Vasopressin inhibits diuresis induced by water immersion in humans

Abstract

We tested the hypothesis that 1-desamino-8-D-arginine vasopressin (DDAVP), a V2-receptor agonist, could inhibit the diuresis induced by water immersion in humans. Water and electrolyte excretion, plasma atrial natriuretic factor concentration, and plasma aldosterone concentration were measured initially and after 3 h of water immersion in 13 healthy sodium-replete men given either placebo or 20 micrograms of intranasal DDAVP. Guanosine 3',5'-cyclic monophosphate and urea excretion and urine osmolality were also determined. DDAVP inhibited the diuresis induced by water immersion in men: 758 +/- 168 (SE) ml/3 h in the placebo group vs. 159 +/- 28 ml/3 h in the DDAVP group (P less than 0.05). After 3 h of water immersion, plasma atrial natriuretic factor concentrations were increased from 11 +/- 2 to 20 +/- 4 pg/ml in the placebo group and from 14 +/- 2 to 33 +/- 4 pg/ml in the DDAVP group (P less than 0.05). Plasma aldosterone concentrations were decreased from 98 +/- 18 to 45 +/- 6 pg/ml in the placebo group (P less than 0.05) and from 54 +/- 17 to 25 +/- 5 pg/ml in the DDAVP group (P less than 0.05). Despite these changes in aldosterone and atrial natriuretic factor concentrations, which should increase sodium excretion, DDAVP decreased the natriuresis induced by water immersion in humans: 56 +/- 8 meq Na+/3 h in the placebo group vs. 36 +/- 6 meq Na+/3 h in the DDAVP group (P less than 0.05). DDAVP may be used to prevent the diuresis associated with central redistribution of blood volumes that occur during water immersion.(ABSTRACT TRUNCATED AT 250 WORDS)

Aqua walking as an alternative exercise modality during cardiac rehabilitation for coronary artery disease in older patients with lower extremity osteoarthritis

“…Furthermore, the increased central blood volume affects the renal blood flow and the right atrial filling pressure, suppressing the arginine vasopressin and plasma renin activity, and activating atrial natriuretic factors. These hormones induce natriuresis and diuresis, which in turn decrease blood pressure [ 26 – 28 , 31 ]. Figure 2 shows that SBP and DBP decreased in both the TW and AW groups without any significant difference between them (−6% and −4% in SBP, and −8% and −5% in DBP, respectively).…”

“…These reductions in blood pressure are meaningful and consistent with those of other exercise training studies [ 3 , 32 ]. Whether the observed blood pressure reductions are due to the “normal” exercise training effect and/or from the aforementioned mechanism of activating natriuresis and diuresis in water-based exercises remains to be determined [ 26 – 28 , 31 ]. The resting heart rate decrease observed in both the TW and AW groups is an expected adaptation to aerobic exercise related to the increased parasympathetic activation [ 33 ] and appears to be similar between the two groups.…”

Neurohumoral Stimulation

“…In addition to the ABR, cardiovascular reflexes emanating from the low pressure side of the circulation may be very important in modulation of fluid balance and sympathetic outflow in CHF. In normal humans, translocation of blood from the periphery to the thoracic circulation evokes a brisk diuresis and natriuresis 31-34 . Neural activity from sensory endings located in the atria and ventricles has been shown to be markedly reduced in animals with CHF 35-42 .…”

Pathophysiological and diagnostic implications of cardiac biomarkers and antidiuretic hormone release in distinguishing immersion pulmonary edema from decompression sickness

“…[ 19 , 25 ] The increase in the copeptin level, and hence in ADH production, in IPE supports a role of ADH via its well-known capacity of inhibiting diuresis and inducing renal vasoconstriction. [ 14 , 15 ] More specifically, we propose that IPE occurs in a context of decreased diuresis, which increases volemia and eventually blood pressure. The situation observed in IPE contrasts with that observed in healthy divers for whom water immersion is associated with increased diuresis.…”

“…Third, the pathogenesis of IPE implies environmental (e.g., pressure and cold) and emotional stressors that induce hemodynamic and volemic changes via the release of various effectors, notably the antidiuretic hormone vasopressin (ADH). [ 1 , 2 , 10 , 11 , 14 , 15 ] Because ADH controls volemia and affects the cardiovascular system, [ 14 , 15 ] it may be a key player in IPE and its measure via a surrogate marker, copeptin, the stable C-terminal domain of the hormone precursor, [ 16 – 19 ] is feasible. Additionally, copeptin is a nonspecific but early marker of severe stress reactions, [ 16 , 17 ] and its release has been described in acute coronary syndrome, [ 18 ] congestive heart failure, and lung injury.…”