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Endocrinology Vol. 139, No. 4 1481-1486
Copyright © 1998 by The Endocrine Society

ARTICLES

Regulation of Vasopressin Synthesis and Release by Area Postrema in Rats1

Hiroshi Arima, Kunikazu Kondo, Takashi Murase, Hisashi Yokoi, Yasumasa Iwasaki, Hidehiko Saito and Yutaka Oiso

First Department of Internal Medicine, Nagoya University School of Medicine, Nagoya 466, Japan

Address all correspondence and requests for reprints to: Dr. Hiroshi Arima, First Department of Internal Medicine, Nagoya University School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466, Japan. E-mail: harima-ngy{at}umin.u-tokyo.ac.jp


   Abstract
Top
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
There is evidence indicating that the area postrema (AP), the most caudal circumventricular organ located on the dorsal surface of the medulla, is involved in several physiological regulations. In this study, we investigated the role of AP in the regulation of arginine vasopressin (AVP) synthesis and release, using rats of which the AP was lesioned 6 weeks previously. The level of plasma AVP in the AP lesioned (APX) group was significantly lower than in the sham operated (Sham) group in the basal state. AVP release induced by either hyperosmolality or hypovolemia was significantly attenuated by APX. To clarify the role of AP in AVP synthesis in the hypothalamus, we examined the AVP gene expression using in situ hybridization. AVP messenger RNA levels in paraventricular (PVN) and supraoptic nuclei (SON) in the APX group were significantly lower than in the Sham group in the basal state. Moreover, the AVP messenger RNA levels in PVN and SON in the APX group were also significantly lower than in the Sham group after water deprivation for 3 days. These results suggest that AVP synthesis and release are tonically stimulated by AP in the basal state and that AVP synthesis and release in stimulated states are also regulated, at least partially, by AP.


   Introduction
Top
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
ARGININE vasopressin (AVP), the antidiuretic hormone, is synthesized within the neurons of paraventricular (PVN) and supraoptic nuclei (SON) in the hypothalamus and released into the systemic circulation from the nerve ending in the neurohypophysis (1, 2). The level of plasma AVP is regulated physiologically by changes in plasma osmolality and in blood volume or pressure (1, 2, 3). The osmoregulation is so precise that only 1% increase in plasma osmolality could stimulate AVP release (2), and the role of the anterior third ventricular regions (AV3V), which include the organum vasculosum of the lamina terminalis, nucleus medianus and median preoptic nucleus, has been extensively investigated in the osmoregulation (4, 5, 6). On the other hand, it is generally accepted that the low pressure receptor in the atrium tonically inhibits the AVP release via a pathway involving the nucleus tractus solitarius (NTS), and AVP release induced by hypovolemia occurs through the reduction in inhibitory input activity (1, 2, 3). Although there are abundant evidences to support the role of the AV3V and the low pressure receptor in the regulation of AVP release, the afferent pathways controlling AVP release appear to be more complex, and it has been suggested that other mechanisms might also be involved in the regulation (1, 7, 8).

The area postrema (AP) is one of circumventricular organs (CVOs) located adjacent to the NTS on the dorsal surface of the medulla in rats. The AP has an extremely rich capillary plexus that lacks a blood brain barrier (9). High densities of receptors for various intrinsic substances such as angiotensin II are reported to be within the AP (10, 11), and these substances activate AP neurons (12, 13). It is also shown that AP projects to various brain regions (14), and thus AP has been postulated to be a "window" through which circulating peripheral substances may influence the central nervous system. Previous studies have revealed that AP lesion (APX) attenuates stress-induced ACTH and corticosterone secretion in rats (15, 16), suggesting the possibility that AP might be involved in the neuroendocrine regulatory system. Along with other CVOs such as the organum vasculosum of the lamina terminalis and the subfornical organ (4), AP has been indicated to play some role in the water and sodium balance (17). Although APX is reported to cause polyuria in rats (18, 19), the role of AP in the hypothalamo-neurohypophyseal system is still uncertain.

In this study, we examined the effects of APX on basal plasma AVP level and on AVP release induced by either hyperosmolality or hypovolemia in unanesthetized rats to see whether AP is involved in the regulation of AVP release. We also examined AVP gene expression in the hypothalamus using in situ hybridization, to clarify the role of AP in AVP synthesis as well.


   Materials and Methods
Top
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
Animals and maintenance conditions
Male Sprague-Dawley rats (250–300 g) were housed individually in cages under controlled conditions (23.0 ± 0.5 C; lights on, 0900–2100 h) and provided with standard rat chow and water ad libitum. In separate groups, body weight (BW), water and food intake, and urine output were monitored in metabolic cages. All procedures were performed in accordance with institutional guidelines for animal care at Nagoya University School of Medicine.

AP lesion
The rats were anesthetized with ip injection of pentobarbital (50 mg/kg) and placed in a stereotaxic instrument with incisor bar 10 mm below the center of the aural bars. A midline incision was made from the skull to the second cervical vertebra, and the underlying muscle was retracted laterally. The meninges were incised to expose the dorsal medulla, and the AP was aspirated through a blunted 25-gauge needle with a surgical microscope. Sham operation was performed in the same fashion except that the AP was not aspirated. After completion of the studies, the brain stem was cut in 25-µm sections coronally. The sections were stained with cresyl violet and examined microscopically to determine the completeness of AP lesion. All experiments were performed in unanesthetized rats 6 weeks after the operation.

Stimuli for AVP release
To examine the effect of APX on hyperosmolality-induced AVP release, hypertonic saline (2% BW, 600 mosmol/kg) or isotonic saline (2% BW) was injected ip 30 min before decapitation in both APX and Sham groups. Polyethylene glycol (PEG) is known to reduce plasma volume without altering plasma osmolality (20). To examine the effect of APX on hypovolemia-induced AVP release, PEG (2% BW, MW 3,000; Wako Pure Chemical Industries Ltd., Osaka, Japan) dissolved in isotonic saline (20% wt/vol) or isotonic saline (2% BW) was injected ip 90 min before decapitation in both APX and Sham groups. The time points used in the analyses were selected in consideration of previous studies (21, 22).

Plasma AVP, Na, total protein (TP), pituitary AVP content, and blood pressure
After decapitation, trunk blood was collected into chilled tubes containing EDTA (potassium salt) for plasma AVP, Na, and TP assay. After immediate separation at 4 C, AVP was extracted from 1 ml volume of plasma sample through a Sep-Pak C18 Cartridge (Waters Associates Inc., Milford, MA) and measured using a RIA kit (AVP-RIA kit, kindly provided by Mitsubishi Chemical Co., Ltd., Tokyo, Japan). The sensitivity of the assay for AVP was 0.063 pg/tube with less than 0.01% cross-reactivity with oxytocin, and plasma AVP values were log-transformed before statistical analyses (20). AVP concentrations in plasma were corrected for recovery, which averaged 83.0–90.8%. Plasma Na and TP were measured using an autoanalyzer (Hitachi Ltd., Tokyo, Japan) for estimation of plasma osmolality and change in plasma volume, respectively (23, 24). Immediately after decapitation, pituitary glands were removed and kept in acetone at -20 C. The glands were homogenized and stirred in 0.1 N HCl at 4 C for 24 h. After centrifugation, the supernates were diluted in buffer and assayed. Systolic blood pressure was measured by a tail cuff method using a programmable sphygmomanometer (Model PS-100; Rikenkaihatsu Co., Tokyo, Japan).

In situ hybridization
The levels of AVP messenger RNA (mRNA) in PVN, SON, and suprachiasmatic nucleus (SCN) were examined in both basal and dehydrated states. For dehydration, rats in both APX and Sham groups were deprived of water for 3 days while food was available ad libitum. After decapitation, brains were removed as soon as possible and kept at -80 C. Coronal brain sections were cut in 12 µm by a cryostat, thaw-mounted onto gelatin/chrome alum-coated slides, and kept at -80 C until hybridization. They were warmed to room temperature, allowed to dry, fixed in 4% formaldehyde in PBS for 5 min, washed twice in PBS, placed in 0.9% NaCl containing 0.25% acetic anhydride and 0.1 M triethanolamine for 10 min, then passed through 70, 80, 95, and 100% ethanol, 100% chloroform, and 100 and 95% ethanol before air drying. The AVP probe, directed against bases encoding the last sixteen amino acids of the glycopeptide sequence (25), was labeled using 35S-deoxy ATP and terminal deoxynucleotidyl transferase, and applied to each section (2 x 105 cpm). Hybridization was performed overnight at 37 C. The sections were then washed in 1 x SSC (0.15 M NaCl and 0.015 M sodium citrate) for 4 x 15 min at 55 C and 2 x 30 min at room temperature. After two water dips to remove salts, the sections were exposed to hyperfilm MP (Amersham International plc, Buckinghamshire, UK) together with the [14 C] microscale (Amersham) (26). The relationship between the signal intensities and exposure time was examined by exposing sections to the x-ray films for various periods, and then the exposure times yielding appropriate signal intensities within the linear range of the detection system were determined (24 h for PVN and SON, and 5 days for SCN). The autoradiographic images were quantified using a Macintosh IIci computer equipped with an image capture board (Data Translation, Inc., Marlboro, MA) running the program Image (Image 1.41; Wayne Rasband, NIMH, Bethesda, MD), and the data representing the hybridization signals were expressed as percentages from control level. No attempt was made to differentiate between signals present in parvocellular and magnocellular divisions of PVN.

Statistics
Results were expressed as mean ± SE. Comparison between groups was performed by Student’s t test, except where multiple comparisons were made, when Fisher PLSD was employed. Differences were considered statistically significant at P < 0.05. The group size was six in all experiments.


   Results
Top
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
Histology
Histological examination revealed that at least 90% of the AP was removed by aspiration. Whereas some rats in the APX group sustained moderate damage to the commissural subnucleus of the NTS, there was no damage to the dorsal motor nucleus of the vagus or to the hypoglossal nucleus in any rat. The extent of lesion did not seem to be related with the effects in the following studies, and all rats in the APX group were included in the statistical analyses. A photomicrograph of a representative APX rat is shown in Fig. 1Go.



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  		Figure 1. Photomicrographs of coronal sections through caudal medulla from a Sham rat (top) and from an APX rat (bottom). Sections were stained with cresyl violet. AP, Area postrema; NTS, nucleus tractus solitarius.

 
Effect of APX on basal plasma AVP level
The APX group showed the transient hypophagia and BW loss after the operation as previously reported (18, 19). However, the food intake and the rate of BW increase in the APX group became similar to those in the Sham group by 2 weeks and continued until 6 weeks after the operation (Table 1Go), when the BW in the APX group was still less than in the Sham group (APX, 357 ± 13 g; Sham, 416 ± 8 g; P < 0.01). The urine output in the APX group became higher than in the Sham group by 2 weeks after the operation, and the polyuria continued (Table 1Go). Six weeks after the operation, the plasma AVP level in the APX group was significantly lower than in the Sham group (APX, 1.03 ± 0.06 pg/ml; Sham, 1.65 ± 0.04 pg/ml; P < 0.01; Fig. 2Go and Table 2Go). There was no significant difference between the groups in the levels of plasma Na, TP, AVP content in pituitary (Tables 2Go and 3Go) or blood pressure (APX, 117.5 ± 1.9 mmHg; Sham, 117.8 ± 2.3 mmHg).


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  		Table 1. Urine output, food intake, and BW change 6 weeks after operation

 


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  		Figure 2. Plasma AVP levels of APX and Sham groups. Hypertonic saline (HS; 2% BW, 600 mosmol/kg) was injected ip 30 min before decapitation. Polyethylene glycol (PEG; 2% BW) dissolved in isotonic saline (20% wt/vol) was injected ip 90 min before decapitation. Isotonic saline (IS) was injected ip 30 or 90 min before decapitation for control. The injection of isotonic saline had no significant effect on the plasma AVP level at either 30 or 90 min after the injection, and the value at 30 min is shown. Results are expressed as mean ± SE (n = 6). Comparisons between the groups were made by one-way ANOVA followed by Fisher PLSD. a, P < 0.01 vs. corresponding Sham group; b, P < 0.01 vs. control (IS) Sham group; c, P < 0.01 vs. control (IS) APX group.

 

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  		Table 2. Levels of plasma AVP and pituitary AVP content

 

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  		Table 3. Plasma Na and TP levels

 
Effect of APX on AVP release induced by hyperosmolality
Thirty minutes after ip injection of isotonic saline, the level of plasma Na, TP (Table 3Go), or AVP (APX, 1.12 ± 0.10 pg/ml; Sham, 1.61 ± 0.09 pg/ml; P < 0.01; Fig. 2Go) was not significantly different from each basal level in both APX and Sham groups. Following ip injection of hypertonic saline, the plasma Na increased similarly in both APX and Sham groups but the plasma TP was not affected (Table 3Go). The plasma AVP level in the APX group was significantly lower than in the Sham group (APX, 4.88 ± 0.42 pg/ml; Sham, 9.09 ± 0.68 pg/ml; P < 0.01; Fig. 2Go), whereas the plasma AVP levels were significantly increased from control levels in both groups (APX, 335%; Sham, 465%; increase of each control level; Fig. 2Go).

Effect of APX on AVP release induced by hypovolemia
Ninety minutes after ip injection of isotonic saline, the level of plasma Na, TP (Table 3Go), or AVP (APX, 1.05 ± 0.11 pg/ml; Sham, 1.60 ± 0.10 pg/ml; P < 0.01) was not significantly different from each basal level in both APX and Sham groups. Following ip injection of PEG, the plasma TP increased similarly in both APX and Sham groups, but the plasma Na was not affected (Table 3Go), and the estimated decrease in plasma volume was about 11%. The plasma AVP level in the APX group was significantly lower than in the Sham group (APX, 3.54 ± 0.55 pg/ml; Sham, 9.37 ± 0.99 pg/ml; P < 0.01; Fig. 2Go), whereas the plasma AVP levels were significantly increased from control levels in both groups (APX, 237%; Sham, 486%; increase of each control level; Fig. 2Go).

Effect of APX on AVP gene expression in PVN, SON, and SCN
The levels of AVP mRNA in the APX group were significantly lower than in the Sham group in the basal state in both PVN (100 ± 11 vs. 76 ± 6%; P < 0.05) and SON (100 ± 8 vs. 82 ± 3%; P < 0.05) (Figs. 3Go and 4Go). After water deprivation for 3 days, plasma Na and TP were increased in both groups, and there was no significant difference in the levels between the groups (Table 3Go). The plasma AVP level in the APX group after dehydration was significantly lower than in the Sham group, indicating impaired AVP release in the APX group during dehydration (APX, 6.25 ± 1.77 pg/ml; Sham, 12.88 ± 2.43 pg/ml; P < 0.05; Table 2Go). As shown in Fig. 4Go, the AVP mRNA levels in PVN and SON after dehydration were significantly lower in the APX group than in the Sham group, whereas the AVP mRNA levels were significantly increased from the basal levels in both groups (APX, 45% and 30%; Sham, 46% and 38%; increase of each basal level in PVN and SON, respectively). There was no significant difference in the levels of pituitary AVP content between the groups after dehydration (Table 2Go). The level of AVP mRNA in SCN was not affected by dehydration in both groups, and there was no significant difference in the levels between APX and Sham groups in both basal and dehydrated states (Figs. 3Go and 4Go).



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  		Figure 3. Representative autoradiographs demonstrating hybridized AVP mRNA in PVN, SON, and SCN of basal Sham and APX groups.

 


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  		Figure 4. Semiquantitative in situ hybridization histochemical analysis of AVP mRNA levels in PVN, SON, and SCN in Sham and APX groups. The mRNA values are expressed as percentages from the level of PVN, SON, or SCN in the basal Sham group (mean ± SE, n = 6). Comparisons between the groups were made by one-way ANOVA followed by Fisher PLSD. a, P < 0.05 vs. corresponding Sham group; b, P < 0.01 vs. basal Sham group; c, P < 0.05 vs. basal APX group.

 

   Discussion
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
In the present study, we elucidated the role of the AP in AVP synthesis and release. The levels of plasma AVP and the mRNA in PVN and SON in the APX group were significantly lower than in the Sham group in both basal and stimulated states. These data indicate that AP has a significant effect on AVP synthesis and release in both states.

We showed that the level of basal plasma AVP was decreased by APX and that the decrease of plasma AVP level was not associated with the changes of variables such as plasma Na, TP, and blood pressure. These data indicate that AVP release is tonically stimulated in the basal state by the neuronal input from the AP to the hypothalamo-neurohypophyseal system. This tonic stimulation is supported by a previous study which showed that APX reduced the firing rate of AVP cells in the SON in the basal state of rats (27). While we first elucidated the tonic stimulation of AVP release by AP, this result is not in accordance with previous studies which showed no significant effects of APX on the level of basal plasma AVP (28, 29). Considering the transient hypophagia by APX, our study was performed 6 weeks after the operation. As the previous studies examined the effects 5–12 days after the APX, this discrepancy might be attributed to their relatively short recovery period. Alternatively, it might be due to a difference in the sensitivity of the assay as the detection limit of the AVP RIA used in this study is very low.

Although the role of AP in the osmoregulation of AVP release has been controversial (27, 29), we clearly showed that AVP release induced by hyperosmolality was attenuated by APX. It is reported that AP neurons are responsive to sodium ion (30), and that ip injection of hypertonic saline induced immediate early gene c-fos expression in AP (31). Thus, it is likely that AP is sensitive to plasma osmolality and that AVP release induced by hyperosmolality is regulated, at least partially, by AP. It is well known that the AV3V are critically involved in the osmoregulation of AVP release, and AVP release induced by hyperosmolality is reported to be impaired in AV3V lesioned rats (4, 5, 6). The reciprocal connections between CVOs have been shown, and AP is supposed to be embedded within the network (14). Collectively, it might be appropriate to consider that AP coordinates with AV3V in the osmoregulation.

The ip injection of hypertonic saline is supposed to be not only an osmotic stimulus but also a painful stress (31). In contrast to the critical role of plasma osmolality in the regulation of AVP release, the effect of stress such as pain on plasma AVP level is ambiguous (2). Although stressors are generally not considered to stimulate AVP release (32, 33, 34), there is a study suggesting that stimuli of ip structures might induce AVP release (35). We showed that ip injection of isotonic saline had no significant effect on plasma AVP level. Nevertheless, one cannot exclude the possibility that the pain accompanying hypertonic saline injection had an effect on the plasma AVP level.

It is widely accepted that AVP release induced by hypovolemia occurs through reduction in tonic inhibitory input from the baroreceptor to the NTS (1, 2, 3), even though some studies disagree as to the tonic inhibition (7, 8). Schreihofer et al. (8) showed that NTS lesion did not prevent AVP release induced by hypovolemia, suggesting that baroreceptor input to the NTS might not be necessary for hypovolemia-induced AVP release. It should be noted that AP and the commissural portion of NTS, which receives dense projections from AP (36), were spared in their lesions. It is also reported that humoral factors such as angiotensin II, which could act at CVOs, might be involved in the baroregulation, and that glucose utilization was increased in AP after hypovolemia (37). Our study does not address the issue whether the tonic inhibitory input from the baroreceptor to the NTS is involved in the baroregulation. Instead, we first showed that the inputs for hypovolemia-induced AVP release are mediated, at least partially, via the AP.

In the present study, we showed the levels of AVP mRNA in PVN and SON in the basal state were decreased by APX, indicating that the AVP synthesis is tonically stimulated by the neuronal mechanism involving AP. We also showed that the levels of AVP mRNA in PVN and SON in the APX group after dehydration were significantly lower than in the Sham group. This could not be attributed to a difference in the degree of dehydration because the levels of plasma Na and TP in the APX group were not significantly different from those in the Sham group after dehydration. Thus, it is indicated that AP regulates, at least partially, the AVP synthesis in PVN and SON reflecting plasma osmolality and/or plasma volume. The similar levels of pituitary AVP content between APX and Sham groups in both basal and dehydrated states might be attributed to the fact that both synthesis and release of AVP were decreased by APX. We also showed that the level of AVP mRNA in SCN, which is not directly involved in water balance (38), was not affected by APX, indicating that AP stimulates AVP synthesis exclusively in PVN and SON.

Whereas the plasma AVP level in the hypertonic or hypovolemic state and the AVP mRNA levels in PVN and SON in the dehydrated state were lower in the APX group than in the Sham group, both AVP release and synthesis in the APX group were increased by stimuli and the responses were still robust, which was shown by the percentage changes relative to the control values. This suggests that some other than AP-related mechanisms are involved in the regulation of AVP release and synthesis and that AP might play a critical role, especially in the regulation of the set point for AVP release and synthesis.

AP is exposed to the substances borne in the peripheral circulation as it lacks a blood brain barrier (9). In addition to humoral inputs, AP receives neuronal inputs from not only the vagus (39) but also the central nervous system, such as NTS, parabrachial nucleus, and PVN (14). On the other hand, heavy inputs are directed from the AP to the catecholaminergic neurons in the caudal NTS (36), which in turn give rise to substantial inputs to the hypothalamus (40). The A1 noradrenergic neurons in the ventral medulla receive the projection from the NTS (41) as well as from the AP (14) and are well known to project to AVP cells in the hypothalamus (40, 42). Moreover, the existence of a direct projection from AP to SON is also suggested (29). Thus, it is likely that AP receives neuronal as well as humoral inputs, transmits the influence to the hypothalamo-neurohypophyseal system directly or via other brain stem regions such as the NTS and the A1 neurons, and stimulates both synthesis and release of AVP.

In conclusion, AVP synthesis and release are stimulated by the input from the AP to the hypothalamo-neurohypo-physeal system.


   Footnotes
 
1 This work was supported by the Research for the Future Program of the Japan Society for the Promotion of Science (JSPS-RFTF97I00201). Back

Received July 21, 1997.


   References
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

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