Vasopressin inhibits diuresis induced by water immersion in humans.

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)

Altered coriolis stress susceptibility in essential hypertension.

Patients with hypertension frequently have vague complaints of dizziness and many other symptoms experienced by healthy individuals with motion sickness. We examined vestibular function in patients with essential hypertension, and we determined whether patients with essential hypertension are more prone to motion sickness using Coriolis stress testing. Vestibular function and Coriolis stress susceptibility were measured in 12 normotensive (NT) and seven asymptomatic patients with mild essential hypertension (HT). The Coriolis stress susceptibility index (CSSI) was calculated from the number of head movements in the four cardinal directions an individual could complete while being rotated in a computerized chair at increasing velocity before they developed motion sickness. The patients with hypertension had normal vestibular function and normal vestibuloocular responses as measured by standard techniques. Subjects with hypertension had significantly decreased Coriolis stress susceptibility scores compared to normotensive subjects (NT, 29.70 +/- 4.8; v HT, 5.48 +/- 2.0, P less than .001) and significantly decreased suppression of postrotatory nystagmus (NT, 44.5% +/- 3.8; v HT, 19.1% +/- 6.9, P less than .05). Medical treatment of hypertension did not result in an increased tolerance to provocative stimuli for motion sickness. It is suggested from our data that an increased susceptibility to motion sickness and abnormal vestibular responses to normal motion may account for many of the vague symptoms of "dizziness" reported by a large number of hypertensive patients.

Effect of the alpha 2-adrenergic antagonist yohimbine on orthostatic tolerance.

We studied the effect of yohimbine, a drug that inhibits presynaptic alpha 2-adrenergic receptors and increases the neuronal release of norepinephrine from the central and sympathetic nervous systems, on tolerance to cardiovascular stress in 10 untrained, healthy subjects. Using radioligand binding of tritiated yohimbine to platelets, these subjects were found to have a normal complement of alpha 2-adrenergic receptors (174 +/- 18 [+/- SEM] receptors/platelet) with normal Kd (1.93 +/- 0.17 nmol/l). Lower body negative pressure was used to test responses to cardiovascular stress in the subjects after they received either placebo or 20 mg yohimbine. Graded lower body negative pressure from 0 to -40 mm Hg significantly decreased systolic blood pressure from 116 +/- 3.7 to 106 +/- 5.8 mm Hg, increased heart rate from 54 +/- 3 to 68 +/- 7 beats/min, decreased forearm blood flow from 1.8 +/- 0.21 to 1.36 +/- 0.25 ml/100 ml/min, and increased forearm vascular resistance from 55.76 +/- 12.1 to 77.26 +/- 15.8 mm Hg/ml/min. Yohimbine increased the blood pressure at rest and during lower body negative pressure, but these changes were not significantly different from values recorded from the individuals when they were given placebo. Compared with placebo, however, yohimbine significantly increased forearm blood flow at rest (1.80 +/- 0.21 vs. 2.66 +/- 0.31 ml/100 ml/min, p less than 0.05) and during -40 mm Hg of lower body negative pressure (1.36 +/- 0.25 vs. 1.91 +/- 0.28 ml/100 ml/min, p less than 0.05). We also found that yohimbine significantly increased the plasma insulin concentration in these fasted subjects (9.4 +/- 2.4 vs. 14.5 +/- 1.4 ng/ml, p less than 0.05) without inducing hypoglycemia.(ABSTRACT TRUNCATED AT 250 WORDS)