The interrelationship between the release of renin and vasopressin as defined by orthostasis and propranolol.

Davies, R.; Forsling, Mary L.; Slater, J. D. H.

doi:10.1172/jci108905

Cited by 34 publications

(9 citation statements)

References 18 publications

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“…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.

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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.

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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.

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“…exercise, nausea) may increase plasma AVP levels to the 20-50 pg/ml range (25,26); at these levels, the V2 vasodilator effect may cause skeletal muscle vasodilation and, in concert with other endothelial, myogenic, and metabolic vasodilator stimuli may act to counterbalance sympathetic vasoconstriction. More profound stress (e.g., hypovolemic hypotension, surgical trauma, congestive heart failure) may increase AVP levels to the 50-500 pg/ml range, and the VI vasoconstrictor effect on skin, splanchnic, and skeletal muscle may predominate (23,24,(27)(28)(29)(30).…”

Section: Discussionmentioning

confidence: 99%

“…Plasma AVP levels increase in response to orthostasis, hypotension, dehydration, exercise, nausea, and are elevated in some patients with congestive heart failure (23)(24)(25)(26)(27)(28)(29)(30). AVP is a potent splanchnic vasoconstrictor (31), but when infused intravenously into normal subjects at high physiologic doses (achieving plasma levels of 200-300 pg/ml), the expected rise in blood pressure is either absent or quite modest (32,33).…”

Section: Introductionmentioning

confidence: 99%

Vasopressin-mediated forearm vasodilation in normal humans. Evidence for a vascular vasopressin V2 receptor.

et al. 1989

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Arginine vasopressin (AVP) is a potent vasopressor and antidiuretic neurohormone. However, when administered intravenously to humans, AVP causes forearm vasodilation. This effect has been attributed to sympathetic withdrawal, secondary to AVP-induced sensitization of baroreceptors. The possibility that AVP also causes forearm vasodilation directly has not been examined.Accordingly, the direct effect of AVP was determined by studying the forearm blood flow (FBF) response to intraarterial (IA) AVP infusion (0.01-1.0 ng/kg per min). Infusion of IA AVP increased FBF (96%) in the infused arm, but not the control arm, in a dose-dependent manner. The role of specific AVP Vl receptors in mediating this FBF response was determined before and after pretreatment with a Vl antagonist (AVP-A). AVP-A alone had no effect on FBF, but coadministration of AVP and AVP-A potentiated the vasodilatory response (223%). IA infusion of the V2 agonist, 1-desaminol8-Dargininej vasopressin, caused a dose-dependent increase in FBF. These findings suggest that AVP causes direct, dose-dependent vasodilation in the human forearm that may be mediated by V2 vasopressinergic receptors. In contrast, AVP infusion caused digital vasoconstriction that was blocked by AVP-A, whereas dDAVP did not affect digital blood flow.Thus, AVP induces regionally selective vascular effects, with concurrent forearm vasodilation and digital vasoconstriction.

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“…The increase in AVP, however, cannot be attributed to the concomitant enhancement of the renin-angiotensin system , because no significant correlation was observed between percent changes in AVP and PRA. There is another report describing how propranolol inhibits the renin-angiotensin system but does not suppress the orthostatic increase in AVP (Davies et al, 1977). Our results showing that upright posture causes a significant increase in hematocrit without a change in plasma osmolality suggest that plasma volume reduction might stimulate the AVP secretion mediated by cardiac volume receptor and vagal afferent fibers (Robert et al, 1979;Egan et al, 1984;Menninger 1985;Drieu et al , 1986).…”

Section: Discussionmentioning

confidence: 62%

Effects of Sodium Depletion and Orthostasis on Plasma and Urinary Vasopressin in Normal Subjects.

et al. 1989

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We investigated the effects of sodium depletion and orthostasis on the plasma concentration and urinary excretion of vasopressin (AVP) in eight normal female subjects. After 4 days on a sodium controlled diet (130 mEq/ day), the subjects were placed on a low sodium diet (30 mEq/day) for 3 days and 120mg of furosemide was administered orally on the first day of the low sodium regimen.Sodium depletion in the present study reduced body weight by 1.6 kg and increased hematocrit by 3.5%.A significant (p<0.05) increase in plasma AVP and a significant (p<0.05) decrease in 24-h urinary excretion of AVP were observed during sodium depletion.One-hour ambulation significantly increased plasma AVP in both control and sodium depleted phases (p<0.01).The percent change in plasma AVP tended to correlate with that in mean blood pressure in the control phase (r= 0.69, 0.05

show abstract

The interrelationship between the release of renin and vasopressin as defined by orthostasis and propranolol.

Cited by 34 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

Vasopressin-mediated forearm vasodilation in normal humans. Evidence for a vascular vasopressin V2 receptor.

Effects of Sodium Depletion and Orthostasis on Plasma and Urinary Vasopressin in Normal Subjects.

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