Altered sensitivity of osmotically stimulated vasopressin release in quadriplegic subjects

1990 ◽  
Vol 258 (4) ◽  
pp. R827-R835
Author(s):  
B. M. Wall ◽  
H. H. Williams ◽  
D. N. Presley ◽  
J. T. Crofton ◽  
E. G. Schneider ◽  
...  
Keyword(s):  
Linear Regression Analysis ◽  
Plasma Osmolality ◽  
Plasma Renin ◽  
Erect Posture ◽  
Vasopressin Release ◽  
Enhanced Sensitivity ◽  
Arterial Blood ◽  
Healthy Control ◽  
Plasma Arginine ◽  
Altered Sensitivity

Osmoregulation of vasopressin release was studied in 15 quadriplegic subjects (Quad) and 7 healthy control subjects (Con). Hypertonic NaCl (0.85 M) was infused intravenously (0.05 ml.kg-1.min-1) over 90 min in studies on supine subjects and in comparable studies on the same subjects erect (sitting). Erect posture in Quad, but not in Con, was accompanied by orthostatic reductions in arterial blood pressure and by significantly increased plasma aldosterone (P less than 0.001) and cortisol (P less than 0.001) concentrations and increased plasma renin activity (P less than 0.025). Changes in plasma arginine vasopressin concentration (PAVP) during hypertonic NaCl infusions were also greater in erect than in supine Quad (P less than 0.005), despite identical changes in plasma osmolality (Posm). Linear regression analysis of the PAVP/Posm relationship during hypertonic NaCl infusions showed highly significant correlations (P less than 0.0002) in both Quad and Con. Mean slope values for regression lines, however, were significantly higher in erect than in supine Quad (P less than 0.005) but did not differ in relation to posture in Con. Differences in posture were not associated with differences in abscissal intercepts in either Quad or Con. These studies show significant alterations in the sensitivity of osmotically stimulated vasopressin release related to differences in posture in Quad, characterized by enhanced sensitivity in erect posture due to nonosmotic stimuli not evident in Con.

VASOPRESSIN RELEASE DURING VENTRICULO-CISTERNAL PERFUSION WITH PROSTAGLANDIN E2 IN THE DOG

1976 ◽  
Vol 71 (3) ◽  
pp. 325-331 ◽  
Author(s):  
MANABU YAMAMOTO ◽  
L. SHARE ◽  
R. E. SHADE
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Plasma Concentrations ◽  
Plasma Osmolality ◽  
Plasma Renin ◽  
Prostaglandin E ◽  
Temperature Plasma ◽  
Vasopressin Release ◽  
Control Value ◽  
Arterial Blood

SUMMARY In an attempt to determine whether prostaglandin E2 (PGE2) can act centrally to affect the release of vasopressin (ADH), the ventriculo-cisternal system of anaesthetized dogs was perfused with PGE2. When PGE2 was perfused at a rate of 76·4 ng/min (0·19 ml/min), the plasma ADH concentration was unchanged. However, perfusion of PGE2 at a rate of 152·8 ng/min (0·19 ml/min) resulted in a significant increase in the plasma ADH concentration from the control value of 9·0 ± 2·2 (s.e.m.) to 18·8 ± 3·9 μu./ml at 10 min and to 41·0 ± 16·7 μu./ml at 30 min after the start of the perfusion. There were no changes in arterial blood pressure, rectal temperature, plasma osmolality, and the plasma concentrations of sodium and potassium. In additional experiments, i.v. injection of indomethacin (2 or 20 mg/kg) decreased the plasma ADH concentration by approximately 50%. Although this finding is consistent with a role of PGE2 in the control of ADH release, it could also have been due to the observed increases in arterial blood pressure and effective left atrial pressure. Plasma renin activity was unchanged in the indomethacin experiments. It is concluded that PGE2 can act in the central nervous system to stimulate ADH release.

The osmotic thresholds for thirst and vasopressin release are similar in healthy man

1986 ◽  
Vol 71 (6) ◽  
pp. 651-656 ◽  
Author(s):  
C. J. Thompson ◽  
J. Bland ◽  
J. Burd ◽  
P. H. Baylis
Keyword(s):  
Arginine Vasopressin ◽  
Analogue Scale ◽  
Linear Regression Analysis ◽  
Plasma Osmolality ◽  
Physiological Saline ◽  
Linear Increase ◽  
Vasopressin Release ◽  
Wide Range ◽  
Plasma Arginine ◽  
The Relationship

1. The relationship between thirst perception and plasma osmolality was studied during hypertonic and physiological saline infusion in ten healthy volunteers. 2. Thirst perception was quantified using a linear visual analogue scale which volunteers marked at intervals during the infusion periods. 3. Infusion of hypertonic saline caused a steady rise in plasma osmolality together with a progressive linear increase in thirst perception and also plasma arginine vasopressin. No significant changes in thirst, plasma osmolality or plasma arginine vasopressin occurred during infusion of physiological saline. 4. Linear regression analysis of the results defined the functions. Thirst (cm) = 0.3 (plasma osmolality −281) (r = + 0.92, P < 0.001) and plasma arginine vasopressin (pmol/l) = 0.4 (plasma osmolality −285) (r = + 0.96, P < 0.001). The osmolar threshold for thirst onset thus defined (281 mosmol/kg) was much lower than in previous studies and similar to the theoretical osmolar threshold for vasopressin release (285 mosmol/kg). 5. We conclude that thirst perception rises in a progressive fashion throughout a wide range of plasma osmolality and that the osmolar threshold for thirst onset is similar to the theoretical osmolar threshold for vasopressin release. 6. The results are compatible with the concept of either a single osmoreceptor subserving both thirst and vasopressin release, or two osmoreceptors sharing similar functional characteristics.

Stimulation of brain mast cells by compound 48/80, a histamine liberator, evokes renin and vasopressin release in dogs

2008 ◽  
Vol 294 (3) ◽  
pp. R689-R698 ◽  
Author(s):  
Itsuro Matsumoto ◽  
Yasuhisa Inoue ◽  
Toshio Shimada ◽  
Tomoe Matsunaga ◽  
Tadaomi Aikawa
Keyword(s):  
Mast Cells ◽  
Receptor Antagonist ◽  
Third Ventricle ◽  
Plasma Osmolality ◽  
Plasma Renin ◽  
Vasopressin Release ◽  
Arterial Blood ◽  
Endogenous Histamine ◽  
Before And After ◽  
Anesthetized Dogs

Because degranulation of brain mast cells activates adrenocortical secretion ( 41 , 42 ), we examined whether activation of such cells increases renin and vasopressin (antidiuretic hormone: ADH) secretion. For this, we administered compound 48/80 (C48/80), which liberates histamine from mast cells, to pentobarbital-anesthetized dogs. An infusion of 37.5 μg/kg C48/80 into the cerebral third ventricle evoked increases in plasma renin activity (PRA), and in plasma epinephrine (Epi) and ADH concentrations. Ketotifen (mast cell-stabilizing drug; given orally for 1 wk before the experiment) significantly reduced the C48/80-induced increases in PRA, Epi, and ADH. Resection of the bilateral splanchnic nerves (SPX) below the diaphragm completely prevented the C48/80-induced increases in PRA and Epi, but potentiated the C48/80-induced increase in ADH and elevated the plasma Epi level before and after C48/80 challenge. No significant changes in mean arterial blood pressure, heart rate, concentrations of plasma electrolytes (Na+, K+, and Cl−), or plasma osmolality were observed after C48/80 challenge in dogs with or without SPX. Pyrilamine maleate (H1histaminergic-receptor antagonist) significantly reduced the C48/80-induced increase in PRA when given intracerebroventricularly, but not when given intravenously. In contrast, metiamide (H2histaminergic-receptor antagonist) given intracerebroventricularly significantly potentiated the C48/80-induced PRA increase. A small dose of histamine (5 μg/kg) administered intracerebroventricularly increased PRA twofold and ADH fourfold (vs. their basal level). These results suggest that in dogs, endogenous histamine liberated from brain mast cells may increase renin and Epi secretion (via the sympathetic outflow) and ADH secretion (via the central nervous system).

Factors associated with vasopressin release in exercising swine

1994 ◽  
Vol 266 (1) ◽  
pp. R118-R124 ◽  
Author(s):  
C. L. Stebbins ◽  
J. D. Symons ◽  
M. D. McKirnan ◽  
F. F. Hwang
Keyword(s):  
Plasma Volume ◽  
Plasma Concentrations ◽  
Plasma Osmolality ◽  
Plasma Renin ◽  
Treadmill Running ◽  
Maximal Heart Rate ◽  
Ang Ii ◽  
Strong Correlations ◽  
Vasopressin Release ◽  
Lysine Vasopressin

This study examined the effect of dynamic exercise on vasopressin release in the miniswine and factors that may elicit this response (n = 15). Thus lysine vasopressin (LVP), the catecholamines epinephrine and norepinephrine (EPI and NE), plasma renin activity (PRA), and plasma volume, Na+, and osmolality were measured before and during treadmill running at work intensities of 60, 80, and 100% of each swine's maximal heart rate reserve (HRR). LVP increased in a progressive manner similar to that of humans, ranging from 5.9 +/- 0.4 pg/ml before exercise to 30.1 +/- 4.5 pg/ml during maximal exercise. EPI, NE, and PRA [an index of angiotensin II (ANG II) activity] demonstrated a pattern of response comparable to LVP. Although these hormones can influence the release of LVP, only PRA displayed a strong correlation with LVP (r = 0.84). When ANG II synthesis was blocked (captopril, 1-3 mg/kg, intra-atrial injection) during exercise (80% HRR), plasma LVP was reduced from 9.9 +/- 0.6 to 7.5 +/- 0.6 pg/ml (P < 0.05). In addition, moderate-to-strong correlations were found between plasma concentrations of LVP and plasma osmolality (r = 0.79) and body temperature (r = 0.78). Plasma LVP also correlated with decreases in plasma volume (r = 0.84). These data suggest that the miniswine model is a good one for studying vasopressin effects during exercise and that ANG II appears to be a particularly strong stimulus for the release of this hormone.

Vasopressin-independent alterations in renal water excretion in quadriplegia

1993 ◽  
Vol 265 (2) ◽  
pp. R460-R466 ◽  
Author(s):  
B. M. Wall ◽  
H. H. Williams ◽  
D. N. Presley ◽  
J. T. Crofton ◽  
L. Share ◽  
...  
Keyword(s):  
Cervical Spinal Cord ◽  
Free Water ◽  
Renal Tubules ◽  
Erect Posture ◽  
Free Water Clearance ◽  
Water Excretion ◽  
Vasopressin Release ◽  
Control Subjects ◽  
Cord Injury ◽  
Healthy Control

Postural effects on water excretion are known to be increased in patients with cervical spinal cord injury and may result in marked impairment of the ability to excrete a water load, especially in erect posture. Both vasopressin-dependent and vasopressin-independent mechanisms have been implicated. To assess the roles of these mechanisms and further identify the factors involved in the renal response to erect posture, sustained water loading studies were performed on 11 quadriplegic subjects and 9 healthy control subjects, supine and erect (sitting). Renal blood flow was assessed by p-aminohippurate clearance (CPAH) measurements in 7 quadriplegic and 5 control subjects. During maximal water diuresis, plasma vasopressin concentrations were reduced to unquantifiable levels in all subjects. Osmolar clearance, free water clearance (CH2O), and distal delivery of filtrate (DDF) were all lower in quadriplegic than in control subjects, supine and erect. The relationship between CH2O and DDF was the same in quadriplegic as in control subjects and was not altered by change in posture in either group. Creatinine clearance and CPAH were lower in erect than in supine posture in quadriplegic subjects but not in control subjects. We conclude that impairment of water excretion in stable normonatremic quadriplegic subjects can be attributed primarily to vasopressin-independent mechanisms involving reduced filtrate delivery to diluting segments of the renal tubules rather than to resistance to normal suppression of vasopressin release.

Increased plasma osmolality stimulates peripheral and central vasopressin release in male and female rats

1994 ◽  
Vol 267 (4) ◽  
pp. R923-R928 ◽  
Author(s):  
M. Ota ◽  
J. T. Crofton ◽  
H. Liu ◽  
G. Festavan ◽  
L. Share
Keyword(s):  
Interstitial Fluid ◽  
Plasma Osmolality ◽  
Female Rats ◽  
Microdialysis Probe ◽  
Vasopressin Release ◽  
Arterial Blood ◽  
Plasma Vasopressin ◽  
Male And Female Rats ◽  
Supraoptic Nuclei

It has been demonstrated that the neurohypophysial hormones can be released intrahypothalamically by the paraventricular (PVN) and supraoptic nuclei. The present experiments were undertaken to determine whether a physiological stimulus for vasopressin release, increased plasma osmolality, will stimulate the release of vasopressin by the PVN into the surrounding interstitial fluid, and whether the responses are affected by gender. Intravenous infusion of 2.5 M NaCl for 60 min (0.1 ml.kg-1.min-1) in conscious rats resulted in an increased vasopressin concentration in the dialysate from a microdialysis probe adjacent to the PVN. This response was greater in nonestrous females than in males. On the other hand, the rise in the plasma vasopressin concentration was greater in males than in nonestrous females. Mean arterial blood pressure increased and heart rate decreased, but these responses were not affected by gender. The role of centrally released vasopressin in the control of the peripheral release of vasopressin is conjectural, but both responses may be modulated by the gonadal steroid hormones.

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.

Atrial natriuretic peptide inhibits osmolality-induced arginine vasopressin release in man

1988 ◽  
Vol 75 (1) ◽  
pp. 35-39 ◽  
Author(s):  
M. J. Allen ◽  
V. T. Y. Ang ◽  
E. D. Bennett ◽  
J. S. Jenkins
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Arginine Vasopressin ◽  
Plasma Osmolality ◽  
Random Order ◽  
Vasopressin Release ◽  
Plasma Arginine ◽  
Placebo Infusion ◽  
Atrial Natriuretic

1. Eight normal volunteers were infused with 5% saline (5 g of NaCl/100 ml) at a rate of 0.06 ml min−1 kg−1 for 120 min to increase plasma osmolality and plasma arginine vasopressin. Human atrial natriuretic peptide (α-hANP; 100 μg) or placebo was given in random order in a double-bind cross-over design for the last 20 min of the saline infusion. 2. Compared with the placebo infusion, atrial natriuretic peptide (ANP) produced a 43% greater sodium excretion and a 34% greater urinary volume in the subsequent hour. 3. Mean plasma immunoreactive ANP did not increase in response to changes in osmolality and rose to a peak of 118 pg/ml during the α-hANP infusion. α-hANP produced significant suppression of mean plasma arginine vasopressin over the 60 min after the infusions. 4. We conclude that ANP is not released in response to increased osmolality in vivo, and that it inhibits osmolality-induced arginine vasopressin release in man.

scholarly journals Water deprivation-induced sodium appetite: humoral and cardiovascular mediators and immediate early genes

2002 ◽  
Vol 282 (2) ◽  
pp. R552-R559 ◽  
Author(s):  
Laurival A. De Luca ◽  
Zhice Xu ◽  
Guus H. M. Schoorlemmer ◽  
Robert L. Thunhorst ◽  
Terry G. Beltz ◽  
...  
Keyword(s):  
Water Deprivation ◽  
Plasma Osmolality ◽  
Plasma Renin ◽  
Preoptic Nucleus ◽  
Adult Rats ◽  
Sodium Appetite ◽  
Arterial Blood ◽  
Fos Expression ◽  
Total Body ◽  
Operational Criteria

10.1152/ajpregu.00295.2000. Adult rats deprived of water for 24–30 h were allowed to rehydrate by ingesting only water for 1–2 h. Rats were then given access to both water and 1.8% NaCl. This procedure induced a sodium appetite defined by the operational criteria of a significant increase in 1.8% NaCl intake (3.8 ± 0.8 ml/2 h; n = 6). Expression of Fos (as assessed by immunohistochemistry) was increased in the organum vasculosum of the lamina terminalis (OVLT), median preoptic nucleus (MnPO), subfornical organ (SFO), and supraoptic nucleus (SON) after water deprivation. After rehydration with water but before consumption of 1.8% NaCl, Fos expression in the SON disappeared and was partially reduced in the OVLT and MnPO. However, Fos expression did not change in the SFO. Water deprivation also 1) increased plasma renin activity (PRA), osmolality, and plasma Na+; 2) decreased blood volume; and 3) reduced total body Na+; but 4) did not alter arterial blood pressure. Rehydration with water alone caused only plasma osmolality and plasma Na+concentration to revert to euhydrated levels. The changes in Fos expression and PRA are consistent with a proposed role for ANG II in the control of the sodium appetite produced by water deprivation followed by rehydration with only water.

Cardiac nerve blockade by infusion of procaine into the pericardial space of conscious dogs

1991 ◽  
Vol 260 (6) ◽  
pp. R1176-R1182 ◽  
Author(s):  
C. P. O'Donnell ◽  
D. A. Scheuer ◽  
L. C. Keil ◽  
T. N. Thrasher
Keyword(s):  
Plasma Osmolality ◽  
Plasma Renin ◽  
Systemic Circulation ◽  
Plasma Norepinephrine ◽  
Nerve Blockade ◽  
Conscious Dog ◽  
Cardiac Nerve ◽  
Drinking Response ◽  
Reflex Tachycardia ◽  
Plasma Arginine

A technique was developed to produce acute, reversible cardiac nerve blockade (CNB) in the conscious dog by infusion of 2% procaine into the pericardial (PC) space. During CNB, reflex changes in heart rate (HR) in response to intravenous bolus injections of phenylephrine (100 micrograms) and nitroglycerin (300 micrograms) and the reflex tachycardia and hypotension after a 50-micrograms bolus injection of veratridine into the left atrium were abolished. In response to CNB, HR increased from 79 +/- 10 to 142 +/- 10 beats/min and mean arterial pressure (MAP) increased from 101 +/- 5 to 117 +/- 6 mmHg. Baseline values for plasma arginine vasopressin (AVP), plasma renin activity (PRA), and plasma norepinephrine (NE) were unchanged by CNB, but there was a small increase in plasma cortisol levels (1.4 +/- 0.3 to 2.3 +/- 0.3 micrograms/dl) during CNB. There was no significant change in the baseline levels of any of these hormones during PC infusion of 0.9% saline. To control for the possibility that procaine leaked into the systemic circulation, identical amounts of procaine were infused intravenously. Systemic administration of procaine caused a rise in MAP but had no effect on HR and did not alter plasma levels of AVP, PRA, NE, or cortisol. The relationship between plasma osmolality and plasma AVP, as well as the drinking response to a 60-min infusion of hypertonic NaCl, was unaltered by CNB. We conclude that PC procaine infusion is an effective technique for producing acute, reversible blockade of the cardiac nerves in the conscious dog.

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