Departments of Internal Medicine and Physiology, Wayne State University School of Medicine and John D. Dingell Veterans Affairs Medical Center, Detroit, Michigan 48201
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ABSTRACT |
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Because
dopamine influences arginine vasopressin (AVP) release, the present
studies were designed to ascertain the dopamine receptor subtype that
potentiates angiotensin II-induced AVP secretion in cultured
hypothalamo-neurohypophysial explants. Dopamine (a nonselective
D1/D2 agonist), apomorphine (a
D2 D1 agonist), and SKF-38393 (a
selective D1 agonist) dose dependently increased AVP
secretion. Maximal AVP release was observed with 5 µM
dopamine, 307 ±
66% · explant
1 · h
1,
1 µM SKF-38393, 369 ± 41% · explant
1 · h
1,
and 0.1 µM apomorphine, 374 ± 67% · explant
1 · h
1.
Selective D1 antagonism with 1 µM SCH-23390 blocked AVP
secretion to values no different from basal. Domperidone
(D2 antagonist), phenoxybenzamine (nonselective adrenergic
antagonist), and prazosin (
1-antagonist) failed to
prevent release. D1 antagonism also prevented AVP secretion
to 1 µM angiotensin II [angiotensin II, 422 ±
87% · explant
1 · h
1
vs. angiotensin II plus SCH-23390,
169 ± 28% · explant
1 · h
1
(P < 0.05)], but D2 and
1-adrenergic blockade did not. In contrast, AT1 receptor inhibition with 0.5 µM losartan blocked
angiotensin II- but not dopamine-induced AVP release. AT2
antagonism had no effect. Although subthreshold doses of the agonists
did not increase AVP secretion (0.05 µM dopamine,
133 ± 44% · explant
1 · h
1;
0.01 µM SKF-38393, 116 ±
26% · explant
1 · h
1;and
0.001 µM angiotensin II, 104 ± 29% · explant
1 · h
1
), the combination of dopamine and angiotensin II provoked a
significant rise in AVP [420 ± 83% · explant
1 · h
1
(P < 0.01)]. Similar results were observed with
SKF-38393 and angiotensin II, and the AVP response was blocked to basal
levels by either D1 or AT1 antagonism. These
findings support a role for D1 receptor activation to
increase AVP release and mediate angiotensin II-induced AVP release
within the hypothalamo-neurohypophysial system. The data also suggest
that the combined subthreshold stimulation of receptors that use
distinct intracellular pathways can prompt substantial AVP
release.
angiotensin receptors; dopamine receptors; hypothalamo-neurohypophysial system; supraoptic nucleus
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INTRODUCTION |
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MAGNOCELLULAR NEURONS within the supraoptic and paraventricular nuclei of the hypothalamus, along with their axonal projections via the infundibular stalk to the neurohypophysis, form the final link in the neural network that controls arginine vasopressin (AVP) secretion. This neurosecretory system receives an elaborate array of neural inputs, including a dense catecholaminergic innervation that is predominantly noradrenergic, but also includes a dopaminergic component (3, 6).
These dopaminergic pathways influence AVP secretory rate. Most of the evidence supports a stimulatory action by dopamine (7, 15, 20, 31), but data showing no change or inhibition also exist (23, 25, 27). Specifically, intracerebroventricular injection of dopamine (7, 15, 20) or direct injection of dopamine into supraoptic or paraventricular nuclei (17) in euvolemic or water-loaded rats provokes antidiuresis and increases plasma AVP levels. This rise in AVP is inhibited by nonselective dopamine receptor antagonism (7).
Dopamine has been implicated in the osmotic release of AVP in rats (31, 40). In addition, Brooks and Claybaugh (2) have shown that haloperidol blocks the increase in plasma AVP associated with infusion of angiotensin II in dehydrated dogs, consistent with facilitation of a nonosmotic mechanism for AVP release. Stimulation of AT1 angiotensin receptors within the brain potentiates dopamine release (11). The central loci involved in AVP release are replete with AT1 receptors (14).
Both D1 and D2 receptor subtypes have been identified in the hypothalamo-neurohypophysial system (1, 5). For the most part, D1 receptor activation has been associated with stimulation and D2 receptor with inhibition of AVP release (28). Most recently, D1A receptor mRNA has been detected and D1A receptors have been identified on neurophysin-expressing cells from the supraoptic nucleus in culture (8, 18). However, selective dopamine agonists and antagonists have been used in only a limited number of studies on AVP secretion (31, 32, 41). Although noradrenergic modulation of angiotensin II-stimulated AVP release has been studied (24, 37), the dopamine receptor subtype mediating the response to angiotensin II has not been identified.
The present studies used rat hypothalamo-neurohypophysial explants to characterize pharmacologically the dopamine receptor subtype that induces AVP release and to identify the selective dopaminergic actions that regulate angiotensin II-stimulated AVP secretion.
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METHODS |
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Experiments were performed on male Long-Evans rats weighing 125-150 g. The rats were housed at constant temperature with a 12:12-h light-dark cycle. They were given free access to water and standard rodent chow. All procedures were reviewed and approved by the institutional Animal Investigation Committee and were in compliance with the National Institutes of Health guidelines.
Dissection and culture of explants. Explants of the hypothalamo-neurohypophysial system were dissected as previously described (30, 34). Each explant contained supraoptic nuclei with intact axonal projections to the neural lobe. The arcuate, suprachiasmatic, preoptic, and ventromedial nuclei were present as well as the organum vasculosum of the lamina terminalis and the intermediate lobe. The paraventricular nuclei and subfornical organ were absent.
Each explant was placed into a separate incubation well (Falcon, Oxnard, CA) and was supported ventral side down by Teflon mesh (Spectrum, Los Angeles, CA). The culture medium was Ham's F-12 nutrient mixture with 5.5 mM dextrose, 100 U/ml penicillin, and 100 µg/ml streptomycin (Life Technologies, Grand Island, NY) fortified with 20% fetal bovine serum (Hyclone, Logan, UT). Medium osmolality was 299 ± 1 mosmol/kgH2O. Explants were incubated at 37°C under a humidified atmosphere of 95% O2-5% CO2. Medium was changed at 24-h intervals.Sampling procedures. Protocols were performed 48 h after dissection and follow the sampling techniques reported earlier (34). All experiments were performed in the presence of the peptidase inhibitor bacitracin, 0.05 mg/ml to prevent degradation of released AVP (30). Immediately before the protocol, ascorbic acid was added to each well to bring the final concentration to 10 µM to retard the oxidation of dopamine and its analogs.
During the basal period, AVP release rate was ascertained after 1 h of exposure to standard medium. This was followed immediately by a 1-h test period. All test agent(s) were dissolved in medium containing 10 µM ascorbic acid. Vehicle controls were performed whenever applicable. Samples were obtained for determination of AVP release rates and degradation during both basal and test periods. AVP release rates were corrected for volume of medium and degradation (34). Samples for AVP radioimmunoassay were frozen and stored atProtocols.
The following protocols were performed: 1) dose-response curves
for 0.01-10 µM dopamine (nonselective
D1/D2 agonist), 0.01-10 µM SKF-38393
(selective D1 agonist), and 0.01 nM to 1 µM apomorphine (D2 D1 agonist); 2) nonselective
dopaminergic antagonism of dopamine-induced AVP release by 1 µM
haloperidol; 3) antagonism of maximally stimulating doses of
each agonist (1 µM angiotensin II, 5 µM dopamine, 1 µM SKF-38393,
and 0.1 µM apomorphine) using the selective D1
antagonist, 1 µM SCH-23390, or the D2 antagonist, 1.5 µM domperidone, and the nonselective adrenergic antagonist, 1 µM
phenoxybenzamine; 4) angiotensin receptor blockade of each agonist with the nonselective antagonist 1 µM saralasin, the
AT1 antagonist, 0.5 µM losartan, or the AT2
antagonist, 0.5 µM CGP-42112A; 5) antagonism of 1 µM
SKF-38393 or 1 µM angiotensin II with 1 µM SCH-23390 or the
selective 1 µM
1-prazosin alone or in combination; 6) the combination of submaximally stimulating concentrations of 0.05 µM dopamine or 0.01 µM SKF-38393 with a subthreshold dose of 0.01 µM angiotensin II; and 7) dopaminergic or
angiotensinergic receptor inhibition of the combined effect of
submaximal angiotensin II and dopamine agonists. Doses of the
antagonists were chosen based on reported values for inhibition
constants.
Analytic methods. AVP content of the medium was measured by radioimmunoassay using methods reported earlier from our laboratory (30). All standards and samples were assayed in duplicate; samples were diluted 1:100 with buffer and assayed directly. Standards were prepared with purified AVP (Ferring, Malmo, Sweden). The tracer was [125I]iodotyrosyl AVP (Amersham, Arlington Heights, IL). Anti-AVP serum no. 2849 was used at a final dilution of 1:3.6 × 105. Assay buffer contained 0.15 M sodium phosphate, 0.01 M sodium EDTA, 0.1 g/100 ml sodium azide, and 0.1 g/100 ml bovine serum albumin (ICN-Miles, Irvine, CA) at pH 7.4. Assay sensitivity and cross-reactivities have been reported previously (30).
Medium osmolality was measured by freezing point depression (Precision Systems 5004, Sudbury, MA). Domperidone was obtained from Janssen Pharmaceutica (Piscataway, NJ). Losartan was provided by Merck (Rahway, NJ). Dopamine, SKF-38393, SCH-23390, CGP-42112A, and phenoxybenzamine were obtained from Research Biochemicals (Natick, MA). Unless otherwise stated, all other chemicals were obtained from Sigma (St. Louis, MO).Statistics. All comparisons between basal and test period release rates were performed on the absolute release rates. Because basal AVP release rates varied among the groups of explants, the release of AVP during the test hour was normalized as the percentage of AVP released during the preceding basal hour for the same explant. Each explant acted as its own control.
Differences between basal and test hour release of AVP in the same explants were compared using the paired t-test. Analyses among the test period secretory rates were performed on the normalized values. Comparisons between two test periods from separate explants were performed by Student's t-test. When multiple comparisons were made, significant differences were assessed by analysis of variance for repeated measures and the Tukey-Kramer test for multiple comparisons. All data are expressed as means ± SE. P < 0.05 was taken as significant. ![]() |
RESULTS |
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Overall basal AVP release rate at 48 h was 79 ± 2 pg · explant1 · h
1
(n = 418). Basal medium osmolality was 305 ± 1 mosmol/kgH2O and did not change by the end of the test
period (307 ± 2 mosmol/kgH2O). AVP release did not vary
during time control experiments with standard medium administered
during both basal and test periods [basal, 100 ± 25 vs. test,
115 ± 6% · explant
1 · h
1
(P > 0.05, n = 7)].
Dose-response curves for the dopamine agonists are shown in Fig.
1. AVP release was significantly increased
by concentrations of dopamine or SKF-38393 >1 µM or apomorphine
>10 nM. Nonselective dopaminergic receptor blockade with haloperidol
inhibited dopamine-induced AVP secretory activity (Fig.
2). The vehicle for haloperidol, 0.0038%
methanol, did not alter AVP release [basal (no methanol) 100 ± 35
vs. test (methanol vehicle)
128 ± 28% · explant1 · h
1].
The dose-response relationship to dopamine was unchanged by the
presence of methanol [compare Figs. 1 (without methanol) and 2 (with
methanol)]. Haloperidol alone did not alter basal AVP secretory rate
[basal, 100 ± 31 vs. haloperidol,
86 ± 20% · explant
1 · h
1
(n = 8; P > 0.05)].
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Figure 3 shows the effect of the selective
D1 and D2 dopamine receptor antagonists and the
nonselective adrenergic blocker on dopamine-induced AVP release.
Significant inhibition occurred only with SCH-23390. The D1
dopaminergic blocker also blocked AVP release by maximally stimulating
doses of SKF-38393 or apomorphine, as depicted in Table
1. Domperidone also failed to inhibit AVP release by 1 µM SKF-38393 (369 ± 41) vs. SKF-38393 with
domperidone [397 ± 72% · explant1 · h
1
(P > 0.05, n = 6 and 6, respectively)] or 0.1 µM apomorphine (392 ± 67) vs. apomorphine with domperidone
[309 ± 33% · explant
1 · h
1
(P > 0.05, n = 6 and 7, respectively)].
SCH-23390 alone did not change AVP release [basal, 100 ± 21 vs.
SCH-23390,
165 ± 25% · explant
1 · h
1
(P > 0.05, n = 7)] nor did domperidone [basal,
100 ± 10 vs. domperidone, 104 ± 15% · explant
1 · h
1
(P > 0.05, n = 6)].
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D1 antagonism prevented the AVP secretory response to a
maximally stimulating dose of angiotensin II as well as the response to
the D1 agonists. D2 antagonism did not alter
the effect of any of the agonists (Fig. 4).
Figure 5 shows that
1-adrenergic blockade with prazosin did not inhibit AVP
release to either SKF-38393 or angiotensin II. No significant
additional inhibition occurred with the combined D1
dopaminergic and
1-adrenergic antagonists. In contrast,
AT1 receptor blockade inhibited only angiotensin II-stimulated but not dopamine- or SKF-38393-induced AVP release. AT2 receptor inhibition did not prevent AVP secretion (Fig.
6). Given alone, neither losartan nor
CGP-42112A changed basal AVP secretory rate [82 ± 27 and
60 ± 19% · explant
1 · h
1,
respectively (P > 0.05 vs. basal)].
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A submaximal concentration of either dopamine or SKF-38393 in combination with a subthreshold dose of angiotensin II prompted a significant release of AVP. Stimulation by the combined agonists was blocked by both D1 and AT1 inhibitors as well as nonselective angiotensin receptor antagonism (Table 2).
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DISCUSSION |
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The present study reports four major findings. First, dopamine and its agonists increase basal AVP release dose dependently via D1 receptor activation. Second, angiotensin II-induced AVP secretion occurs via an AT1 receptor. Third, the AVP secretory response to angiotensin II is blocked by selective D1 receptor antagonism, but dopamine-stimulated AVP release is not altered by angiotensin II receptor inhibition. Fourth, D1 agonism potentiates the stimulatory effect of a subthreshold dose of angiotensin II.
Before attempting to assess the effect of dopamine on angiotensin II secretion by hypothalamo-neurohypophysial explants, it was necessary to characterize the response of these explants to dopamine. Previous studies reported that intracerebroventricular injections as well as direct injections of dopamine into the supraoptic and paraventricular nuclei increased plasma AVP and resulted in antidiuresis in euvolemic, water-loaded rats (7, 15, 17, 20), but some investigators observed suppression or no change in AVP secretion with dopamine (4, 39). The variability of the response to dopamine was highly dependent on the initial activity of the neurohypophysial system. Dopamine had little, if any, effect on AVP release when hormone levels were already elevated, but when AVP levels were low, as in water-loaded rats, dopamine increased AVP (7, 31). In our explants, where the confounding effects of osmolality, extracellular volume, systemic arterial pressure, or anesthesia can be controlled or eliminated, dopamine stimulated AVP secretion.
Our findings clearly implicate a D1 receptor as responsible
for the increase in AVP. Earlier studies were compelled to rely on
nonselective ligands, and stimulation of other catecholaminergic receptors, such as -adrenergic receptors, often was not excluded (7,
15, 17, 25, 26). The present studies extend observations made in
perifused explants and in cultured neurons from supraoptic nucleus by
Sladek and colleagues (18, 32) by showing the concentration dependency
and the D1 selectivity of the AVP stimulatory response.
Dopamine fibers terminate synaptically on magnocellular neuron cell bodies within the supraoptic nucleus (3, 6). These cells express D1A mRNA and exhibit D1 receptors on the cell membrane (8, 18). Dopaminergic fibers also project from the arcuate nucleus to the neurointermediate lobe and end in close proximity to the AVP neurosecretory endings (3, 17, 23). Experiments in these explants do not distinguish between these sites of action. D1 receptors at either or both of these loci could potentially have been activated. Data exist showing that, at least at the level of the neural lobe, D1 agonists facilitate electrically evoked AVP release (25, 26).
Numerous studies have shown that angiotensin II stimulates AVP
secretion (30, 31, 33). AT1 receptors identified within hypothalamic loci have been implicated in AVP release (19, 22, 24).
Qadri et al. (24) have shown that microinjection of losartan into
supraoptic nuclei reduced AVP release after angiotensin II was
administered intracerebroventricularly, but AVP secretion was still
twofold higher than baseline levels. In the present experiments,
losartan inhibited AVP secretion by the explants to basal levels. A
plausible explanation for this disparity is that the explants do not
contain the subfornical organ or the paraventricular nuclei. Thus
angiotensin II in the medium was only able to act upon AT1
receptors on the magnocellular cell body itself or on neuronal pathways
within the explant (33). Angiotensin II administered in vivo may have
acted on the circumventricular organs to elicit AVP release not only
via well-characterized angiotensinergic pathways (12) but also via
1-adrenergic pathways (37).
In dogs, nonselective dopamine receptor antagonism prevented AVP release in response to intravenous angiotensin II (2). Our data indicate that a D1 dopamine receptor mechanism is responsible. Clearly, when the D1 antagonist was present, AVP secretion in response to a maximally stimulating concentration of angiotensin II was reduced by 84% to a level that did not differ from the basal release rate. Within the substantia nigra, AT1 receptor activation potentiated dopamine release from nerve terminals (11). A similar scheme in the hypothalamo-neurohypophysial system would result in angiotensin II inducing dopamine release from nerve terminals within the explant. Dopamine, in turn, would act upon D1 receptors on the magnocellular cell body, along the axon, or on the neural lobe. In the absence of D1 receptor activation, as seen with D1 receptor antagonism, angiotensin II stimulation of the magnocellular neuron fails to release AVP. This does not imply that a dopaminergic neuron or a D1 receptor mediates angiotensin II actions. These findings do provide evidence, however, that D1 input at either the cell body or the axon of the magnocellular neuron is required for AT1 activation to stimulate AVP release (Fig. 7).
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The involvement of an 1-adrenergic pathway in supraoptic
nucleus mediating the angiotensin II effect has also been suggested; however, AVP levels were reduced only by 50% when prazosin was microinjected bilaterally (24). The residual AVP concentrations after
1-adrenergic blockade remained at least threefold higher than baseline levels reported using the same paradigm. Veltmar et al.
(37) have shown that the effect of
1- and
2-adrenergic antagonism was more pronounced on AVP
release prompted by angiotensin II within the paraventricular nuclei,
which are not contained within the hypothalamo-neurohypophysial
explants. In fact,
1-adrenergic blockade did not change
AVP release to angiotensin II by the explants. The small additional
decrement that prazosin elicited when used in conjunction with
SCH-23390 was not significant. Thus our findings suggest that dopamine
plays a major role in mediating AVP release stimulated by angiotensin
II acting at the supraoptic nucleus.
The D1 dopamine receptor is linked to adenylate cyclase (13, 16). Several investigators have also observed that D1 dopamine receptor activation increases cytosolic free calcium (9, 36). Although influx of extracellular calcium is not required, cytoplasmic calcium concentration is an important determinant of the response to dopamine in vasopressinergic magnocellular neurons (29). In contrast, AT1 receptor signaling occurs by activation of the phosphoinositide cascade in the central nervous system (10, 21, 35). Because coadministration of subthreshold concentrations of D1 agonists and angiotensin II potentiated AVP secretion, it appears that simultaneous occupation of D1 and AT1 receptors at low levels on the magnocellular neurons leads to sufficient activation of these separate pathways so as to elicit a rise in intracellular calcium sufficient to provoke a large secretory response. Such an interaction between dopamine and angiotensin II to augment intracellular calcium could quite conceivably occur at the nerve terminal. If the interaction is at the level of the cell body, the mechanisms for modulating the propagation of action potentials to the neural lobe may be more varied and complex. For example, it could involve the participation of excitatory and/or inhibitory amino acid receptors via activation of protein kinase A or protein kinase C by dopamine and angiotensin II. Finally, an action at the level of the soma does not necessarily exclude an action at the level of the axon or nerve terminal.
Taken together, the present data provide evidence that D1 dopamine receptor activation concentration dependently increases AVP secretion. The findings further support the concept that activation of a D1 dopaminergic pathway is required for angiotensin II-induced AVP release within the hypothalamo-neurohypophysial explant. We can speculate that the need for dual inputs would allow for integration and fine tuning of AVP in the whole organism. Finally, the potentiation of AVP secretion by combined subthreshold D1 and AT1 agonism is consistent with sufficient activation of apparently distinct intracellular pathways to increase intracellular calcium to a level that prompts secretion. Additional studies are warranted to localize the site of dopaminergic modulation of the angiotensin II response more precisely, such as magnocellular cell body versus neurointermediate lobe.
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ACKNOWLEDGEMENTS |
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This work was supported by a Merit Award from the Office of Research and Development of the Department of Veterans Affairs.
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FOOTNOTES |
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The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.
Address for reprint requests: N. F. Rossi, Dept. of Medicine, Wayne State University School of Medicine, 4160 John R #908, Detroit, MI 48201.
Received 14 April 1998; accepted in final form 19 June 1998.
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