Plasma vasopressin response to peripheral administration of angiotensin in conscious rats

European Journal of Endocrinology

Hama²,

Watanabe

1998

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.

Section: Measurements and Statistical Analysesmentioning

confidence: 99%

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

European Journal of Endocrinology

Hama²,

Watanabe

1998

“…Values are means ± sem for number of rats shown in parentheses. The ip injection (2 ml/100 g) of isotonic (IT; 150 mmol/1) or hypertonic (HT; 600 mmol/1) saline was given 10 min after the icv injection ( Our earlier study in conscious rats indicates that after ip injection of 600 mmol/1 NaCl, plasma AVP increases significantly at 15 and 30 min, and re¬ turns to an approximate control level at 60 min (24). Therefore, we examined in this investigation the effects of the dopamine antagonists on plasma AVP levels 15 and 30 min after the ip treatments.…”

Section: Discussionmentioning

confidence: 99%

“…The length of the inner cannula was 0.5-1.0 mm longer than the implanted one. The doses of the drugs, and the time intervals between the second icv or ip injection and blood sampling were determined on the basis of previous studies (14,22,24 30). The values given for plasma AVP were corrected using the average recovery of 55.8%.…”

Section: Animals and Experimentsmentioning

confidence: 99%

Participation of periventricular dopamine receptors in vasopressin secretion elicited by hypertonicity of systemic blood in rats

Hama²

1991

Acta Endocrinologica

The aim of this study was to examine in conscious rats the role of periventricular dopamine receptors in vasopressin secretion caused by hypertonicity of the systemic blood. Intracerebroventricular injections of dopamine (0.15 or 0.75 \g=m\mol)produced dose-related increases in plasma AVP 90 sec or 5 min later, without affecting plasma osmolality, concentrations of electrolytes, hematocrit, arterial pressure or heart rate. The AVP response to 0.75 \g=m\moldopamine was blocked by its antagonists, SCH 23390, sulpiride and haloperidol, given intracerebroventricularly at a dose of 0.15 \g=m\mol 10 or 40 min before the injection of dopamine. The ip injections (2 ml/100 g) of 600 mmol/l NaCl produced, 15 or 30 min later, augmentations in plasma AVP accompanied by elevations in plasma osmolality, sodium and chloride. At a dose of 0.15 \g=m\molgiven intracerebroventricularly 10 min before the injection of 600 mmol/l NaCl, SCH 23390 or sulpiride inhibited the AVP response at 15 min, and sulpiride or haloperidol inhibited that at 30 min. The increases in plasma osmolality and the electrolytes owing to hypertonic saline were not reduced by these dopamine antagonists. The intracerebroventricular applications of the antagonists followed by those of vehicles for dopamine or by ip injections of 150 mmol/l NaCl were without any effect on plasma AVP or the other plasma variables. On the basis of these results, we concluded that dopamine receptors in the periventricular regions may contribute to AVP secretion in response to hypertonicity of the systemic blood.Dopamine neurons project to both the cell bodies of the hypothalamic vasopressin (AVP) neurons and the posterior pituitary containing their termi¬ nals (1,2). Dopa accumulation or dopamine con¬ centration in the neurohypophysis increased ac¬ companied by an elevation in plasma osmolality, which is a representative stimulus for accelerating AVP secretion (3-5). However, the role of the brain dopaminergic system in regulating AVP release re¬ mains unclear: central applications of dopamine have been reported to stimulate, inhibit or to have no effect on AVP release (6,7). We have recently observed in rats that intracerebroventricular (icv) injections of a dopamine antagonist, haloperidol, inhibit increases in plasma AVP caused by dopa¬ mine and a hypertonic solution given icv (8), sug¬ gesting that dopamine receptors in the periventri¬ cular regions may participate in AVP release in re¬ sponse to a rise in cerebrospinal fluid (CSF) osmo¬ lality. Action sites of an icv administered hypertonic solution may include the regions encompassing the anteroventral third ventricle (AV3V) (9,10) which may function to respond to hypertonicity of the circulating blood (11,12). Therefore, it is possible that periventricular dopamine receptors, which may be involved in AVP release stimulated by hy¬ pertonicity of CSF, may contribute to the release facilitated by hypertonicity of systemic blood. How¬ ever, this view is not beyond doubt. Although icv injections of dopamine antagonists blocked ...

“…The assay procedures have been described in detail elsewhere (20). Briefly, the AVP antiserum raised in the rabbit showed negligible cross-reaction with oxytocin (less than 5.9xl0~6%), lysine vasopressin (3.2xl0_1%), arginine vasotocin (8.9xlO~3%) or deamino-D-AVP (2.6 x 10~2%).…”

Section: Methodsmentioning

confidence: 99%

Effect of dopamine injection into the anteroventral third ventricular region and the paraventricular nucleus on vasopressin secretion in conscious rats

Hama²,

Watanabe³

et al. 1992

Acta Endocrinologica

Effect of dopamine injection into the anteroventral nucleus on vasopressin secretion in conscious rats. 598To investigate the role of dopamine receptors situated in the paraventricular nucleus and the anteroventral third ventricular region in regulating vasopressin release, responses of plasma AVP and its controlling factors to injections of dopamine into these regions and the lateral cerebral ventricle were examined in conscious rats. The injections of 156 nmol (30 \g=m\g)dopamine into the cerebral ventricle produced transient rises in plasma AVP 5 min later. When the dose of dopamine was reduced to 26 nmol (5 \g=m\g), the increase in plasma AVP was not provoked any more. However, injections of 26 nmol dopamine into the paraventricular nucleus greatly augmented plasma AVP 5 and 15 min later. This dose of dopamine was without effect on plasma AVP when injected into the anteroventral third ventricular region, including the organum vasculosum lamina terminalis, median preoptic nucleus, medial preoptic area and the periventricular preoptic nucleus. These dopamine administrations in the cerebral ventricle, paraventricular nucleus and the anteroventral third ventricular region did not significantly change AVP-controlling factors such as plasma osmolality, sodium and arterial pressure. On the basis of these results, we conclude that dopamine receptors in the paraventricular nucleus may function to facilitate AVP secretion, whereas those in the anteroventral third ventricular region may not play an important role in the regulation of AVP release. Dopamine stimulates vasopressin (AVP) secretion when applied to the incubation medium of the isolated rat hypothalamic tissue (1), and enhances plasma AVP concentration when given intracerebroventricularly (icv) in conscious rats (2-6). However, location in the brain of dopamine receptors contributing to facilitation of AVP release remains uncertain. It is possible to presume two periventricular regions as the candidate for the locus. One is the region surrounding the anteroven¬ tral third ventricle (AV3 V) which is known as a primary reception site for angiotensin II and an osmotic stimulus (7-9). The conceivable role of dopamine receptors in this area can be speculated from the observations that the AV3V region contains dopaminergic fibers and dopa¬ mine sensitive neurons (10, 11) which may be involved in the regulation of water balance, and that the inhibitory effects of electrical or chemical destruction of the AV3 V region on the angiotensin II-and the hyperosmolality-induced AVP release (12-16) could be mimicked by the icv administration of the antagonists (3-6) which may block dopamine receptors in the AV3V region. The other possible region is the paraventricular nucleus (PVN) where the AVP neurosecretory cells exist.Since the PVN is also located close to the ventricular system, the drugs given icv may be able to act on this nucleus. Therefore, if neural information arising from the reception sites for angiotensin II and the osmotic stimulus is transmitted to the PVN AVP...