Central noradrenergic neurons and the hypertensive effects of intracerebroventricularly administered prostaglandin E2 in anaesthetized rabbits

Otorii, Takeshi; Ohkubo, Kei; Suzuki, Kenichi

doi:10.1016/0090-6980(85)90148-0

Cited by 8 publications

(3 citation statements)

References 16 publications

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“…These results are consistent with those reported previously (Morimoto et al 1992). Because the pressor response following the i.c.v, administration of PGE 2, the treatment which may permit PGE 2 to affect the AV3V (Phillips and Hoffman 1977), was attenuated by phenoxybenzamine, phentolamine, or 6-hydroxydopamine (Hoffman and Schmid 1979;Otorii et al 1985), it seems likely that PGE 2 injected into the AV3V may have exert the cardiovascular effects via activation of the sympathetic nervous system. Therefore, the changes in those variables by PGE 2 may be attributable to its actions on the AV3V neural mechanism subserving the cardiovascular homeostasis.…”

Section: Discussionmentioning

confidence: 99%

Possible roles of prostaglandins in the anteroventral third ventricular region in the hyperosmolality-evoked vasopressin secretion of conscious rats

Yamaguchi

Hama²,

Watanabe

1997

Exp Brain Res

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This study explored the roles of prostaglandins in the anteroventral third ventricular region, a cerebral osmoreceptor site, in the osmoregulation mechanism of vasopressin release. We injected (1 microliter) prostaglandin E2 (12.8 nmol) or meclofenamate (78.3 nmol), an inhibitor of prostaglandin biosynthesis, into the brain region or the lateral cerebral ventricle of conscious rats, examining their effects on plasma vasopressin and its controlling factors in the presence or absence of an osmotic stimulus. The injection of prostaglandin E2 into the anteroventral third ventricular region augmented plasma vasopressin and arterial pressure after 5 min and 15 min, without influencing plasma osmolality, sodium, potassium, or chloride. In contrast, intraventricular injection of prostaglandin E2 did not cause any significant effect on those variables. The i.v. infusion (0.1 ml.kg-1.min-1) of hypertonic saline (2.5 mol/l) enhanced plasma vasopressin after 15 min and 30 min; this was accompanied by increased plasma osmolality, sodium, and chloride, and by unaltered or elevated arterial pressure. Meclofenamate given into the anteroventral third ventricular region 30 min before starting the hypertonic saline infusion abolished the osmotic vasopressin response without significantly changing the responses of the other variables. Histological analysis showed that the injection sites of meclofenamate in these rats were close to those of prostaglandin E2 in the anteroventral third ventricular region and included the organum vasculosum of the lamina terminalis and the surrounding area, the medial preoptic area, and periventricular and median preoptic nuclei. When injection cannulae for meclofenamate deviated from those areas incidentally or when the drug was expressly administered into the cerebral ventricle, the osmotic vasopressin response was not inhibited. Plasma vasopressin and the other variables observed during the i.v. infusion of isotonic saline (0.15 mol/l) were not affected significantly by meclofenamate administration into the anteroventral third ventricular region or the cerebral ventricle. On the basis of these results, we concluded that prostaglandins synthesized in and/or near the anteroventral third ventricular region might contribute to the facilitation of vasopressin release in the hyperosmotic state.

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Section: Discussionmentioning

confidence: 99%

Possible roles of prostaglandins in the anteroventral third ventricular region in the hyperosmolality-evoked vasopressin secretion of conscious rats

Yamaguchi

Hama²,

Watanabe

1997

Exp Brain Res

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“…Because the pressor and tachycardiac responses following the i.c.v. administration of PGE 2 were diminished, respectively, by a-and b-adrenergic blockers (42,43), it seems likely that PGE 2 administered into the AV3V may have produced the cardiovascular actions by stimulating the sympathetic nervous system. Hemorrhage activates the sympathetic nervous system (44), and AV3V infusion of meclofenamate intensified the depressor and bradycardic responses to the hemorrhage (Fig.…”

Section: Figure 4 Effects Of Meclofenamate (Mcl) Infusion Into the Acmentioning

confidence: 99%

Possible participation of prostaglandins generated in the anteroventral third ventricular region in the hypovolemia-induced vasopressin secretion of conscious rats

Yamaguchi

Hama²,

Watanabe

1998

European Journal of Endocrinology

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Objective: The aim of this study was to investigate the roles of prostaglandins (PGs) in the anteroventral third ventricular region (AV3V), a cerebral site for cardiovascular homeostasis, in hypovolemiainduced vasopressin (AVP) secretion. Methods: We infused meclofenamate (78.3 nmol in 1 ml), a PG synthesis inhibitor, or PGE 2 (7.1 nmol in 0.5 ml) into the AV3V of conscious rats, examining their effects on plasma AVP and other variables in the presence or absence of hemorrhages. The hemorrhages (about 14% of blood volume) were conducted successively by taking femoral arterial blood over a 30-s period at 10-min intervals.Results: The first hemorrhage increased plasma AVP in blood samples obtained 10 min later, without affecting plasma angiotensin II (ANG II), arterial pressure and heart rate. The second hemorrhage after 10 min raised plasma AVP further and, remarkably, augmented plasma ANG II, and reduced arterial pressure. The AVP responses to both the first and second hemorrhages were attenuated by meclofenamate infusion into the AV3V performed 35 min before the first hemorrhage. The meclofenamate infusion did not alter the response of ANG II, while that of arterial pressure was potentiated and heart rate was decreased after the second hemorrhage. These effects of meclofenamate on plasma AVP and the cardiovascular parameters were not found when the drug was infused into the nucleus accumbens, the region slightly distant from the AV3V, or the lateral cerebral ventricle. In the normovolemic state, meclofenamate administered into the three brain regions did not affect any of the variables monitored. In contrast, application of PGE 2 into the AV3V enhanced plasma AVP, heart rate and arterial pressure after 5 and 15 min. Histological examination indicated that infusion sites of meclofenamate in the AV3V were close to those of PGE 2 in several cases and included areas such as the organum vasculosum of the lamina terminalis, periventricular hypothalamic nucleus, and the median and medial preoptic nuclei. Conclusion: These results suggest that PGs synthesized in and/or near the AV3V may be involved in the regulation of AVP release and cardiovascular function in the hypovolemic state.

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“…Although the present study has examined the effect of CA levels on PG synthesis, previous studies have provided evidence that PGs inhibit NE release from central and peripheral nerve endings (Hedqvist, 1976;Otorii et al, 1985). Thus, the data of the present study showing that the central CA system facilitates basal PG synthesis may lead one to speculate on the existence of a feedback mechanism between the central CA and PG systems.…”

Section: Discussionmentioning

confidence: 55%

Role of the Central Adrenergic System in the Regulation of Prostaglandin Biosynthesis in Rat Brain

Weidenfeld

Kahbha

Reches

et al. 1992

Journal of Neurochemistry

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The role of endogenous catecholamines in the regulation of brain prostaglandin (PG) synthesis was studied in the rat. Male rats were injected in the brain lateral ventricle or in the ventral noradrenergic bundle with either the catecholaminergic neurotoxin 6-hydroxydopamine or vehicle. Other groups of rats were injected intraperitoneally with the tyrosine hydroxylase inhibitor, alpha-methyl-p-tyrosine, or with the inhibitor of dopamine-beta-hydroxylase, FLA-63. All these drugs produced a significant depletion of norepinephrine (NE) content in the cortex and hypothalamus. The rats that had lower levels of NE exhibited reduced capacity to synthesize PGE2 but not thromboxane B2 and 6-keto-PGE1 alpha in the cortex and hypothalamus. However, induced production of PG, stimulated by the bacterial endotoxin lipopolysaccharide (LPS), remained unchanged, namely, a similar (2- to 2.5-fold) increase of PG synthesis was noted in control and in NE-depleted rats. We suggest that the regulation of PG synthesis under basal condition requires intact adrenergic input, whereas LPS-induced production of PG is independent of the adrenergic innervation.

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Central noradrenergic neurons and the hypertensive effects of intracerebroventricularly administered prostaglandin E2 in anaesthetized rabbits

Cited by 8 publications

References 16 publications

Possible roles of prostaglandins in the anteroventral third ventricular region in the hyperosmolality-evoked vasopressin secretion of conscious rats

Possible roles of prostaglandins in the anteroventral third ventricular region in the hyperosmolality-evoked vasopressin secretion of conscious rats

Possible participation of prostaglandins generated in the anteroventral third ventricular region in the hypovolemia-induced vasopressin secretion of conscious rats

Role of the Central Adrenergic System in the Regulation of Prostaglandin Biosynthesis in Rat Brain

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