Transient vasopressin release and thirst in response to prolonged intracerebroventricular infusions of hypertonic mannitol in saline

In the conscious goat infusions of 0.4 M mannitol in 0.15 M NaCl into the lateral cerebral ventricle (40 or 100 min, 0.02 ml/min) caused slight, transient vasopressin release and temporary thirst, whereas infusions or pure, hypertonic (0.7 M) mannitol did not elicit thirst and inhibited the basic vasopressin release in the nonhydrated animal. In contrast, infusions of equiosmolal (0.35 M) NaCl induced persistent thirst and pronounced elevation of the plasma vasopressin concentration throughout the infusion period. The cerebrospinal fluid (CSF) osmolality was raised by the same order of magnitude (= 13%) after the mannitol/NaCl and the hypertonic NaCl infusions. The CSF Na+ concentration was elevated by greater than 10% at 5 min after hypertonic NaCl infusions, but it was reduced by approximately 10% at 5 min after the mannitol/NaCl infusions. There was no appreciable difference in the CSF K+ concentration after the infusions. The results are discussed with regard to the possible importance of CSF Na+-concentration as opposed to strict osmotic factors for the excitation of receptors involved in the control of water balance.     

Natriuresis induced by intracarotid infusion of hypertonic NaCl.

The intracarotid infusion of hypertonic sodium chloride in anesthetized dogs pretreated with vasopressin and mineralocorticoid resulted in an increase in sodium excretion as well as an increase in the percent of the filtered load of sodium excreted. This increase was not due to changes in renal hemodynamics or arterial blood pressure. The change in fractional sodium excretion was approximately 1%. Intracarotid infusion of isotonic sodium chloride did not result in a natriuretic response. The intracarotid infusion of hyperosmotic glucose did not evoke an increase in sodium excretion. Femoral vein infusions of hypertonic sodium chloride failed to evoke any natriuretic response. These data indicate that a sodium-sensing mechanism may exist in the brain that can alter the renal handling of sodium. The efferent mechanism of the response is discussed.     

Efferent renal nerve activity during intracarotid and intracerebroventricular infusions of hypertonic sodium chloride solutions and isotonic volume expansion in the rat

The change in renal nerve activity under conditions known to increase renal sodium excretion was studied. In adult Sprague Dawley rats, anaesthetized with Inactin®, nor-motonic and hypertonic NaCl solutions were infused into 1) a vein, 2) a carotid artery and 3) the third ventricle. The left kidney was freed and placed in a plastic cup. A renal nerve was dissected free and placed on a stainless bipolar electrode. The nerve was cut distal to the electrode. The nerve signals were amplified and recorded on a tape recorder. Simultaneously integrated nerve signals and also arterial and venous pressures were recorded. Intracarotid infusion of a 1 M NaCl solution increased sodium output and temporarily decreased renal nerve activitv by some 35%. Corresponding intravenous (i.v.) infusion gave an increase in renal nerve activity and also in sodium output. The latter increase was delayed compared with that caused by the intracarotid infusion. No variations in blood pressure were noted. In control experiments with a slow i.v. infusion of physiological saline, renal nerve activity increased throughout the experiment, while sodium excretion remained constant. During infusion of a 1 M NaCl solution into the third ventricle, renal nerve activity decreased in about half of the cases. This reduction was often accompanied by an increased arterial blood pressure and an increased sodium output. Arterial blood pressure increases were especially pronounced at the highest infusion rate, i.e. 800 nl-min-¹. Isotonic volume expansion of 2% of the body weight resulted in a transient decrease in renal nerve activity by about 30%. Venous blood pressure rose and sodium output increased six-fold. The decrease in nerve activity was observed both when the vagal nerves were intact and when they were cut.     

Effects of intracerebroventricular infusions of arginine vasopressin in sheep

In sheep, neither the in vivo effect of vasopressin administered by a method other than systemic infusion nor the central effects on behavior from the perspective of stress regulation has been fully elucidated in an intact animal. We examined changes in behavioral, adrenocorticotropic, and autonomic nervous functions after intracerebroventricular infusions of arginine vasopressin (AVP) to elucidate its central role. Intracerebroventricular infusions of AVP (0, 0.12, 1.2 and 12 microg/500 microl/30 min) evoked a dose-related increase in plasma cortisol concentration. There were significant treatment-related effects on the total duration of sham-chewing (Friedman's test, X2=12.75, p=.0052), on the total duration of bar-biting (Friedman's test, X2=15.0, p=.0018), and on the total duration of rubbing (Friedman's test, X2=12.0, p=.0074). AVP 12 microg treatment induced a greater degree of sham-chewing and bar-biting than the other three treatments did (Nemenyi multiple comparisons: p<0.1). These findings indicate, together with our previous findings, that AVP has the same corticotropic potential as corticotropin-releasing hormone infused intracerebroventricularly in equal molar concentrations. Although the degree to which central stress signaling pathways are involved in these responses remains speculative, the relationships between stereotypies and central AVP are of particular interest.     

Water drinking caused by intracerebroventricular infusions of hypertonic solutions in cattle

Infusions into the lateral cerebral ventricle of hypertonic solutions of NaCl, mannitol or sucrose all induced water drinking in cattle. However, infusion of hypertonic NaCl caused a significantly greater water drinking response than did the infusions of mannitol or sucrose, despite the fact that CSF osmolality increase was similar. In contrast, hypertonic solutions of NaCl or mannitol had similar dipsogenic effects when infused intravenously. The intracerebroventricular infusions of hypertonic NaCl or mannitol did not affect the intakes of food or Na solution. The results are consistent with the hypothesis that both cerebral osmoreceptors and Na sensors are involved in regulating thirst in cows.     

Mechanism of inhibition of gastric acid secretion by hypertonic solutions and vasopressin

Summary An experiment was performed in female rats in order to assess the influence and mechanism underlying the effects of hyperglycemia, hypertonic saline and vasopressin upon the gastric acid secretion and mucosal blood flow (MBF). Infusion of isotonic saline did not alter acid output and gastric clearance of plasma aminopyrine whereas hypertonic solutions (20% glucose or 3% NACl) significantly increased plasma osmolality and decreased the acid secretion within 30 min and recovered to normal levels after 2 h. Vasopressin also effectively inhibited acid secretion. Both hypertonic solutions and vasopressin decreased the mucosal blood flow. However, the ratio (R) of MBF to gastric secretory rate which is a helpful guide to the mechanism of secretory inhibition did not significantly change in either case. We concluded that all three agents probably had a direct action on secretion rather than decreasing MBF. The mechanism of inhibition of acid secretion and its relationship to MBF was suggested and discussed.     

Effects of saline infusions on calcium concentration in plasma ultrafiltrate and on the ultrastructure of the parathyroid glands of the rat

Summary Experiments have been performed in adult female rats to examine the effects of saline infusion on calcium concentration in plasma ultrafiltrate and on the ultrastructure of the parathyroids as studied with the electron microscope. Intravenous infusions of isotonic saline of at least 10 ml within 30 min decreased calcium concentration in plasma ultrafiltrate from 3.04±0.15 mEq/l to 2.79±0.11 eEq/l (P<0.001). Saline infusions of 2 h duration at a rate of 0.5 ml/min decreased significantly the number of secretory granules in the parathyroid cells and induced considerable growth of the Golgi apparatus. It is concluded, that saline infusions in the rat decrease the ionized fraction of plasma calcium concentration thereby increasing parathormone secretion rate.This work was supported in part by a grant from the Deutsche Forschungsgemeinschaft.