Plasma arginine vasopressin (PAV) concentration was determined by radioimmunoassay during the diurnal cycle in 8 recombent healthy male subjects. Two subjects were studied again 3 weeks later while receiving 1 mycles. In 8 out of 10 cycles, a nocturnal increase in PAV was found; there was a progressive rise during the night in 5 subjects and a peak occurred at 2400 or 3400 h. In 1 subject no variation was detected and in another, the pattern was compleetly different. The mean PAV in the 10 cycles was significantly (P less than 0.001) higher during the night than during the day. Dexamethasone did not modify the pattern of variation, but induced a significant (P less than 0.001) decrease in PAV. Hematocrit remained stable throughout the study as did osmolality, except at 2000 h, when a significant (P less than 0.001) increase (5 mOsm) on average occurred in every subject. Blood sugar, sodium or chloride did not account for the observed rise in osmolality and no simultaneous change in PAV occurred. A rise in PAV explains, to some extent, the known nocturnal decrease in urine output. Diurnal variations in PAV must be taken into account in clinical investigations involving vasopressin.
In human plasma, the concentration of free dopamine (DA) is approximately equal to that of epinephrine (E). Like norepinephrine (NE) and E its concentration may increase during physical effort and stress (Fig. 1). Most of the stress-related increase in plasma DA is derived from peripheral noradrenergic nerve terminals and the adrenal medulla. Because virtually all of the DA is rapidly conjugated upon release, it is necessary to measure plasma total (free + conjugated) DA. When dietary sources are controlled, the total DA concentration can be used as an indicator of the intensity of the sympathetic response and possibly the level of training in animals and humans. In normal individuals, plasma DA and blood pressure (BP) are usually negatively correlated since during a low level sympathetic discharge the hypotensive action of DA via dopaminergic vascular receptors predominates. The DA action on BP is, however, biphasic and dependent on its concentration. In many hypertensive patients, hypertensive peaks, which cannot be accounted for by rises in NE and E, are associated with very large stimulus-elicited increases in total DA into a range in which its hypertensive action via beta and alpha-receptors could temporarily predominate. Alternatively, this rise in DA could be a marker of the sympathetic discharge or a negative modulator of other hypertensive influences rather than the cause of the elevated BP. In primary aldosteronism, there is a more sustained increase in circulating DA. In both groups of patients the DA levels decrease with successful treatment. Concentrations of total DA and of free + conjugated NE + E in plasma are a more sensitive measure of sympathetic activity than are levels of free catecholamines, and they may provide a clinically useful biochemical index for categorizing hypertension and following its treatment.
S U M M A R Y1. The role of the adrenergic nervous system in the regulation of plasma renin activity was investigated in fourteen healthy volunteers. Special attention was devoted to 3,4dihydroxyphenethylamine (dopamine) because this amine is not only a precursor of noradrenaline, but also a catecholamine with its own functions. The adrenergic nervous system was activated by a change of posture because this offers a simple and reproducible stimulus; its effects were studied during a normal diet and also after restriction of sodium.2. With both diets, the expected increase in plasma renin activity was observed after changing from recumbency to an upright posture. This was associated with a decrease in the urinary excretion of dopamine and an increase in the urinary excretion of noradrenaline and adrenaline. In addition, a positive and significant correlation was found between the urinary excretion of dopamine and sodium.3. Our data suggest that dopamine and noradrenaline may play a complementary role in the regulation of renin secretion, but they do not necessarily act in the same direction or through similar mechanisms. Dopamine is known to be a pharmacological natriuretic agent. It may have a similar role in the physiological regulation of urinary sodium excretion.
We have studied several parameters of peripheral dopamine synthesis and metabolism in spontaneously hypertensive rats during the development of hypertension. Compared to Wistar-Kyoto rats, there was an increased dopamine content in 8-week-old spontaneously hypertensive rats in the adrenals (1.6 +/- 0.1 vs. 1.2 +/- 0.1 nmol/pair in Wistar-Kyoto rats) and kidneys (97 +/- 12 vs. 63 +/- 7 pmol/g tissue in Wistar-Kyoto rats), but the dopamine content in peripheral organs from normotensive 4-week-old spontaneously hypertensive rats did not differ from Wistar-Kyoto rats. In the heart, the dopamine increase was observed in 14-week-old spontaneously hypertensive rats (systolic blood pressure: spontaneously hypertensive rats, 189 +/- 9; Wistar-Kyoto rats, 106 +/- 2 mm Hg;) in both atrium (spontaneously hypertensive rats, 133 +/- 14; Wistar-Kyoto rats, 86 +/- 20 pmol/g tissue) and ventricle (spontaneously hypertensive rats, 41 +/- 6; Wistar-Kyoto rats, 23 +/- 5 pmol/g tissue). Urinary free dopamine and dihydroxyphenylacetic acid, but not norepinephrine or normetanephrine, in spontaneously hypertensive rats significantly increased between the ages of 7 and 11 weeks, reflecting the dopamine changes in tissue and suggesting a selective increase of the rate of dopamine synthesis and release.(ABSTRACT TRUNCATED AT 250 WORDS)
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.