Aspects of Cerebrospinal Fluid Pressure Control in Conscious Rats During Central Infusions of Angiotensin and Vasopressin

Severs, Walter B.; Spaeth, H. J.; Wurpel, John N.D.; Dundore, Ronald L.; Henry, R. T.; Keil, L. C.

doi:10.1007/978-1-4757-0366-5_21

Cited by 3 publications

(3 citation statements)

References 11 publications

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“…Venous con striction at the right atrium did not elevate CSF-p relative to the sham-operated animals (p > 0.05) and the CSF-p of individual ani mals did not change over the interval mea sured (p > 0.05). The CSF-p of all rats were within the normal limits for conscious rats tested under similar conditions [15]. The times evaluated encompass the immediate stimulus period (postoperative), a time when thoracic volume overload causes diuresis/natriuresis (1 day) and a time when equilib rium could be anticipated [3] (10 days).…”

Section: Resultsmentioning

confidence: 99%

“…These times were selected to detect any slowly developing changes in CSF-p after surgery. The 25-gauge guide probe described above was connected to the rat in its home cage for 15 min of recording according to the method described pre viously [14,15]. The transducer was calibrated with a water manometer, and the dome was 2 cm above the cage floor ( approximate height of the rat head during sleep).…”

Section: Methodsmentioning

confidence: 99%

“…It is of interest to consider that soma tostatin [12] and vasopressin [13] concentra tions in CSF are elevated when CSF-p is high. Also, cerebroventricular infusions of vasopressin blunt the rise in CSF-p induced by cerebroventricular angiotensin infusions [14,15].…”

Section: Introductionmentioning

confidence: 99%

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Cerebrospinal Fluid Pressure of Conscious Rats after Venous Constriction at the Right Atrium

Severs

Hartman²,

Morrow³

et al. 1991

Pharmacology

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Thoracic shifts of blood stimulate diuresis and natriuresis during spaceflight. The available literature is not conclusive as to whether thoracic afferent neurons are essential for this response. Possibly, an acute elevation in cerebrospinal fluid pressure (CSF-p) activates central compensatory mechanisms. This is because central venous pressure is elevated by thoracic blood shifts and may reduce the pressure gradient for drainage of CSF into the venous sinuses. We tested whether rats with constriction of the venous return at the level of the heart (0.4 mm maximum diameter) had CSF-p different from sham-operated controls. CSF-p in the immediate postoperative period, as well as 1 and 10 days after surgery, were within normal limits and did not differ (p > 0.05). Blood collected at the end of the experiment showed no group differences (p > 0.05) in the hematocrit, or concentrations of sodium, potassium or vasopressin. Thus, changes in CSF-p, per se, appear to be insufficient to explain the cardiovascular or salt/water balance readjustments observed in spaceflight. It is likely that compensatory systems are highly redundant.

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Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Cerebrospinal Fluid Pressure of Conscious Rats after Venous Constriction at the Right Atrium

Severs

Hartman²,

Morrow³

et al. 1991

Pharmacology

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Mechanism of delayed intracranial hypertension after cerebroventricular infusions in conscious rats

Morrow¹,

Holt²,

Starčević³

et al. 1992

Brain Research

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Interaction of changes in the third ventricular CSF tonicity, central and systemic AVP concentrations and water intake

Eriksson¹,

Simon-Oppermann²,

Simón³

et al. 1987

Acta Physiologica Scandinavica

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Arginine vasopressin (AVP) is assumed to be involved as a central transmitter or modulator in the control of autonomic functions including thirst. In conscious dogs AVP concentration in cerebrospinal fluid (CSF) from the anterior part of the third ventricle (A3V) was analysed before and after local elevation of CSF osmolality by intracerebroventricular (i.c.v.) infusion of 0.35 M NaCl and after i.c.v. AVP infusion at 46 and 138 fmol ml-1 for 10 min. In addition, the effects of these i.c.v. infusions on water intake, plasma AVP concentration and blood pressure were investigated. In euhydrated dogs 0.35 M NaCl i.c.v. did not alter AVP concentration in the CSF during the subsequent 2 h. In contrast, plasma AVP concentration had increased significantly from 3.4 +/- 0.3 (control) to 6.4 +/- 0.7 and 4.7 +/- 0.3 fmol ml-1, 4 and 16 min, respectively, after the hypertonic stimulus. Drinking was stimulated with an average water intake of 14.5 +/- 3.7 ml kg-1 body wt. However, AVP infusion into the A3V did not elicit water intake despite increases of AVP concentration in the A3V by factors up to 40 above control. The same animals responded with spontaneous drinking to 0.35 M NaCl i.c.v. administered 160 min after the end of AVP infusions. Exogenously administered AVP disappeared from the A3V with a time constant of 13.8 min. The results do not support the view that AVP in the A3V CSF per se stimulates drinking.

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Aspects of Cerebrospinal Fluid Pressure Control in Conscious Rats During Central Infusions of Angiotensin and Vasopressin

Cited by 3 publications

References 11 publications

Cerebrospinal Fluid Pressure of Conscious Rats after Venous Constriction at the Right Atrium

Cerebrospinal Fluid Pressure of Conscious Rats after Venous Constriction at the Right Atrium

Mechanism of delayed intracranial hypertension after cerebroventricular infusions in conscious rats

Interaction of changes in the third ventricular CSF tonicity, central and systemic AVP concentrations and water intake

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