The increase in free water excretion during induced re-entrant supraventricular tachycardias in man is not due to changes in plasma arginine-vasopressin

1988 ◽  
Vol 22 (4) ◽  
pp. 413
Author(s):  
G.C. Kaye ◽  
P.J. Lowry ◽  
P. Baylis ◽  
A.J. Camm
1988 ◽  
Vol 75 (4) ◽  
pp. 441-444 ◽  
Author(s):  
David J. Leehey ◽  
Alicia A. Picache ◽  
Gary L. Robertson

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.


1992 ◽  
Vol 82 (1) ◽  
pp. 33-37 ◽  
Author(s):  
Gerald C. Kaye ◽  
Peter Bayliss ◽  
Philip J. Lowry ◽  
P. L. Drury ◽  
A. John Camm

1. A symptomatic diuresis, polyuria, sometimes accompanies paroxysmal tachycardias in man. A study was undertaken in patients with inducible supraventricular tachycardia, irrespective of the symptom of polyuria, to measure simultaneous changes in urine output and plasma hormone levels during the arrhythmia. 2. During 14 episodes of induced tachycardia in 10 patients, there was a significant increase in mean urine flow, which was independent of the state of patient hydration. During a mean tachycardia duration of 30 ± 3 min, the mean group urine flow increased from 3.2 ± 2.3 ml/min to 7.6 ± 3.7 ml/min (P<0.001). This was characterized by a consistent increase in free water excretion and a variable increase in sodium excretion. 3. The plasma atrial natriuretic peptide level (five patients) significantly increased from 7.6 ± 4.6 pg/ml to 34.6 ± 21.7 pg/ml (P<0.02) during the arrhythmia. There was no significant change in the plasma argininevasopressin level and a non-significant reduction in plasma renin activity. 4. This study has shown that induced supraventricular tachycardias in man are accompanied by a significant diuresis. The mechanisms responsible remain unknown, but do not appear to involve the plasma arginine-vaso-pressin level alone.


1986 ◽  
Vol 250 (5) ◽  
pp. E564-E569
Author(s):  
M. G. Ross ◽  
M. G. Ervin ◽  
R. D. Leake ◽  
O. Habeeb ◽  
D. A. Fisher

Chronically prepared third trimester fetal lambs were administered intravenous infusions of nitropruside. Mean basal systolic and diastolic blood pressure (59.8 and 42.4 mmHg, respectively) decreased significantly during the infusion (49.2 and 36.8 mmHg, respectively) and increased significantly during the recovery period (66.4 and 48.5 mmHg, respectively). Fetal plasma arginine vasopressin (AVP) significantly increased from a mean basal level of 1.25 +/- 0.09 to 6.81 +/- 0.39 pg/ml during the hypotensive period. Urinary AVP basal levels of 1.21 +/- 0.13 pg/ml increased to 3.18 +/- 0.66 pg/ml during the hypotensive period and 5.87 +/- 0.82 pg/ml during the recovery period (P less than 0.05). The fetal urinary response to nitroprusside appeared biphasic. The hypotensive phase was marked by decreases in both free water and osmolar clearances. During the recovery phase free water clearance remained decreased, while osmolar clearance returned to basal levels. Thus AVP secretion represents an important mechanism for ovine fetal modulation of solute and water excretion in response to utero hypotensive stress.


2008 ◽  
Vol 294 (3) ◽  
pp. F638-F644 ◽  
Author(s):  
Timo Rieg ◽  
Kanishka Pothula ◽  
Jana Schroth ◽  
Joseph Satriano ◽  
Hartmut Osswald ◽  
...  

Activation of adenosine A1 receptors (A1R) can inhibit arginine vasopressin (AVP)-induced cAMP formation in isolated cortical and medullary collecting ducts. To assess the in vivo consequences of the absence of A1R, we performed experiments in mice lacking A1R (A1R−/−). We assessed the effects of the vasopressin V2 receptor (V2R) agonist 1-desamino-8-d-arginine vasopressin (dDAVP) on cAMP formation in isolated inner medullary collecting ducts (IMCD) and on water excretion in conscious water-loaded mice. dDAVP-induced cAMP formation in isolated IMCD was significantly greater (∼2-fold) in A1R−/− compared with wild-type mice (WT) and, in contrast to WT, was not inhibited by the A1R agonist N6-cyclohexyladenosine. A1R−/− and WT had similar basal urinary excretion of vasopressin, expression of aquaporin-2 protein in renal cortex and medulla, and acute increases in urinary flow rate and electrolyte-free water clearance in response to the V2R antagonist SR121463 or acute water loading; the latter increased inner medullary A1R expression in WT. Dose dependence of dDAVP-induced antidiuresis after acute water loading was not different between the genotypes. However, A1R−/− had greater inner medullary expression of cyclooxygenase-1 under basal conditions and of the P2Y2 and EP3 receptor in response to water loading compared with WT mice. Thus vasopressin-induced cAMP formation is enhanced in isolated IMCD of mice lacking A1R, but the adenosine-A1R/V2R interaction demonstrated in vitro is likely compensated in vivo by multiple mechanisms, a number of which can be “uncovered” by water loading.


1982 ◽  
Vol 63 (3) ◽  
pp. 47P-48P
Author(s):  
J. Brown ◽  
H.P. Henneberry ◽  
J.D.H. Slater

2011 ◽  
Vol 2011 ◽  
pp. 1-5 ◽  
Author(s):  
Katsunobu Yoshioka ◽  
Nagaaki Tanaka ◽  
Keiko Yamagami ◽  
Takeshi Inoue ◽  
Masayuki Hosoi

A 28-year-old man was admitted to our hospital because of reduced livido and increased fatigability. Four months before admission, he noticed polyuria, which was gradually relieved by admission. Magnetic resonance imaging revealed enhancing lesion centrally in the pituitary stalk. Biopsy from the skin revealed noncaseating granuloma composed of epithelioid cells, and a diagnosis of sarcoidosis was made. Although plasma arginine vasopressin (AVP) was undetectable after administration of hypertonic saline, urinary output was within normal range (1.5 to 2.2 L/day). The urine osmolality became above plasma levels during the hypertonic saline test. Hormonal provocative tests revealed partial glucocorticoid deficiency. Soon after the glucocorticoid therapy was begun, moderate polyuria (from 3.5–4.0 liters daily) occurred. At this time, plasma AVP was undetectable, and urine osmolality was consistently below plasma levels during the hypertonic saline test. In conclusion, we showed in human study that masked diabetes insipidus could be mediated by AVP-independent mechanisms.


1985 ◽  
Vol 69 (s12) ◽  
pp. 49P-50P
Author(s):  
G.C. Kaye ◽  
A. Shennan ◽  
A.W. Nathan ◽  
A. J. Camm

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