In order to investigate the role of central noradrenergic neurons in the control of vasopressin (ADH) release and cardiovascular regulation, norepinephrine (1.4 microgram/kg), clonidine (0.1 microgram/kg), and isoproterenol (1.4 microgram/kg were infused into the lateral cerebral ventricle of the anesthetized dog. The drugs were given over a 20-min period, dissolved in 0.9% saline at a volume rate of 10 microliter/min. Both norepinephrine and clonidine markedly reduced ADH release and lowered arterial blood pressure and heart rate. Isoproterenol had no effect on ADH release and produced a slight reduction in arterial pressure and a large increase in heart rate. Pretreatment with phenoxybenzamine (100 microgram/kg, iv) completely blocked the effects of norepinephrine on blood pressure and heart rate but only partially (about 50%) inhibited the norepinephrine effect on ADH release. Intravenous isoproterenol lowered blood pressure and increased ADH release and heart rate. In none of the experiments could changes in ADH release be attributed to changes in plasma osmolality or plasma sodium and potassium concentrations. It is concluded that, in the anesthetized dog, intraventricular norepinephrine and clonidine decreased ADH release, blood pressure, and heart rate by stimulating alpha-adrenoreceptors. The increased release of ADH after peripheral administration of isoproterenol was presumably due to the reduction in blood pressure and decreased baroreceptor inhibition of ADH release.
In the anesthetized dog, the concentrations of vasopressin (ADH) in plasma and cerebrospinal fluid (CSF) were similar under basal conditions, and there was a highly significant positive correlation between them (r = 0.71, p < 0.01). Although hemorrhage was capable of increasing the ADH concentration in both plasma and CSF, the threshold for the increase in plasma ADH was much lower than for the increase in the concentration of ADH in CSF. In addition, the magnitude of the increase in the concentration of ADH in plasma was considerably greater than that in CSF at a comparable degree of hemorrhage. Our results suggest that ADH released into CSF during hemorrhage may have a different origin from that released into blood.
In the anesthetized dog, intravenous infusion of 2.5 M saline (40 µl/kg·min) increased plasma and cerebrospinal fluid (CSF) osmolality and the plasma vasopressin (ADH) concentration, but did not increase the CSF ADH concentration. The increase in the plasma ADH concentration coincided with the increase in plasma osmolality, but preceded the increase in CSF osmolality. Intracerebroventricular infusion of hypertonic artificial CSF (2,000 mosm/kg·H2O, 10 µl/min) increased CSF osmolality and plasma and CSF ADH concentrations; plasma osmolality did not increase. Thus, receptors which sense changes in plasma osmolality appear to be outside the blood-brain barrier; different receptors may sense changes in CSF osmolality.
A study was undertaken to evaluate the role of vasopressin in the pathogenesis of hypertension in New Zealand genetically hypertensive (NZGH) rats. During the course of development of hypertension in NZGH rats from 4 to 11 weeks of age, the 24 h urinary excretion of vasopressin did not differ from that of the New Zealand normotensive control rats (NZNR). Furthermore, at the conclusion of the study (rats 13 to 14 weeks old), the plasma vasopressin concentrations in NZGH and NZNR rats were not significantly different. Although there was no evidence for a difference in secretion of vasopressin from the neurohypophysis in the NZGH rats, there was a substantially increased pressor responsiveness to vasopressin in these rats. This was not specific since NZGH rats also had an increased pressor responsiveness to angiotensin II. The importance of increased pressor responsiveness to vasopressin in the hypertensive process in the NZGH rat requires further study.
The effects of a high-sodium meal on plasma atrial natriuretic peptide (atriopeptin) and renal sodium excretion were studied in eight normal human subjects. As expected, sodium excretion and urine osmolality increased following the meal. Plasma atriopeptin levels did not increase, however, after the high-sodium meal. In a control experiment, consumption of a low-sodium meal by six of the same subjects did not increase either urinary sodium excretion or plasma atriopeptin concentration. We conclude that the natriuresis elicited by a high-salt meal is not mediated by the atrial peptides.
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