Blood–cerebrospinal fluid barrier to arginine-vasopressin, desmopressin and desglycinamide arginine-vasopressin in the dog

Ang, V. T. Y.; Jenkins, Janis H.

doi:10.1677/joe.0.0930319

Cited by 88 publications

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“…For vasopressin, it is difficult to decide whether some of the drug in the CSF originated from direct transport from nose-to-brain or all the drug reached the CSF via transport across the blood±brain barrier. It has been shown in dogs that arginine±vasopressin was transported across the blood±brain barrier from the blood to the CSF after intravenous injection (Ang & Jenkins 1982). Support for (at least some) drug reaching the CSF via the olfactory region is found in the studies by Pietrowsky et al (1996aPietrowsky et al ( , b, 2001, showing event related effects on the brain potential after nasal but not after intravenous administration of the drug.…”

Section: Direct Evidence Of Nose-to-brain Transport As Arguedmentioning

confidence: 96%

Is nose-to-brain transport of drugs in man a reality?

Illum¹

2004

Journal of Pharmacy and Pharmacology

399

262

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The blood-brain barrier that segregates the brain interstitial fluid from the circulating blood provides an efficient barrier for the diffusion of most, especially polar, drugs from the blood to receptors in the central nervous system (CNS). Hence limitations are evident in the treatment of CNS diseases, such as Parkinson's and Alzheimer's diseases, especially exploiting neuropeptides and similar polar and large molecular weight drugs. In recent years interest has been expressed in the use of the nasal route for delivery of drugs to the brain, exploiting the olfactory pathway. A wealth of studies has reported proof of nose-to-brain delivery of a range of different drugs in animal models, such as the rat. Studies in man have mostly compared the pharmacological effects (e.g. brain functions) of nasally applied drugs with parenterally applied drugs and have shown a distinct indication of direct nose-to-brain transport. Recent studies in volunteers involving cerebrospinal fluid sampling, blood sampling and pharmacokinetic analysis after nasal, and in some instances parenteral administration of different drugs, have in my opinion confirmed the likely existence of a direct pathway from nose to brain.

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Section: Direct Evidence Of Nose-to-brain Transport As Arguedmentioning

confidence: 96%

Is nose-to-brain transport of drugs in man a reality?

Illum¹

2004

Journal of Pharmacy and Pharmacology

399

262

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“…Recent neuroanatomic studies, however, indicate that AVP is also present in parvocellular neurons of the hypo thalamus, particularly in cells of the suprachiasmatic nu cleus, and projections from both magnocellular and parvo cellular AVP-containing neurons pass to a variety of central sites other than the neurohypophysis [6,45]. AVP has been detected in cerebrospinal fluid (CSF) by both bioassay and radioimmunoassay (RIA) [13,17,39], and since AVP does not normally appear to cross the blood-brain barrier [2,42], it seems that AVP present in CSF may be derived from nonneurohypophysial AVP tract terminals.…”

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confidence: 99%

Vasopressin in Plasma and Cerebrospinal Fluid of Hydrated and Dehydrated Steers

Doris¹,

Bell²

1984

Neuroendocrinology

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Levels of arginine-vasopressin (AVP), the antidiuretic hormone, have been concurrently measured by radioimmunoassay (RIA) in plasma (p) and cerebrospinal fluid (CSF) from conscious, unrestrained steers. During 4 days of dehydration, plasma osmolarity (posm) rose progressively from control hydrated levels of 301.3 ± 0.632 mosm/1 (mean ± SE) to 338.5 ± 3.00 mosm/1 (p < 0.001). Packed cell volume also rose from 39.9 ± 0.64% to 44.7 ± 1.24% (p < 0.001). Associated with these changes was a progressive increase in pAVP from control levels of 1.3 ± 0.19 µU/ml to 16.9 ± 1.88 µU/ml (p < 0.001) after 4 days without water. Log pAVP was linearly related to posm (r = 0.82, p < 0.001). Mean level of CSF-AVP in control animals was 5.4 ± 0.97 µU/ml. During dehydration, CSF-AVP levels also rose, becoming significantly greater than control levels (p < 0.01) after 3 days without water and further increasing to reach 15.2 ± 1.83 µU/ml after 4 days without water (p < 0.001). Log CSF-AVP could also be linearly related to posm (r = 0.62, p < 0.01). Termination of dehydration by restoration of ad libitum water supply was accompanied by return of pAVP and CS F-AVP to predehydration levels. Regression analysis of concurrent levels of pAVP and CSF-AVP indicates that CSF-AVP levels are linearly correlated to pAVP levels in hydrated and dehydrated animals (r = 0.70, p < 0.001). These experiments suggest that neurosecretory neurons secreting AVP at sites accessible to CSF respond to similar stimuli during dehydration as those neurons secreting AVP into blood.

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“…It is unlikely that the effects of AVP within the NTS can be acounted for by diffusion of drug into the peripheral circulation, since most evidence suggests that the blood-brain barrier limits the access of physiologically significant amounts of AVP in the cerebrospinal fluid to the blood (Vorherr et al, 1968;Ang & Jenkins, 1982;Ermisch et al, 1985). We have also shown previously that systemic administration of AVP produced different responses from those due to central injections of AVP (King et al, 1985).…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular effects of injections of vasopressin into the nucleus tractus solitarius in conscious rats

King

Pang

1987

British J Pharmacology

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1The effects of injections of arginine vasopressin (AVP) into the nucleus tractus solitarius (NTS) on mean arterial pressure (MAP), heart rate (HR) and plasma concentrations of noradrenaline and adrenaline were investigated in conscious, unrestrained rats. 2 Injection of 2 ng AVP into the NTS significantly increased MAP but not plasma catecholamine concentrations, while injection of 10 ng AVP significantly increased MAP and plasma noradrenaline and adrenaline levels. 3 Neither dose of AVP produced any change in HR. The vehicle did not affect MAP, HR or plasma catecholamine levels. 4 Injection of a specific pressor antagonist of AVP, d(CH2)5Tyr-(Me)AVP (10 ng), did not change MAP, HR or plasma noradrenaline or adrenaline levels. 5 These results suggest that the NTS is a central site of the pressor action of AVP. However, since the injection of the AVP antagonist did not reduce MAP or plasma noradrenaline or adrenaline levels, it suggests that AVP does not act tonically at the NTS to influence sympathoadrenal outflow.

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Blood–cerebrospinal fluid barrier to arginine-vasopressin, desmopressin and desglycinamide arginine-vasopressin in the dog

Cited by 88 publications

References 0 publications

Is nose-to-brain transport of drugs in man a reality?

Is nose-to-brain transport of drugs in man a reality?

Vasopressin in Plasma and Cerebrospinal Fluid of Hydrated and Dehydrated Steers

Cardiovascular effects of injections of vasopressin into the nucleus tractus solitarius in conscious rats

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