Neurohypophysial hormones

Bisset, G. W.

doi:10.1007/978-1-349-02718-7_9

Cited by 13 publications

(7 citation statements)

References 203 publications

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“…Much less is known about the reflex which controls the release of vasopressin in response to changes in blood volume and distribution (for reviews see Bisset, 1975;Bisset & Jones, 1975). The afferent pathway of this reflex consists of fibres arising from baroand stretch receptors which enter the brain stem in the sinus and vagus nerves.…”

Section: Discussionmentioning

confidence: 99%

“…The afferent pathway of the milk-ejection reflex from the mammary glands to the oxytocin releasing cells of the paraventricular nuclei has been worked out in detail and defined almost in its entirety (Cowie & Tindal, 1971). Much less is known about the reflex which controls the release of vasopressin in response to changes in blood volume and distribution (for reviews see Bisset, 1975;Bisset & Jones, 1975). The afferent pathway of this reflex consists of fibres arising from baroand stretch receptors which enter the brain stem in the sinus and vagus nerves.…”

Section: Discussionmentioning

confidence: 99%

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Vasopressin Release by Nicotine: The Site of Action

Bisset

Feldberg

Guertzenstein

et al. 1975

British J Pharmacology

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In cats anaesthetized with chloralose the release of neurohypophysial hormones was examined after injection of nicotine into the cerebral ventricles or cisterna magna or its topical application through perspex rings to the ventral surface of the brain stem. The release was measured by assaying the hormones in samples of venous blood Injected into a lateral or the third cerebral ventricle, nicotine (0.5 to 1 mg) produced release of vasopressin without oxytocin. When the aqueduct was cannulated, preventing access to the fourth ventricle and to the subarachnoid space, this release did not occur. Vasopressin was also released without oxytocin when nicotine (0.25 to 2 mg) was injected into the subarachnoid space through the cisterna magna. With this route of administration the nicotine did not enter any part of the ventricular system. Applied through paired perspex rings placed across the ventral surface of the brain stem, nicotine again produced release of vasopressin without oxytocin. The amount of nicotine placed in each ring was usually 80 μg, but a release was obtained with 10 μg and in one experiment with as little as 5 μg. The bilateral region on the ventral surface of the brain stem where nicotine acts when producing release of vasopressin lies lateral to the pyramids and in a longitudinal direction, 6 to 9 mm caudal to the trapezoid bodies. The vasopressin release by nicotine injected intraventricularly or intracisternally, or applied topically to the ventral surface of the brain stem was not due to absorption of nicotine into the blood stream, nor to blood pressure effects. It is concluded that nicotine acts on the ventral surface of the brain stem probably by activating the central projection to the supra‐optic and possibly also the paraventricular nuclei of afferent pathways in the sinus and vagus nerves which control the release of vasopressin in response to changes in blood volume or distribution.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Vasopressin Release by Nicotine: The Site of Action

Bisset

Feldberg

Guertzenstein

et al. 1975

British J Pharmacology

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“…The changes in blood volume which control the release of vasopressin are monitored by cardiovascular receptors in both the low-pressure and high-pressure systems (for reviews see Share & Claybaugh, 1972;Share, 1974Share, , 1976Bisset & Jones, 1975;Bisset, 1976). The low-pressure system comprises 80-85 % of the blood volume and consists of the capacitance vessels of the systemic circulation, the right heart and the pulmonary circuit and the left heart in diastole: the intrathoracic blood volume is equivalent to 60 % of the total volume (Henry, Gauer & Sieker, 1956;Gauer & Henry, 1963).…”

Section: Afferent Pathways For Volume Controlmentioning

confidence: 99%

Control of Release of Vasopressin by Neuroendocrine Reflexes

1988

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“…Vasopressin (VP) and oxytocin (OT), nonapeptides synthesized in the magnocellular neurons of the hypothalamus, are secreted via axons in the neurohypophysis and regulate water conservation, cardiovascular functions, and smooth muscle contractions (1). Both peptides are synthesized as precursors in covalent linkages with neurophysin peptides, termed preproVP-neurophysin and preproOT-neurophysin (2)(3)(4).…”

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confidence: 99%

Vasopressin gene is expressed at low levels in the hypothalamus of the Brattleboro rat.

Majzoub¹,

Pappey²,

Burg³

et al. 1984

Proc. Natl. Acad. Sci. U.S.A.

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The Brattleboro rat carries as a recessive trait the inability to synthesize hypothalamic vasopressin and its related neurophysin but is able to synthesize oxytocin and its neurophysin. Brattleboro rats homozygous for this trait have no immunologically detectable circulating vasopressin and manifest a complete syndrome of diabetes insipidus, which is corrected with vasopressin replacement therapy. Such a defect could be due to absence of the gene encoding vasopressin, the presence of an abnormal gene, or a variety of transcriptional or posttranscriptional abnormalities. We report here that the hypothalamus of the Brattleboro rat contains detectable, although markedly reduced, levels of an mRNA indistinguishable in size with and similar in sequence to authentic vasopressin mRNA. Corresponding levels of oxytocin mRNA were the same in Brattleboro and normal rat hypothalami. These findings indicate that the Brattleboro rat expresses a vasopressin gene, but at a reduced level.Vasopressin (VP) and oxytocin (OT), nonapeptides synthesized in the magnocellular neurons of the hypothalamus, are secreted via axons in the neurohypophysis and regulate water conservation, cardiovascular functions, and smooth muscle contractions (1). Both peptides are synthesized as precursors in covalent linkages with neurophysin peptides, termed preproVP-neurophysin and preproOT-neurophysin (2-4). The Brattleboro rat carries as a semirecessive trait the inability to synthesize VP or its related neurophysin but is able to synthesize OT and its neurophysin (5). Brattleboro rats homozygous for this trait have severe diabetes insipidus, which is completely corrected by VP replacement therapy. Although the Brattleboro rat has been used extensively in the study of VP deficiency, nothing is known regarding the nature of its genetic defect. Therefore, we examined this issue using molecular biological techniques. Such studies might shed some light on the nature of the analogous genetic defect in hereditary human VP deficiency. Our findings indicate that the Brattleboro rat does possess the gene for VP and expresses this gene, although at a markedly reduced level. MATERIALS AND METHODSPreparation and 5'-End Labeling of Synthetic Oligonucleotides. Oligonucleotides were synthesized by the triester method and were purified by reversed-phase high-pressure liquid chromatography on C18 resin (Waters Associates) (6).For use in subsequent studies, the oligonucleotides were 5'-end-labeled using [y32P]ATP (Amersham) and T4 polynucleotide kinase (Bethesda Research Laboratories) to a final specific activity of 4-6 x 106 cpm/pmol (7). Nucleotide sequences of the oligonucleotides were confirmed using the chemical degradation method (8).Preparation of Hypothalamic mRNA. Adult female (180-200 gm) homozygous Brattleboro rats were deprived of water for 24 hr prior to decapitation. They were confirmed to be homozygous for the Brattleboro trait by two criteria: (i) they all lost >20% of their body weight after 24 hr of water deprivation, compared with <5% loss in ...

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Neurohypophysial hormones

Cited by 13 publications

References 203 publications

Vasopressin Release by Nicotine: The Site of Action

Vasopressin Release by Nicotine: The Site of Action

Control of Release of Vasopressin by Neuroendocrine Reflexes

Vasopressin gene is expressed at low levels in the hypothalamus of the Brattleboro rat.

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