Different pharmacological anatomy in the paraventricular hypothalamic nucleus, supraoptic nucleus, and suprachiasmatic nucleus of rats: Quantitative autoradiography on angiotensin II receptor binding sites

Hwang, Bang H.; Wu, Jang‐Yen; Wieczorek, Caroline; Harding, Joseph W.; Erickson, Joel B.; Wamsley, James K.

doi:10.1002/aja.1001760212

Cited by 12 publications

(9 citation statements)

References 15 publications

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“…However, essentially equivalent OT secretory responses were obtained after administration of Ang II directly into the PVN/ACN, PVNcnt, SON and MBH. To our knowledge, this is the First report that OT release can be increased after direct Ang II stimulation of the magnocellular nuclei, but this finding is consistent with previous observations that Ang II receptors are present within the PVN and SON [41 ], that Ang 11 increases neuronal activity of a subpopu lation of putative SON OT neurons in vitro [39,42], and that Ang Il-immunopositive fibers, derived from subfor nical organ, innervate the SON [43]. The response to Ang 11 in the MBH may be indirect as this region is known to project to the PVN [ 18].…”

Section: Discussionsupporting

confidence: 82%

Activation of Central D-1 Dopamine Receptors Stimulates Oxytocin Release in the Lactating Rat: Evidence for Involvement of the Hypothalamic Paraventricular and Supraoptic Nuclei

Parker

Crowley

1992

Neuroendocrinology

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The stimulatory effect of dopamine (DA) on the release of oxytocin (OT) in lactating rats is exerted at the D-1 DA receptor subtype. Because the neural loci mediating this effect have not been identified, the objective of the present studies was to test whether OT release in the lactating rat would be elevated after central administration of a D-1 DA receptor agonist into the third ventricle (3V) or directly into either the rostral paraventricular/anterior commissural nucleus area (PVN/ACN), the central paraventricular nucleus area, or the supraoptic nucleus (SON), all of which contain OT neurosecretory cells. Lactating rats were implanted with a stainless steel cannula directed into one of the above areas or into the arcuate-ventromedial region of the medial basal hypothalamus (MBH), or sites dorsal to the PVN/ACN or SON, which served as anatomical controls. After 6-7 days of recovery, each animal received an intra-atrial cannula for sequential blood sampling, and was used in experiments 24 h later. Animals were separated from their litters, and following a period of basal blood sampling, received central microinjections of either vehicle, the D-1 DA receptor agonist SKF-38393, or the D-2 DA receptor agonist quinpirole, and blood samples were removed periodically for 60 min. An injection of angiotensin II (Ang II, 100 ng) was made into each site as a positive control for OT release. Injection of SKF-38393 (12.5 or 50 µg/5 µl) into the 3V resulted in a statistically significant and dose-releated increase in plasma OT concentrations, which was attenuated by intravenous pretreatment with the specific D-1 DA receptor antagonist, SCH-23390 (1.2 mg/kg). Unilateral injection of SKF-38393 (8 µg) into the SON region also produced a significant increase in plasma OT concentrations, while more modest increases followed injection of this agent into the PVN sites. Systemic pretreatment with the D-1 DA antagonist also blocked the effect of SKF-38393 in the SON. Plasma OT concentrations were not significantly changed after administration of SKF-38393 into the MBH or to dorsal control sites, or after any central injections of vehicle or the D-2 agonist quinpirole. Ang II markedly stimulated OT release after administration to 3V, PVN, SON and MBH, but not to the control sites dorsal to the PVN and SON. The present findings extend previous observations that D-1 DA receptors mediate the central dopaminergic stimulation of OT secretion in the lactating rat, and suggest that the SON region may be an important locus for this effect.

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Section: Discussionsupporting

confidence: 82%

Activation of Central D-1 Dopamine Receptors Stimulates Oxytocin Release in the Lactating Rat: Evidence for Involvement of the Hypothalamic Paraventricular and Supraoptic Nuclei

Parker

Crowley

1992

Neuroendocrinology

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“…Therefore, the Ang II-induced effects are inhibited by a lower dose of [Sar1, Ile$]Ang II in the SON than in the PVN. Also, this is consistent with evidence from auto radiographic binding studies that the Ang II receptor concentration is higher in the PVN than in the SON (8,10). It is suggested that Ang II receptors exist on cell bodies of vasopressin-containing neurons in the nuclei and direct ly promotes vasopressin release (11)(12)(13)(14).…”

Section: Effects Of Antagonists On Ang Ii-induced Antidiuresessupporting

confidence: 77%

“…Vasopres sin-containing neurons are activated by Ang II (12 14). Also, Ang II receptors, neurons and terminals of Ang II containing neurons are involved in the SON, as well as in the PVN (6,8,15).…”

mentioning

confidence: 99%

Microinjections of Angiotensin II into the Supraoptic and Paraventricular Nuclei Produce Potent Antidiureses by Vasopressin Release Mediated through Adrenergic and Angiotensin Receptors

Tsushima

Mori

Matsuda

1994

Japanese Journal of Pharmacology

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ABSTRACT-We investigated the effects of angiotensin II (Ang II), microinjected into the supraoptic (SON) and paraventricular (PVN) nuclei of rats, on the urine outflow rate and underlying mechanisms. Ang II produced antidiuretic effects in a dose-dependent manner with ED50 values of 0.1 and 0.05 nmol in the SON and PVN, respectively. [Sar', Ile8]Ang II at 0.1 nmol diminished the Ang II (0.5 nmol)-induced anti diureses in the SON more markedly than in the PVN. A high dose of [Sar', Ile8]Ang II, 1 nmol, completely inhibited the effects in both the nuclei. In addition, the Ang II (1 nmol)-induced antidiuretic effects were par tially inhibited by phenoxybenzamine (80 nmol) in the SON and by phenoxybenzamine, timolol (100 nmol) and propranolol (100 nmol) in the PVN. The microinjection of Ang II (1 nmol) into both the nuclei, after pretreatment with a vasopressin V1V2-antagonist, d(CH2)5-u-Tyr(Et)VAVP (i.v.), significantly increased the urine outflow rate. These findings suggest that 1) Two mechanisms account for the Ang II receptor mediated antidiureses resulting from an increase in vasopressin release: direct stimulation on vasopressin containing neurons and indirect stimulation on them through a-adrenoceptors in the SON and a and ã drenoceptors in the PVN; 2) The Ang II-induced antidiuretic effect in the SON is slightly less potent than that in the PVN; and 3) Ang II receptors in the nuclei may possibly produce the diureses through mecha nisms that are not presently understood.

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“…All of the components of the renin-an giotensin system, including angiotensin II itself, are found in the brain [10, II], Specific angiotensin II receptors have been demonstrated throughout the central nervous system [10,12,24,29,31]. It has been shown repeatedly that the injection of angiotensin II into the cerebral ventricular system stimulates vasopressin release in many species [16,28,37,48].…”

Section: Introductionmentioning

confidence: 99%

Effect on Vasopressin Release of Microinjection of Angiotensin II into the Paraventricular Nucleus of Conscious Rats

Miyake¹,

Share²,

Crofton³

1989

Neuroendocrinology

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We have studied in conscious unrestrained rats the role of angiotensin II receptors in the paraventricular nucleus (PVN) in the control of vasopressin secretion under basal conditions and after 24 h of water deprivation. In euhydrated rats, the microinjection rostral to the PVN of 1 and 5 ng of angiotensin II produced a transient, dose-dependent increase in the plasma vasopressin concentration. There was also a transient, but not dose-dependent, rise in mean arterial blood pressure (MABP), without a change in heart rate. However, the microinjection of angiotensin II into the PVN and sites caudal to it was without effect on the measured variables. In dehydrated rats, on the other hand, microinjection of 5 ng angiotensin II, both into the PVN and rostral to it, resulted in a prolonged increase in the plasma vasopressin concentration. The reponse from the rostral site was more rapid and was associated with an increased MABP. These findings suggest that angiotensin II receptors rostral to the PVN may participate in the control of vasopressin release in both euhydrated and dehydrated states, whereas angiotensin II receptors in the PVN are effective only following dehydration.

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Different pharmacological anatomy in the paraventricular hypothalamic nucleus, supraoptic nucleus, and suprachiasmatic nucleus of rats: Quantitative autoradiography on angiotensin II receptor binding sites

Cited by 12 publications

References 15 publications

Activation of Central D-1 Dopamine Receptors Stimulates Oxytocin Release in the Lactating Rat: Evidence for Involvement of the Hypothalamic Paraventricular and Supraoptic Nuclei

Activation of Central D-1 Dopamine Receptors Stimulates Oxytocin Release in the Lactating Rat: Evidence for Involvement of the Hypothalamic Paraventricular and Supraoptic Nuclei

Microinjections of Angiotensin II into the Supraoptic and Paraventricular Nuclei Produce Potent Antidiureses by Vasopressin Release Mediated through Adrenergic and Angiotensin Receptors

Effect on Vasopressin Release of Microinjection of Angiotensin II into the Paraventricular Nucleus of Conscious Rats

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