Regulation of plasma vasopressin by plasma osmolality and carotid sinus pressure in anesthetized rabbits

1994 ◽  
Vol 266 (3) ◽  
pp. R796-R801
Author(s):  
C. S. Scott ◽  
J. Sharp-Kehl ◽  
C. A. Redekopp ◽  
J. R. Ledsome

The purpose of the experiments was to investigate the effect of changes in carotid sinus baroreceptor stimulation on plasma vasopressin (AVP) at different plasma osmolalities in the anesthetized artificially ventilated rabbit. Both carotid sinuses were isolated and perfused with blood at servo-controlled pressures. The vagus and aortic depressor nerves were sectioned bilaterally to eliminate input from atrial and aortic arch baroreceptors. Saline (0.3%, wt/vol) was infused to lower plasma osmolality, and 5% saline was infused to raise plasma osmolality. At three plasma osmolalities, the carotid sinus pressure (CSP) was changed from 100 mmHg to 40 and 140 mmHg and returned to 100 mmHg. There were no changes in plasma AVP in response to changes in CSP at low plasma osmolality (289 mosmol/kgH2O), but at medium (309 mosmol/kgH2O) and high (323 mosmol/kgH2O) osmolality, plasma AVP was higher at 40 than at 140 mmHg CSP. The relationship between plasma AVP and plasma osmolality was expressed as a linear regression at each CSP. Changes in CSP changed the sensitivity but not the threshold of the osmotic control of AVP release.

1988 ◽  
Vol 255 (5) ◽  
pp. H1199-H1205
Author(s):  
C. A. Courneya ◽  
A. J. Rankin ◽  
N. Wilson ◽  
J. R. Ledsome

The arterial baroreceptors are known to influence the release of vasopressin, but the quantitative relationship between baroreceptor stimulation and plasma vasopressin concentration has not been defined. These experiments examine the effect of stepwise changes in carotid sinus pressure (40-160 mmHg) on the plasma concentration of vasopressin in chloralose-urethan anesthetized rabbits. Plasma vasopressin concentration (9.2 +/- 1.2 pg/ml, n = 27) did not change in response to changes in carotid sinus pressure when the aortic depressor nerves were intact. These results were unaltered by bilateral cervical vagotomy. However, after aortic depressor nerve section, decreases in carotid sinus pressure were associated with increases in plasma vasopressin concentration. There appeared to be a greater redundancy in the baroreceptor control of plasma vasopressin than in the baroreceptor control of arterial pressure or heart rate. The results provided no evidence that receptors with vagal afferents have a tonic influence on the baroreceptor control of vasopressin release in the anesthetized rabbit.


1980 ◽  
Vol 238 (4) ◽  
pp. E313-E317 ◽  
Author(s):  
M. Hammer ◽  
J. Ladefoged ◽  
K. Olgaard

The relationship between plasma osmolality (pOsm) and plasma vasopressin (pAVP) was studied in 13 human subjects during dehydration. The fit of linear, log-linear, parabolic, and exponential models was tested. For all of the data, the nonlinear models had the best fit. However, when individual differences in either gain or threshold were allowed for, the linear models were better than log-linear models. Finally, analyses were made with individual data points. Linear models had the best fit in half of the subjects, whereas for the others the parabolic model gave the best fit. For those subjects investigated in the low range of the osmoregulatory curve, a linear relationship was found, whereas, for those having the most pronounced increase in pOsm, the most significant improvement was found with the parabolic model. This finding indicates that the relationship is not stable during dehydration in the whole range and that hypovolemia probably can influence the secretion rate and/or metabolic clearance rate and thereby the relationship.


1987 ◽  
Vol 253 (3) ◽  
pp. H598-H603
Author(s):  
A. A. Shoukas ◽  
M. J. Brunner ◽  
A. S. Greene ◽  
C. L. MacAnespie

The ability of the aortic arch baroreceptors to change vascular capacity was measured and, in the same animal, compared with carotid sinus reflex changes in capacity. Seven dogs were anesthetized with pentobarbital sodium and perfused with constant flow. Changes in external reservoir volume reflected reciprocal changes in total systemic vascular capacity and changes in arterial pressure parallel changes in total peripheral resistance. The aortic arch and carotid sinus baroreceptor areas were isolated, and the pressures were controlled separately. With carotid sinus pressure held constant at 125 mmHg, aortic arch pressure was increased and decreased between 225 and 50 mmHg, and the changes in reservoir volume and systemic arterial pressure were measured. Results from increasing and decreasing aortic arch or carotid sinus pressure were not significantly different and were averaged. The mean change in reservoir volume was 1.9 +/- 0.2 ml/kg and the change in mean arterial pressure was 18.7 +/- 3.7 mmHg. The changes in reservoir volume and arterial pressure caused by the aortic arch reflex were not influenced by the level of carotid sinus pressure. Carotid sinus pressure changes between 200 and 50 mmHg at a constant aortic arch pressure caused reservoir volume and arterial pressure to change by 7.2 +/- 0.9 ml/kg and 45.1 +/- 4.1 mmHg, respectively. The level of aortic arch pressure did not modify these responses.


1995 ◽  
Vol 78 (5) ◽  
pp. 1699-1709 ◽  
Author(s):  
K. W. Saupe ◽  
C. A. Smith ◽  
K. S. Henderson ◽  
J. A. Dempsey

The purpose of this study was to determine whether acutely raising carotid sinus pressure (Pcs) causes changes in upper airway resistance and/or electroencephalographic (EEG) frequency during wakefulness and non-rapid-eye-movement (NREM) sleep. Five dogs were chronically instrumented so that breathing, tracheal pressure, mouth pressure, EEG, and electrooculogram could be measured while pressure in the vascularly isolated carotid sinus was rapidly increased between 40 and 150 mmHg via an extracorporeal perfusion circuit. Dogs were studied during both wakefulness and NREM sleep. Multiple trials of increased Pcs were conducted in each dog. We observed that increasing Pcs 40–150 mmHg caused not only a reflex cardiovascular response but also a 15–40% decrease in minute ventilation. Raising Pcs caused no physiologically significant changes in upper airway resistance over the range of airway pressures and flow rates encountered during inspiration and expiration. Even dogs that demonstrated moderate to substantial sleep-induced increases in airway resistance did not consistently increase resistance during superimposed baroreceptor stimulation. Small increases in airway resistance were sometimes observed during baroreceptor stimulation, but this was not a consistent finding. Acute increases in Pcs did not cause measurable changes in EEG frequency during wakefulness or NREM sleep. We conclude that acute stimulation of the carotid sinus baroreceptors does not cause physiologically meaningful changes in upper airway resistance or EEG activity in awake or sleeping dogs.


1988 ◽  
Vol 254 (4) ◽  
pp. H742-H750
Author(s):  
D. F. Hanley ◽  
D. A. Wilson ◽  
M. A. Feldman ◽  
R. J. Traystman

Neurohypophysial blood flow responses to hypoxic hypoxia were studied under conditions of vagotomy, carotid sinus denervation, and combined vagotomy and carotid sinus denervation. Arterial O2 tension was lowered from 128 +/- 3 to 31 +/- 1 Torr, whereas pH and arterial CO2 tension remained constant. Denervation of either carotid sinus or aortic arch chemoreceptors alone does not attenuate the dilation of neurohypophysial vessels that accompanies hypoxic hypoxia. Combined denervation, however, completely blocks this response for the neurohypophysis but not for any other brain region studied. Hypoxic hypoxia resulted in an increase in plasma vasopressin (AVP) from approximately 8 to approximately 40 pg/ml. This increase occurred in the intact, vagotomy, and carotid sinus-denervation conditions. This neurosecretory response was also completely inhibited by combined denervation. For most brain regions peripheral chemoreceptors are not involved in the blood flow response; however, the response of the neurohypophysis appears to be mediated via these chemoreceptors, presumably by altering the neuroeffector activity to this region. In addition our data suggest a temporal relationship between neurohypophysial vasodilation and neurosecretion of AVP.


1994 ◽  
Vol 131 (1) ◽  
pp. 86-90 ◽  
Author(s):  
Dirk Terwel ◽  
Jellemer Jolles

Terwel D, Jolles J. The relationship between plasma osmolality and plasma vasopressin concentration is altered in old male Lewis rats. Eur J Endocrinol 1994;131:86–90. ISSN 0804–4643 Kidney dysfunction has been observed in aged humans and rats, the primary cause of which may reside in the kidney itself or in the hypothalamus. The latter possibility is suggested by the increased release of AVP in response to salt infusion in humans. The effect of age on the relationship between plasma osmolality and plasma AVP concentration has never been verified in an animal model. Therefore, in the present study, 9% salt solution was infused into adult and aged Lewis rats, and plasma AVP concentration and osmolality were measured. Basal plasma AVP concentration, osmolality and total water intake were not altered in aged Lewis rats as compared with adult animals, indicating the absence of overt disturbances in water homeostasis. Infusion of 9% salt solution resulted in a linear increase in plasma osmolality in both adult and aged rats. Plasma osmolality increased more with time in aged animals than in adult animals, suggesting an age-related difference in kidney function during salt infusion. Plasma AVP concentration increased 50% less with osmolality at relatively low osmolalities, but not at relatively high osmolalities. The altered relationship between plasma osmolality and plasma AVP concentration in rats with age may be related to changes in neurons monitoring osmolality or to changes in baroreflex regulation. The data suggest that reduced kidney function with age does not result from an altered relationship between plasma osmolality and plasma AVP concentration. D Terwel, University of Limburg, Department of Neuropsychology and Psychobiology, PO Box 616, 6200 MD Maastricht, The Netherlands


1984 ◽  
Vol 246 (3) ◽  
pp. H360-H368 ◽  
Author(s):  
B. C. Wang ◽  
W. D. Sundet ◽  
M. O. Hakumaki ◽  
P. G. Geer ◽  
K. L. Goetz

Changes in blood volume are capable of altering the relationship between plasma osmolality (Posmol) and plasma arginine vasopressin (PAVP), presumably via a reflex elicited from cardiovascular receptors, but the precise location of the receptors involved in this response has not been established. Because cardiac receptors are capable of influencing AVP secretion, their specific effect was examined by producing volume changes in cardiac-denervated (CD) dogs and comparing the Posmol-PAVP relationship in these dogs with data from comparable experiments on sham-operated control dogs (cardiac-sham, CS). Posmol was increased by water deprivation for 96 h (volume depletion) and also by administration of hypertonic saline for 2 h (volume expansion). The slope of the regression line describing the Posmol-PAVP relationship in CS control dogs was steeper (P less than 0.01) during volume depletion (0.390) than it was during volume expansion (0.228), thus suggesting that volume depletion had enhanced and volume expansion had inhibited the secretion of AVP. In contrast, the slope of the regression line delineating the Posmol-PAVP relationship in CD dogs was essentially the same during volume depletion (0.288) as it was during volume expansion (0.291). It would seem that most, if not all, of the volume influences on the Posmol-PAVP relationship are mediated via reflex effects elicited by cardiac receptors.


1982 ◽  
Vol 242 (6) ◽  
pp. F740-F744
Author(s):  
S. S. Daniel ◽  
R. I. Stark ◽  
M. K. Husain ◽  
L. V. Baxi ◽  
L. S. James

The role of vasopressin (VP) and the kidney in the maintenance of solute and volume homeostasis was studied in chronically instrumented fetal lambs during the third trimester. Plasma VP, urine and plasma osmolality, and urine output were measured in 74 simultaneous samples. The results show a strong positive nonlinear correlation between plasma VP and osmolality when a latter is higher than 290 mosmol/kg (r = 0.803, P = 0.03) and between plasma VP and urine osmolality (r = 0.806, P = 0.05). No correlation was found between fetal and maternal plasma VP. However, linear correlations were found in plasma osmolality and sodium concentrations between mother and fetus; mean maternal-fetal gradients were 4 mosmol/kg and 3.1 meq/liter, respectively. The highest values for plasma VP and osmolality found in our study were 7.0 pg/ml and 317 mosmol/kg, respectively. There values corresponded to urine output of 0.02 ml.kg-1.min-1 and osmolality of 517 mosmol/kg. In conclusion, there studies demonstrate that the relationship among plasma osmolality, plasma vasopressin concentration, and urine osmolality in the lamb fetus are qualitatively similar to those of the adult. The results suggest that the fetal neurohypophysis and kidney may participate in the maintenance of fetal osmolar and volume homeostasis.


1979 ◽  
Vol 57 (2) ◽  
pp. 147-151
Author(s):  
Franco Lioy ◽  
Peter M. Szeto

A stretch of the walls of the thoracic aorta, performed in vagotomized cats without obstructing aortic flow, induces increases in heart rate, myocardial contractility, and arterial pressure. These reflex responses are still present after high spinal section. Cats under chloralose–urethane anesthesia were vagotomized and one carotid sinus was isolated and perfused with arterial blood at constant flow. The contralateral carotid sinus nerve and both aortic nerves were sectioned. A stretch of the walls of the thoracic aorta between the 7th and 10th intercostal arteries induced a reflex increase in mean arterial pressure of 29 ± 2 mmHg (mean ± SE). Stepwise increases of carotid sinus pressure (CSP) or electrical stimulation of the carotid sinus nerve induced stepwise decreases of this reflex response. At maximal baroreceptor stimulation (CSP 212 ± 9 mmHg) the reflex response to aortic stretch was reduced by 42%.These experiments show that this spinal cardiovascular reflex is at least partially under the inhibitory control of the baroreceptor input.


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