Effect of Various States of Hydration on Plasma ADH and Renin in Man

Kimura, Tokihisa; Minai, Koji; Matsui, Kuniaki; Mouri, Toraichi; Satô, Tatsuo

doi:10.1210/jcem-42-1-79

Cited by 36 publications

(23 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…4). Finally, these observations are consistent with those of others who have reported no correlation betwen PRA and AVP levels in man during various states of hydration and volume depletion (36), and no diminution of the AVP response to orthostasis during propranolol blockade which, nevertheless, eliminated the PRA response to orthostasis (37). Since angiotensin II may act as a neurotransmitter in some hypothalamic areas it is still possible that central angiotensin II mediates the dipsogenic and vasopressinemic response to 2DG.…”

Section: Resultssupporting

confidence: 91%

Increased Thirst and Plasma Arginine Vasopressin Levels during 2-Deoxy-d-glucose-induced Glucoprivation in Humans

Thompson¹,

Campbell²,

Lilavivat³

et al. 1981

J. Clin. Invest.

View full text Add to dashboard Cite

A B S T R A C T 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 glucoprivation 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 ,tg/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 shaminfused 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 ,3-adrenoreceptors as evidenced by increased MAP and plasma epinephrine, and abolition ofthe RPA increases during 2DG-induced glycoprivation, but did not suppress AVP and thirst responses. A cervical cordsectioned patient lacking descending sympathetic outflow 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.

show abstract

Section: Resultssupporting

confidence: 91%

Increased Thirst and Plasma Arginine Vasopressin Levels during 2-Deoxy-d-glucose-induced Glucoprivation in Humans

Thompson¹,

Campbell²,

Lilavivat³

et al. 1981

J. Clin. Invest.

View full text Add to dashboard Cite

show abstract

“…It seemed to be due to differences in hydration and the activity of other physiological processes of each subject which could affect AVP secretion apart from plasma osmolality (Dunn et al 1973;Kimura et al 1976 Daily urinary excretion of AVP in the normal and the various patients were almost equivalent to the values reported previously by several authors (Miller and Moses 1972;Fressinaud et al 1974;Merkelbach et al 1975). In patients with diabetes insipidus, urinary AVP could be detectable, although extremely low (about 14% of normal values), indicating that most of these patients have a residual function in the neurohypophysis to secrete a small amount of AVP into the blood despite of marked polyuria.…”

Section: Discussionsupporting

confidence: 62%

Radioimmunoassay of arginine vasopressin in human plasma and urine, a resin microcolumn method.

Kimura

Matsui

Ota

et al. 1980

Tohoku J. Exp. Med.

Self Cite

View full text Add to dashboard Cite

“…Angiotensin has been shown in man to potentiate the AVP response to an osmolar stimulus (27,28), conversely Claybaugh (29) showed that hyperosmolality augmented the AVP response to renin infusion in conscious dogs. Thus the angiotensin-AVP interaction would tend to reinforce the defense of dehydration.…”

Section: Discussionmentioning

confidence: 99%

Endogenous Angiotensin Stimulation of Vasopressin in the Newborn Lamb

1979

View full text Add to dashboard Cite

A B S T R A C T 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 ,ug/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 ,uU/ml and 12.8±2.5 ng/dl to 9.8±2.0 ,uU/ml (P < 0.01) and 23.0±7.7 ng/dl (P < 0.05) at 35 min and 13.8±2.1 ,uU/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 ,uU/ml at 35 min, and 7.4 ±2.0 ,.U/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, A 10.8±2.0 ,uU/ ml, was greater than in the lambs with saralasin, A4.0± 1.9 (P < 0.05), and greater than in the anephric lambs, A3.3±2.1 ,uU/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.

show abstract

Effect of Various States of Hydration on Plasma ADH and Renin in Man

Cited by 36 publications

References 18 publications

Increased Thirst and Plasma Arginine Vasopressin Levels during 2-Deoxy-d-glucose-induced Glucoprivation in Humans

Increased Thirst and Plasma Arginine Vasopressin Levels during 2-Deoxy-d-glucose-induced Glucoprivation in Humans

Radioimmunoassay of arginine vasopressin in human plasma and urine, a resin microcolumn method.

Endogenous Angiotensin Stimulation of Vasopressin in the Newborn Lamb

Contact Info

Product

Resources

About