(s):  
Roy Davies ◽  
J. D. H. Slater ◽  
Mary L. Forsling ◽  
Nadia Payne
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Volume ◽  
Arginine Vasopressin ◽  
Plasma Osmolality ◽  
Plasma Renin ◽  
Renin Activity ◽  
Initial Rise ◽  
Constant Rate ◽  
Normal Man ◽  
Plasma Arginine

1. Fourteen mildly hydropenic normal volunteers were slowly tilted at a constant rate from the horizontal to the 85° head-up position in order to study the interrelationship between plasma arginine vasopressin concentration, plasma renin activity and the change of plasma volume. 2. Nine subjects did not develop vaso-vagal symptoms and were studied for 45–60 min. Arginine vasopressin rose biphasically in all subjects: a small initial rise, which was seen at 3 min and persisted for 30 min, was followed by a striking rise between 30 and 45 min, when the fall of plasma volume had reached its maximum (17%). 3. Plasma renin activity reached a maximum at 30 min but fell by 45 min, as plasma concentration of arginine vasopressin rose. 4. Five subjects developed vaso-vagal symptoms 4–24 min after reaching 85° when the study was terminated. A striking increase of arginine vasopressin concentration was seen within 4 min of syncope, but there was no change of plasma osmolality, cortisol concentration or renin activity.

Vasopressin Blood Pressure Dependency after α-Adrenoceptor Blockade in Normotensive and Mineralocorticoid-Salt Hypertensive Rats

1982 ◽  
Vol 63 (s8) ◽  
pp. 101s-103s ◽  
Author(s):  
M. Burnier ◽  
J. Biollaz ◽  
H. R. Brunner ◽  
H. Gavras
Keyword(s):  
Blood Pressure ◽  
Arginine Vasopressin ◽  
Pressor Response ◽  
Control Group ◽  
Hypertensive Rats ◽  
Plasma Vasopressin ◽  
Lysine Vasopressin ◽  
Pressure Dependency ◽  
Plasma Arginine ◽  
Normotensive Control

1. The effect of α-adrenoceptor blockade by phentolamine on plasma arginine vasopressin, on vasopressin dependency of blood pressure and on responsiveness to exogenous lysine vasopressin was studied in conscious normotensive and in deoxycorticosterone (DOC)/salt-treated hypertensive rats. 2. Phentolamine infusion reduced blood pressure of DOC-treated hypertensive rats to levels significantly lower than those of similarly treated Wistar control animals. 3. Plasma vasopressin levels of the DOC-treated hypertensive and normotensive control rats were similar. Phentolamine infusion increased plasma arginine vasopressin levels to 109.4 ±21.8 pg/ml in the DOC-treated rats and to 44.4 ± 8.2 pg/ml in the control animals. It also enhanced the pressor response to exogenous lysine vasopressin in both groups. 4. Administration of the vasopressin analogue dPVDAVP had no effect on blood pressure in either the DOC-treated or the control group but induced a similar fall in blood pressure in both groups during α-adrenoceptor blockade with phentolamine.

Contribution of vasopressin to the maintenance of blood pressure during dehydration

1983 ◽  
Vol 245 (5) ◽  
pp. F615-F621 ◽  
Author(s):  
R. L. Woods ◽  
C. I. Johnston
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
Systolic Blood Pressure ◽  
Arginine Vasopressin ◽  
Cardiovascular Response ◽  
Urine Volume ◽  
Brattleboro Rats ◽  
Continuous Administration ◽  
Plasma Vasopressin ◽  
Long Evans

Normal Long-Evans rats, when dehydrated for up to 72 h, have a progressive rise in plasma vasopressin that is associated with a fall in body weight and urine volume, a rise in plasma and urine osmolality, and the maintenance of normal systolic blood pressure. In contrast, Brattleboro diabetes insipidus rats, genetically deficient in vasopressin, when dehydrated to achieve an equivalent body weight loss, have a significant 15 mmHg fall in systolic blood pressure. Even when fluid balance is corrected in the Brattleboro rats by the continuous administration of 1-desamino-8-D-arginine vasopressin, a synthetic vasopressin analogue with potent antidiuretic properties but minimal pressor activity, blood pressure still falls when the animals are dehydrated. In contrast, Brattleboro rats infused with exogenous arginine vasopressin to produce a plasma vasopressin level of 18.9 +/- 3.5 pg X ml-1 are able to maintain normal blood pressure during 48 h of dehydration. This level of vasopressin is comparable to the level found endogenously in dehydrated Long-Evans rats and is nonpressor in normal rats. These results suggest that both the antidiuretic and vasoconstrictor properties of vasopressin are important in the cardiovascular response to dehydration.

Solitary Kidney and Ageing as Causes of Low Renin and Aldosterone Concentrations: Relevance to ‘Low-Renin’ Essential Hypertension

1976 ◽  
Vol 51 (s3) ◽  
pp. 177s-180s ◽  
Author(s):  
R. Gordon ◽  
Freda Doran ◽  
M. Thomas ◽  
Frances Thomas ◽  
P. Cheras
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Plasma Renin Activity ◽  
Plasma Volume ◽  
Plasma Renin ◽  
Renin Activity ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Normotensive Subjects ◽  
The Mean

1. As experimental models of reduced nephron population in man, (a) twelve men aged 15–32 years who had one kidney removed 1–13 years previously and (b) fourteen normotensive men aged 70–90 years were studied. Results were compared with those in eighteen normotensive men aged 18–28 years and eleven men aged 19–33 years with essential hypertension. 2. While the subjects followed a routine of normal diet and daily activity, measurements were made, after overnight recumbency and in the fasting state, of plasma volume and renin activity on one occasion in hospital and of blood pressure on five to fourteen occasions in the home. Blood pressure was also measured after standing for 2 min and plasma renin activity after 1 h standing, sitting or walking. Twenty-four hour urinary aldosterone excretion was also measured. 3. The measurements were repeated in the normotensive subjects and subjects in (a) and (b) above after 10 days of sodium-restricted diet (40 mmol of sodium/day). 4. The mean plasma renin activity (recumbent) in essential hypertensive subjects was higher than in normotensive subjects. In subjects of (a) and (b) above, it was lower than normotensive subjects, and was not increased by dietary sodium restriction in subjects of (a). 5. The mean aldosterone excretion level was lower in old normotensive subjects than in the other groups, and increased in each group after dietary sodium restriction. 6. Mean plasma volume/surface area was not different between the four groups and in normotensive, essential hypertensive and nephrectomized subjects but not subjects aged 70–90 years was negatively correlated with standing diastolic blood pressure.

Vasopressin Deficiency and Pressor Hypersensitivity In Hemodynamically Unstable Organ Donors

Circulation ◽  
1999 ◽  
Vol 100 (suppl_2) ◽  
Author(s):  
Jonathan M. Chen ◽  
Suzanne Cullinane ◽  
Talia B. Spanier ◽  
John H. Artrip ◽  
Ranjit John ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Diabetes Insipidus ◽  
Low Dose ◽  
Clinical Evidence ◽  
Pressor Response ◽  
Hemodynamic Instability ◽  
Solid Organ ◽  
Organ Donors ◽  
Plasma Vasopressin ◽  
Before And After

Background —Solid organ donors often develop hypotension due to vasodilation, and recently we observed that a variety of vasodilatory states are characterized by vasopressin deficiency and hypersensitivity. Thus, we investigated the prevalence of vasopressin deficiency in hypotensive solid organ donors without clinical evidence of diabetes insipidus; we also investigated the vasopressor effect of vasopressin replacement in hypotensive donors. Methods and Results —Fifty organ donors were evaluated for hemodynamic instability, (mean arterial pressure [MAP]≤ 70 mm Hg despite the use of catecholamine vasopressors), and in those unstable donors who were not already receiving exogenous vasopressin, low-dose vasopressin was administered as a continuous infusion (0.04 to 0.1 U/min). MAP, catecholamine requirements, serum vasopressin, and serum osmolality were obtained before and after vasopressin administration. Ten patients meeting the enrollment criteria received vasopressin and MAP increased from 72.2±3.5 to 89.8±4.2 mm Hg, ( P <0.05), allowing for complete discontinuation of catecholamine pressors in 4 (40%) patients and a decrement in pressor dose in 4 (40%). Plasma vasopressin levels (2.9±0.8 pg/mL) were low for the degree of hypotension. Conclusions —Hemodynamically unstable organ donors without clinically apparent diabetes insipidus display a defect in the baroreflex-mediated secretion of vasopressin. In these patients, low-dose vasopressin significantly increases blood pressure with a pressor response sufficient to reduce catecholamine administration.

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.

Immersion diuresis without expected suppression of vasopressin

1984 ◽  
Vol 57 (1) ◽  
pp. 123-128 ◽  
Author(s):  
S. E. Kravik ◽  
L. C. Keil ◽  
J. E. Silver ◽  
N. Wong ◽  
W. A. Spaul ◽  
...  
Keyword(s):  
Water Balance ◽  
Plasma Volume ◽  
Fluid Intake ◽  
Serum Osmolality ◽  
Renin Activity ◽  
Fluid Restriction ◽  
Angiotensin I ◽  
Plasma Vasopressin ◽  
Immersion Diuresis ◽  
Ad Libitum

To investigate fluid, electrolyte, and plasma vasopressin (PVP) and renin activity (PRA) responses, six men (20–35 yr) were immersed to the neck (NI) in water at 34.5 degrees C for six h after overnight food and fluid restriction. Diuresis was 1,061 +/- 160 (SE) ml/6 h during immersion and water balance was -1,285 +/- 104 ml/6 h. Preimmersion PVP was 0.7 +/- 0.2 pg/ml and increased to 3.0 +/- 0.6 pg/ml (P less than 0.05) at 6 h. PVP was unchanged at 1.2 +/- 0.1 pg/ml in the 6-h seated nonimmersionexperiment at 25 degrees C. Plasma volume increased by 7.8 +/- 1.6% (P less than 0.05) at 60 min of NI and decreased thereafter. Serum osmolality was constant (292 +/- 1 mosmol/kg) throughout NI, whereas PRA decreased progressively from 1.9 to 0.5 ng angiotensin I X ml-1 X h-1 (P less than 0.05) at theend of immersion. In spite of moderate thirst just before NI, thirst sensations were attenuated and no water was consumed ad libitum during immersion. These data indicate that PVP is not suppressed whenthere is no fluid intake during immersion and suggest that the action of factors other than PVP suppression are necessary to explain the mechanism of immersion diuresis.

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