1. This study was designed to evaluate variations in plasma β-endorphin, methionine-enkephalin, adrenocorticotropic hormone and serum prolactin in healthy volunteers during head-out water immersion. 2. Water immersion induced an increase in methionine-enkephalin plasma levels, which was associated with a significant fall in mean arterial pressure and heart rate. 3. Conversely, a suppression of plasma β-endorphin, adrenocorticotropic hormone and serum prolactin was detected during water immersion. 4. We suggest that a dopaminergic inhibitory control mechanism may be involved in regulating circulating levels of β-endorphin, adrenocorticotropic hormone and prolactin in normal subjects undergoing extracellular fluid volume expansion produced by water immersion.
1. Animal studies have shown that arterial baroreflexes are modulated by reflexes originating from the cardiopulmonary volume receptors, and that this modulation consists of a reduction of the inhibitory influence exerted by arterial baroreceptors on the heart and peripheral circulation. This has not been confirmed in man, however, in whom no reduction in the bradycardic response to carotid baroreceptor stimulation has been observed after the mild increase in central venous pressure (right atrial catheter) and cardiopulmonary receptor activity provided by passive leg raising. 2. In seven normotensive subjects carotid baroreceptors were gradedly stimulated by progressively increasing carotid transmural pressure through a neck chamber device, the resulting reflex lengthening in R–R interval being measured in the two–three cardiac cycles immediately after the baroreceptor stimulus. This manoeuvre was performed in control conditions and repeated during a head-out water immersion which increased central venous pressure (right atrial catheter) from 1.5 ± 0.2 to 12.0 ± 0.9 mmHg (mean ± SE), thereby providing a marked increase in the cardiopulmonary receptor stimulus. 3. In the control condition graded stimulation of the baroreceptors caused a progressive lengthening in R–R interval, the maximal effect being + 477.4 ± 57.2 ms. Immersion increased the R–R interval from 774.2 ± 3.2 to 961.6 ± 5.8 ms ( P < 0.01) and reduced mean arterial pressure (cuff measurement) from 96.0 ± 1.0 to 82.3 ± 0.9 mmHg. The changes in R–R interval induced by carotid baroreceptor stimulation were virtually identical with those observed in the absence of immersion. However, owing to the lower baseline heart rate during immersion, this meant a lesser degree of reflex bradycardia to carotid baroreceptor stimulation (maximal reduction − 30.5 ± 3.0 beats/min and −19.3 ± 3.1 beats/min before and during immersion respectively). 4. Thus, although the baroreflex sensitivity as expressed by changes in R–R interval is altered, the arterial baroreceptor ability to modulate heart rate (and perhaps cardiac output) is reduced when cardiopulmonary receptor activity is markedly increased. This may have implications in a number of physiological and pathophysiological settings.
1. Natriuresis was studied during water immersion in eight normal subjects either in the absence or in the presence of dopamine blockade by domperidone. 2. Creatinine clearance showed no significant changes; urine flow remained significantly above control values during water immersion, implying persistent suppression of antidiuretic hormone. 3. The marked natriuresis seen during water immersion alone was significantly blunted ( P < 0.05) but not abolished during water immersion plus domperidone. 4. Suppression of the renin–aldosterone system by water immersion alone was not significantly different from that obtained during water immersion plus dopamine blockade. 5. On the contrary, plasma prolactin levels, previously suppressed during water immersion alone, were significantly stimulated during water immersion plus domperidone, thus indirectly suggesting a role of dopamine in mediating the blunted natriuresis seen during water immersion.
1. We studied renin-aldosterone system behaviour in five renovascular hypertensive patients during central hypervolaemia by water immersion to the neck. 2. Water immersion significantly suppressed the high peripheral renin levels of the patients despite an autonomic renin secretion from the stenotic kidney, a significant reduction of mean blood pressure and an increase in distal tubule sodium concentration. 3. The effect of immersion on plasma aldosterone appeared to be primarily mediated via suppression of plasma renin activity (PRA). 4. Our data suggest that: (a) the renin secretion is mainly modulated by cardiopulmonary receptors activity; (b) the neurogenic reflex control of plasma renin activity is very effective in renovascular hypertension.