Drinking and natriuresis during volume expansion and intracranial angiotensin or carbachol

1986 ◽  
Vol 251 (2) ◽  
pp. R381-R387
Author(s):  
D. A. Fitts ◽  
J. B. Simpson
Keyword(s):  
Body Fluid ◽  
Isotonic Saline ◽  
Plasma Osmolality ◽  
Sodium Concentration ◽  
The Body ◽  
Ang Ii ◽  
Elevated Plasma ◽  
Precipitous Decline ◽  
Infusion Period ◽  
Drinking Fluid

Two methods of sodium loading were used to counteract the body fluid dilution resulting from natriuresis and water drinking during sustained lateral ventricular infusions of carbachol (CBC) or angiotensin II (ANG II) in rats. It was expected that preventing dilution would also prevent the precipitous decline of both drinking and natriuresis during the later hours of CBC infusion. In the first study, rats having isotonic saline as the sole drinking fluid during CBC infusions drank less fluid and had only slightly higher plasma osmolality and sodium concentration than rats drinking water, which showed extreme dilution. In the second study, rats with only water to drink were given intravenous infusions of 0.15, 0.45, or 1.00 M NaCl solutions at 1.8 ml/h concurrently with the intraventricular infusions. Significant dilution of plasma was found at the two lower rates but not at 1.00 M NaCl in CBC-infused rats. Only the latter group showed both persistent drinking and natriuresis throughout the 4-h infusion period, and this was not because of elevated plasma osmolality. Infusions of ANG II generated less severe body fluid dilution and more persistent drinking in both experiments. The study demonstrates that body fluid dilution may control the offset of both drinking and natriuresis during sustained infusions of CBC and that the more persistent drinking to ANG II vs. CBC probably occurs because of a lesser natriuresis and consequent fluid dilution.

Fluid retention after oral loading with water or saline in camels

1992 ◽  
Vol 262 (5) ◽  
pp. R915-R920 ◽  
Author(s):  
S. Benlamlih ◽  
K. Dahlborn ◽  
R. Z. Filali ◽  
J. Hossaini-Hilali
Keyword(s):  
Body Weight ◽  
Plasma Proteins ◽  
Isotonic Saline ◽  
Plasma Osmolality ◽  
Plasma Renin ◽  
The Body ◽  
Plasma Aldosterone Concentration ◽  
Excess Water ◽  
Saline Loading ◽  
Long Time

When dehydrated camels are offered water they drink volumes of water exceeding their body water loss during the water deprivation period. The excess water is excreted during 2-4 days. To investigate the ability to retain fluid in the body, normohydrated camels were loaded with water or isotonic saline (0.1 l/kg body wt) by esophageal tube. After water loading plasma osmolality decreased and a water diuresis was seen, but it took 3 days until the body weight returned to prehydration level. Plasma aldosterone concentration (PAC) increased, but plasma renin activity (PRA) and plasma atrial natriuretic peptide (ANP) concentration did not change. After the saline loading plasma osmolality increased and total plasma proteins and hematocrit decreased. Renal Na excretion increased 4 h after the saline load, but the magnitude of the natriuresis was small, and the camels had not regained their body weight 6 days after the load. PAC and PRA decreased after saline loading, while plasma ANP concentration did not change. These data show that camels are able to retain excess water within the body and to tolerate blood hyposmolality for a relatively long time. With saline the retention of fluid lasts even longer despite an attenuation of PAC.

Osmoregulation in water-deprived rats drinking hypertonic saline: effect of area postrema lesions

2001 ◽  
Vol 280 (3) ◽  
pp. R831-R842 ◽  
Author(s):  
Edward M. Stricker ◽  
Carl F. Craver ◽  
Kathleen S. Curtis ◽  
Kimberly A. Peacock-Kinzig ◽  
Alan F. Sved ◽  
...  
Keyword(s):  
Water Deprivation ◽  
Area Postrema ◽  
Drinking Behavior ◽  
Plasma Osmolality ◽  
Hypertonic Solution ◽  
Elevated Plasma ◽  
Intact Control ◽  
Nacl Load ◽  
Intact Rats ◽  
Drinking Fluid

Rats drank rapidly when 0.3 M NaCl was the only drinking fluid available after overnight water deprivation, consuming ∼200 ml/24 h. Although such large intakes of this hypertonic solution initially elevated plasma osmolality, excretion of comparable volumes of urine more concentrated than 300 meq Na+/l ultimately appears to restore plasma osmolality to normal levels. Rats drank ∼100 ml of 0.5 M NaCl after overnight water deprivation, but urine Na+ concentration (UNa) did not increase sufficiently to achieve osmoregulation. When an injected salt load exacerbated the initial dehydration caused by water deprivation, rats increased UNa to void the injected load and did not significantly alter 24-h intake of 0.3 or 0.5 M NaCl. Rats with lesions of area postrema had much higher saline intakes and lower UNa than did intact control rats; nonetheless, they appeared to osmoregulate well while drinking 0.3 M NaCl but not while drinking 0.5 M NaCl. Detailed analyses of drinking behavior by intact rats suggest that individual bouts were terminated by some rapid postabsorptive consequence of the ingested NaCl load that inhibited further NaCl intake, not by a fixed intake volume or number of licks that temporarily satiated thirst.

Thirst and vasopressin release in the dog: an osmoreceptor or sodium receptor mechanism?

1980 ◽  
Vol 238 (5) ◽  
pp. R333-R339 ◽  
Author(s):  
T. N. Thrasher ◽  
C. J. Brown ◽  
L. C. Keil ◽  
D. J. Ramsay
Keyword(s):  
Plasma Osmolality ◽  
Sodium Concentration ◽  
Plasma Sodium ◽  
Nacl Solution ◽  
Elevated Plasma ◽  
Vasopressin Release ◽  
Hypertonic Glucose ◽  
Hypertonic Solutions ◽  
Vasopressin Secretion ◽  
Plasma Arginine

The effects of intravenous infusion of hypertonic NaCl, sucrose, glucose, urea, or isotonic NaCl solution on thirst and plasma arginine vasopressin concentration (AVP) were studied in five conscious dogs. The changes in osmolality and sodium concentration of plasma and cerebrospinal fluid (CSF) were measured at the threshold of drinking, or after 45 min if no drinking occurred. Hypertonic NaCl and sucrose stimulated drinking in all dogs and significantly elevated plasma AVP. Equally hypertonic glucose, urea, or isotonic NaCl failed to stimulate any drinking or vasopressin secretion. All hypertonic solutions caused significant and similar increases in the osmolality and sodium concentration of CSF. Plasma osmolality was increased by the hypertonic solutions. Plasma sodium was increased by hypertonic NaCl, decreased by sucrose and glucose, and not changed by urea. Isotonic NaCl had no effect on either plasma or CSF composition. These data are not consistent with either a sodium or an osmoreceptor mechanism located within the blood-brain barrier (BBB) or with a peripheral sodium receptor mechanism. An intracranial osmoreceptor located on the blood side of the BBB is proposed to explain these results.

Shift in body fluid compartments after dehydration in humans

1988 ◽  
Vol 65 (1) ◽  
pp. 318-324 ◽  
Author(s):  
H. Nose ◽  
G. W. Mack ◽  
X. R. Shi ◽  
E. R. Nadel
Keyword(s):  
Body Fluid ◽  
Extracellular Fluid ◽  
Plasma Osmolality ◽  
Free Water ◽  
Inverse Correlation ◽  
The Body ◽  
Free Water Clearance ◽  
Before And After ◽  
Body Fluid Compartments ◽  
Fluid Compartments

To investigate the influence of [Na+] in sweat on the distribution of body water during dehydration, we studied 10 volunteer subjects who exercised (40% of maximal aerobic power) in the heat [36 degrees C, less than 30% relative humidity (rh)] for 90-110 min to produce a dehydration of 2.3% body wt (delta TW). After dehydration, the subjects rested for 1 h in a thermoneutral environment (28 degrees C, less than 30% rh), after which time the changes in the body fluid compartments were assessed. We measured plasma volume, plasma osmolality, and [Na+], [K+], and [Cl-] in plasma, together with sweat and urine volumes and their ionic concentrations before and after dehydration. The change in the extracellular fluid space (delta ECF) was estimated from chloride distribution and the change in the intracellular fluid space (delta ICF) was calculated by subtracting delta ECF from delta TW. The decrease in the ICF space was correlated with the increase in plasma osmolality (r = -0.74, P less than 0.02). The increase in plasma osmolality was a function of the loss of free water (delta FW), estimated from the equation delta FW = delta TW - (loss of osmotically active substance in sweat and urine)/(control plasma osmolality) (r = -0.79, P less than 0.01). Free water loss, which is analogous to "free water clearance" in renal function, showed a strongly inverse correlation with [Na+] in sweat (r = -0.97, P less than 0.001). Fluid movement out of the ICF space attenuated the decrease in the ECF space.(ABSTRACT TRUNCATED AT 250 WORDS)

The metabolism of cyanide and the gastrointestinal circulation of the resulting thiocyanate under conditions of chronic cyanide intake in the rat

1982 ◽  
Vol 60 (3) ◽  
pp. 381-386 ◽  
Author(s):  
P. N. Okoh ◽  
G. A. J. Pitt
Keyword(s):  
Body Fluid ◽  
Stomach Contents ◽  
The Body ◽  
Elevated Plasma ◽  
Gastric Contents ◽  
Very High ◽  
Regular Intake

A study of the distribution of 14C-labelled cyanide was carried out in rats exposed to a regular intake of cyanide in the diet for 3 weeks. All tissues contained radioactivity 9 h after injection of 14CN− but very high amounts were found in the stomach, which accounted for 18% of the total injected radioactivity. Most of this was in the contents of the stomach, of which over 80% was in the form of thiocyanate. When a small amount of S14CN− was given by mouth to rats with elevated plasma thiocyanate levels, most of the activity was excreted in the urine and only small amounts were found in the faeces. This indicated the existence of a gastrointestinal circulation of thiocyanate, in which a substantial amount of this substance secreted into the stomach contents of the rat was reabsorbed by the intestine into the body fluid to be partly excreted in the urine and partly resecreted into the gastric contents. The likely implications of this are discussed.

Diverse mechanisms for body fluid regulation in teleost fishes

2014 ◽  
Vol 307 (7) ◽  
pp. R778-R792 ◽  
Author(s):  
Yoshio Takei ◽  
Junya Hiroi ◽  
Hideya Takahashi ◽  
Tatsuya Sakamoto
Keyword(s):  
Body Fluid ◽  
Plasma Osmolality ◽  
The Body ◽  
Fluid Composition ◽  
Teleost Fishes ◽  
Endocrine Control ◽  
Ion Regulation ◽  
Teleost Species ◽  
Fluid Regulation ◽  
Body Fluid Regulation

Teleost fishes are the major group of ray-finned fishes and represent more than one-half of the total number of vertebrate species. They have experienced in their evolution an additional third-round whole genome duplication just after the divergence of their lineage, which endowed them with an extra adaptability to invade various aquatic habitats. Thus their physiology is also extremely diverse compared with other vertebrate groups as exemplified by the many patterns of body fluid regulation or osmoregulation. The key osmoregulatory organ for teleosts, whose body fluid composition is similar to mammals, is the gill, where ions are absorbed from or excreted into surrounding waters of various salinities against concentration gradients. It has been shown that the underlying molecular physiology of gill ionocytes responsible for ion regulation is highly variable among species. This variability is also seen in the endocrine control of osmoregulation where some hormones have distinct effects on body fluid regulation in different teleost species. A typical example is atrial natriuretic peptide (ANP); ANP is secreted in response to increased blood volume and acts on various osmoregulatory organs to restore volume in rainbow trout as it does in mammals, but it is secreted in response to increased plasma osmolality, and specifically decreases NaCl, and not water, in the body of eels. The distinct actions of other osmoregulatory hormones such as growth hormone, prolactin, angiotensin II, and vasotocin among teleost species are also evident. We hypothesized that such diversity of ionocytes and hormone actions among species stems from their intrinsic differences in body fluid regulation that originated from their native habitats, either fresh water or seawater. In this review, we summarized remarkable differences in body fluid regulation and its endocrine control among teleost species, although the number of species is still limited to substantiate the hypothesis.

scholarly journals Neuronal Circuits Involved in Osmotic Challenges

2017 ◽  
pp. 411-423 ◽  
Author(s):  
M. C. DOS SANTOS MOREIRA ◽  
L. M. NAVES ◽  
S. M. MARQUES ◽  
E. F. SILVA ◽  
A. C. S. REBELO ◽  
...  
Keyword(s):  
Body Fluid ◽  
Ion Homeostasis ◽  
Survival Rates ◽  
Sodium Concentration ◽  
The Body ◽  
Plasma Sodium ◽  
Fluid Homeostasis ◽  
Arterial Blood ◽  
Plasma Sodium Concentration ◽  
Body Fluid Homeostasis

The maintenance of plasma sodium concentration within a narrow limit is crucial to life. When it differs from normal physiological patterns, several mechanisms are activated in order to restore body fluid homeostasis. Such mechanisms may be vegetative and/or behavioral, and several regions of the central nervous system (CNS) are involved in their triggering. Some of these are responsible for sensory pathways that perceive a disturbance of the body fluid homeostasis and transmit information to other regions. These regions, in turn, initiate adequate adjustments in order to restore homeostasis. The main cardiovascular and autonomic responses to a change in plasma sodium concentration are: i) changes in arterial blood pressure and heart rate; ii) changes in sympathetic activity to the renal system in order to ensure adequate renal sodium excretion/absorption, and iii) the secretion of compounds involved in sodium ion homeostasis (ANP, Ang-II, and ADH, for example). Due to their cardiovascular effects, hypertonic saline solutions have been used to promote resuscitation in hemorrhagic patients, thereby increasing survival rates following trauma. In the present review, we expose and discuss the role of several CNS regions involved in body fluid homeostasis and the effects of acute and chronic hyperosmotic challenges.

Plasma vasopressin response to peripheral administration of angiotensin in conscious rats

1985 ◽  
Vol 248 (2) ◽  
pp. R249-R256 ◽  
Author(s):  
K. Yamaguchi ◽  
M. Koike ◽  
H. Hama
Keyword(s):  
Angiotensin Ii ◽  
Isotonic Saline ◽  
Plasma Osmolality ◽  
Plasma Sodium ◽  
Ang Ii ◽  
Mannitol Solution ◽  
Injection Volume ◽  
Conscious Rats ◽  
Plasma Vasopressin ◽  
Series Of Experiments

To assess a role for peripherally administered angiotensin II (ANG II) in regulating vasopressin (antidiuretic hormone, ADH) release, the effects on plasma ANG II and ADH of intraperitoneal injections of ANG II dissolved in various solutions were examined in conscious rats. Plasma ANG II and ADH were determined by radioimmunoassay using the trunk blood collected after decapitation. Injections of 150 mM NaCl containing ANG II (6, 12, or 24 micrograms X 2 ml-1 X 100 g body wt-1) caused dose-related increases in plasma ANG II 15 and 30 min after, but plasma ADH remained unchanged. The lack of effect on plasma ADH of the ANG II dissolved in isotonic saline was also confirmed in another series of experiments in which the solution with a higher ANG II concentration was loaded by much smaller injection volume (14.3 micrograms X 0.1 ml-1 X 100 g-1). However, when given together with 600 mM NaCl, ANG II (8 micrograms X 2 ml-1 X 100 g-1) significantly potentiated the plasma ADH response to the vehicle at 15, 30, and 60 min, without affecting those of plasma osmolality, sodium, and hematocrit. The elevations of plasma ANG II and osmolality brought about by the treatment were comparable with those previously observed in rats deprived of water for 46 h. ANG II was without effect on the plasma ADH responses to the intraperitoneal injections of hypertonic sucrose or mannitol solution that did not alter plasma sodium, although these solutions were equipotent to 600 mM NaCl in augmenting plasma ADH and osmolality.(ABSTRACT TRUNCATED AT 250 WORDS)

Fluid volume and osmoregulation in humans after a week of head-down bed rest

2001 ◽  
Vol 281 (1) ◽  
pp. R310-R317 ◽  
Author(s):  
Morten Heiberg Bestle ◽  
Peter Norsk ◽  
Peter Bie
Keyword(s):  
Excretion Rate ◽  
Sodium Intake ◽  
Isotonic Saline ◽  
Plasma Osmolality ◽  
Bed Rest ◽  
Ang Ii ◽  
Plasma Vasopressin ◽  
Saline Loading ◽  
Body Fluid Homeostasis ◽  
Renal Responses

Body fluid homeostasis was investigated during chronic bed rest (BR) and compared with that of acute supine conditions. The hypothesis was tested that 6° head-down BR leads to hypovolemia, which activates antinatriuretic mechanisms so that the renal responses to standardized saline loading are attenuated. Isotonic (20 ml/kg body wt) and hypertonic (2.5%, 7.2 ml/kg body wt) infusions were performed in eight subjects over 20 min following 7 and 10 days, respectively, of BR during constant sodium intake (200 meq/day). BR decreased body weight (83.0 ± 4.8 to 81.8 ± 4.4 kg) and increased plasma osmolality (285.9 ± 0.6 to 288.5 ± 0.9 mosmol/kgH2O, P < 0.05). Plasma ANG II doubled (4.2 ± 1.2 to 8.8 ± 1.8 pg/ml), whereas other endocrine variables decreased: plasma atrial natriuretic peptide (42 ± 3 to 24 ± 3 pg/ml), urinary urodilatin excretion rate (4.5 ± 0.3 to 3.2 ± 0.1 pg/min), and plasma vasopressin (1.7 ± 0.3 to 0.8 ± 0.2 pg/ml, P < 0.05). During BR, the natriuretic response to the isotonic saline infusion was augmented (39 ± 8 vs. 18 ± 6 meq sodium/350 min), whereas the response to hypertonic saline was unaltered (32 ± 8 vs. 29 ± 5 meq/350 min, P< 0.05). In conclusion, BR elicits antinatriuretic endocrine signals, but it does not attenuate the renal natriuretic response to saline stimuli in men; on the contrary, the response to isotonic saline is augmented.

scholarly journals Effect of hypohydration on hyperthermic hyperpnea and cutaneous vasodilation during exercise in men

2008 ◽  
Vol 105 (5) ◽  
pp. 1509-1518 ◽  
Author(s):  
Naoto Fujii ◽  
Yasushi Honda ◽  
Keiji Hayashi ◽  
Narihiko Kondo ◽  
Takeshi Nishiyasu
Keyword(s):  
Oxygen Uptake ◽  
Body Fluid ◽  
Minute Ventilation ◽  
Plasma Osmolality ◽  
Rest Period ◽  
Random Order ◽  
Peak Oxygen Uptake ◽  
The Body ◽  
Fluid Replacement ◽  
End Tidal

We tested the hypothesis that, in humans, hypohydration attenuates hyperthermic hyperpnea during exercise in the heat. On two separate occasions, thirteen male subjects performed a fluid replacement (FR) and a no-fluid replacement (NFR) trial in random order. The subjects performed two bouts of cycle exercise (Ex1 and Ex2, 30–60 min) at 50% peak oxygen uptake (V̇o2 peak) in 35°C separated by a 70- to 80-min rest period, during which they drank water containing 25 mosmol/l sodium in the FR trial but not the NFR trial. The drinking in the FR trial nearly restored the body fluid to the euhydrated condition, so that the body fluid status differed between the trials before Ex2 (the difference in plasma osmolality before Ex2 was 9.4 mosmol/kgH2O; plasma volume was 7.6%, and body weight was 2.5%). The slopes of the linear relationships between ventilatory variables (minute ventilation, ventilatory equivalents for oxygen uptake and carbon dioxide output, tidal volume, respiratory frequency, and end-tidal CO2 pressure) and esophageal temperature (Tes) did not significantly differ between Ex1 and Ex2, or between the FR and NFR trials. On the other hand, during Ex2 in the NFR trial, the Tes threshold for the onset of increased forearm vascular conductance (FVC) was higher, and the slope and peak values of the relationship between FVC and Tes were lower than during Ex1 in the NFR trial and during Ex2 in the FR trial. These findings suggest that hypohydration does not affect the hyperthermic hyperpnea during exercise, although it markedly attenuates the cutaneous vasodilatory response.

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