Plasma AVP, neurophysin, renin activity, and aldosterone during submaximal exercise performed until exhaustion in trained and untrained men

Abstract

The effect of intense muscular work (80% of maximal oxygen uptake) on responses of plasma hormones involved in electrolyte and water balance were measured in 14 male subjects. They were divided into three groups according to their maximal oxygen uptake and the duration of exercise performed until exhaustion: well trained subjects (group I), trained subjects (group II), and untrained subjects (group III). Pulmonary gas exchange, heart rate, rectal and skin temperature, and weight loss were measured as well as hematocrit and plasma and urine sodium and potassium concentrations. Rectal temperature increased significantly in all subjects after exhaustion. The variation of hematocrit was smallest and the weight loss greatest in the well-trained subjects. Plasma aldosterone, renin activity (PRA), vasopressin (AVP), and neurophysin (Np) displayed highly significant increases after exercise in all three groups: PRA was increased 4.5 times (p < 0.01), aldosterone 13 times (p < 0.05), Np 2.6 times (p pe 0.05), and AVP 4.8 times (p < 0.05). Nevertheless, there was no correlation between the changes in PRA and those in plasma aldosterone, nor between aldosterone and plasma sodium or potassium. At the urinary level, the only striking observation was that free water clearance tends to become positive after exercise. Our results provide evidence that this kind of exercise produces a highly significant increase in plasma levels of the hormones involved in electrolyte and water balance. They also indicate that it is among the well-trained subjects that sweat loss is highest though the hematocrit increase is the smallest; this suggests that water is shifted more efficiently from the extravascular compartment.

Arginine Vasopressin Enhances Sympathetic Constriction Through the V 1 Vasopressin Receptor in Human Saphenous Vein

“…The concentration of AVP in this study may be lower than those expected to occur in response to hypotension, dehydration, and exercise and in some patients with hypertension or congestive heart failure. [33][34][35] Consequently, the amplifying effect of AVP on adrenergic-mediated constriction, shown in the present experiments, may importantly contribute to vascular mechanisms involved in acute ischemic syndromes associated with venous grafts. The human saphenous vein can undergo spasm, which is a clinically relevant problem, immediately after autologous grafts in the arterial circulation or coronary bypass surgery.…”

Contractile responses of human thyroid arteries to vasopressin

“…At 10 −8 M, the antagonist produced a 19-fold shift to the right of the control concentration-response curve to vasopressin, presumably due to a competitive agonist-antagonist interaction. Plasma levels of vasopressin increase in response to stimuli such as increased plasma osmolality (Mason, 1980), dehydration, hypotension (Sorenson and Hammer, 1985), exercise (Melin et al, 1980), increased angiotensin II levels (Bonjour and Malvin, 1970), and sympathetic activation (Leng et al, 1999) and in different pathophysiological settings such as, haemorrhage (Fujisawa et al, 1994), and congestive heart failure (Preibisz et al, 1983). In addition, vasopressin may modify the effects of other vasoactive substances that are found in plasma or released from perivascular nerve endings.…”

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

“…Moderate stress (e.g. 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).…”

“…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).…”