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

Miyake, Shoji; Share, Leonard; Crofton, J. T.

doi:10.1159/000125241

Cited by 35 publications

(12 citation statements)

References 38 publications

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“…The slow response is consistent with electrophysiological studies showing that the reversal of ANG II-induced excitation of PVN sympathoexcitatory neurons following washout of the peptide requires several minutes (9,30). Alternatively, the slow time course could be explained by PVN AT1R blockade decreasing vasopressin secretion and its subsequent clearance from plasma, due to reversal of the known stimulatory effect of ANG II in PVN on vasopressin release (39,48). However, our finding that the greatest depressor responses to candesartan were observed in the more caudal regions of PVN, which house sympathoexcitatory neurons that project to the spinal cord and/or to RVLM, but contain few neurohypophysial magnocellular vasopressin neurons (20,35), argues against this possibility.…”

Section: Discussionsupporting

confidence: 82%

AT₁ and glutamatergic receptors in paraventricular nucleus support blood pressure during water deprivation

Freeman¹,

Brooks²

2007

American Journal of Physiology-Regulatory, Integrative and Comp

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ter deprivation activates sympathoexcitatory neurons in the paraventricular nucleus (PVN); however, the neurotransmitters that mediate this activation are unknown. To test the hypothesis that ANG II and glutamate are involved, effects on blood pressure (BP) of bilateral PVN microinjections of ANG II type 1 receptor (AT1R) antagonists, candesartan and valsartan, or the ionotropic glutamate receptor antagonist, kynurenate, were determined in urethane-anesthetized waterdeprived and water-replete male rats. Because PVN may activate sympathetic neurons via the rostral ventrolateral medulla (RVLM) and because PVN disinhibition increases sympathetic activity in part via increased drive of AT1R in the RVLM, candesartan was also bilaterally microinjected into the RVLM. Total blockade of the PVN with bilateral microinjections of muscimol, a GABAA agonist, decreased BP more (P Ͻ 0.05) in water-deprived (Ϫ29 Ϯ 8 mmHg) than in water-replete (Ϫ7 Ϯ 2 mmHg) rats, verifying that the PVN is required for BP maintenance during water deprivation. PVN candesartan slowly lowered BP by 7 Ϯ 1 mmHg (P Ͻ 0.05). In waterreplete rats, however, candesartan did not alter BP (1 Ϯ 1 mmHg). Valsartan also produced a slowly developing decrease in arterial pressure (Ϫ6 Ϯ 1 mmHg; P Ͻ 0.05) in water-deprived but not in water-replete (Ϫ1 Ϯ 1 mmHg) rats. In water-deprived rats, PVN kynurenate rapidly decreased BP (Ϫ19 Ϯ 3 mmHg), and the response was greater (P Ͻ 0.05) than in water-replete rats (Ϫ4 Ϯ 1 mmHg). Finally, as in PVN, candesartan in RVLM slowly decreased BP in water-deprived (Ϫ8 Ϯ 1 mmHg; P Ͻ 0.05) but not in water-replete (Ϫ3 Ϯ 1 mmHg) rats. These data suggest that activation of AT 1 and glutamate receptors in PVN, as well as of AT1R in RVLM, contributes to BP maintenance during water deprivation.angiotensin II; rostral ventrolateral medulla; candesartan; valsartan; glutamate WATER DEPRIVATION IS ASSOCIATED with regional activation of sympathetic nerves (8,37,38). Recent studies indicate that sympathoexcitatory neurons in the paraventricular nucleus (PVN) contribute to this activation, since acute blockade of the PVN results in profound decreases in arterial blood pressure (BP) and sympathetic activity (42,43). Moreover, PVN neurons that project to the spinal cord, which houses sympathetic preganglionic neurons, or to the rostral ventrolateral medulla (RVLM), a hindbrain region responsible for the basal activity of many sympathetic nerves, express c-fos after water deprivation (41, 42), indirectly suggesting activation. However, the neurotransmitters that drive PVN sympathoexcitatory neurons during water deprivation have not been identified. Considerable indirect evidence implicates ANG II or a related peptide. First, water deprivation increases circulating ANG II levels, and increased binding of ANG II to type 1 receptors (AT1R) in circumventricular organs, such as the subfornical organ, increases the release and activity of an ANG II-like peptide in PVN (for a review, see Ref. 17). Second, both water deprivation and increases in osmolali...

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Section: Discussionsupporting

confidence: 82%

AT₁ and glutamatergic receptors in paraventricular nucleus support blood pressure during water deprivation

Freeman¹,

Brooks²

2007

American Journal of Physiology-Regulatory, Integrative and Comp

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“…In addition, the excitation is abolished by the AT 1 antagonist losartan, demonstrating that ANG II's effects on this subset of PVN neurons are mediated by the AT 1 receptor. These observations are particularly intriguing given that the majority of studies thus far have concentrated on the actions of ANG II on magnocellular neurons (9,28,29,38). These reports have themselves garnered considerable debate with respect to AT 1 receptor localization with PVN.…”

Section: Discussionmentioning

confidence: 99%

“…Angiotensinergic fibers, cell bodies, and receptors have been reported in PVN (22,23,25,30,36,39), and ANG II has been shown to influence a variety of neuroendocrine and autonomic functions (7,11,12,23). Early reports have focused primarily on ANG II actions on magnocellular neurons (9,28,29,38). Interestingly, Lenkei et al (23)(24)(25) observed a high level of AT 1 receptor mRNA expression within the parvocellular areas of PVN and the surrounding periventricular area, but no expression in the magnocellular PVN.…”

mentioning

confidence: 99%

Angiotensin depolarizes parvocellular neurons in paraventricular nucleus through modulation of putative nonselective cationic and potassium conductances

Latchford

Ferguson

2005

American Journal of Physiology-Regulatory, Integrative and Comp

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Neurosecretory parvocellular neurons in the hypothalamic paraventricular nucleus (PVN) exercise considerable influence over the adenohypophysis and thus play a critical role in neuroendocrine regulation. ANG II has been demonstrated to act as a neurotransmitter in PVN, exerting significant impact on neuronal excitability and also influencing corticotrophin-releasing hormone secretion from the median eminence and, therefore, release of ACTH from the pituitary. We have used whole cell patch-clamp techniques in hypothalamic slices to examine the effects of ANG II on the excitability of neurosecretory parvocellular neurons. ANG II application resulted in a dose-dependent depolarization of neurosecretory neurons, a response that was maintained in tetrodotoxin (TTX), suggesting a direct mechanism of action. The depolarizing actions of this peptide were abolished by losartan, demonstrating these effects are AT(1) receptor mediated. Voltage-clamp analysis using slow voltage ramps revealed that ANG II activates a voltage-independent conductance with a reversal potential of -37.8 +/- 3.8 mV, suggesting ANG II effects on a nonselective cationic current. Further, a sustained potassium current characteristic of I(K) was significantly reduced (29.1 +/- 4.7%) by ANG II. These studies identify multiple postsynaptic modulatory sites through which ANG II can influence the excitability of neurosecretory parvocellular PVN neurons and, as a consequence of such actions, control hormonal secretion from the anterior pituitary.

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“…In rats, local administration of ANGII onto neurons of the PVN excites neurosecretory cells (Harding and Felix 1987) and increases plasma ADH level (Shoji et al 1989). Lesions of the PVN prevent the release of ADH in response to centrally applied ANGII (Iovino and Steardo 1985).…”

Section: Discussionmentioning

confidence: 99%

Angiotensin II-binding sites in chicken brain and pituitary: autoradiographic localization

Natke¹,

Gerstberger

Großmann³

1996

Cell and Tissue Research

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The distribution of binding sites for 125I-Val5-angiotensin II in the brain and the pituitary of control and dehydrated adult chickens of both sexes was determined by receptor autoradiography. Specific 125I-Val5-angiotensin II binding was mainly located in sensory areas, the limbic system and the hypothalamus including circumventricular organs and the nucleus paraventricularis. Since both the central angiotensin II system and the avian antidiuretic arginine-vasotocin system interact in osmoregulation, possible changes in angiotensin II binding intensities after dehydration were investigated in hypothalamic areas known to be involved in body-fluid homeostasis. There was an obvious increase in binding sites neither in areas where arginine-vasotocin synthesizing neurons were located, e.g. the nucleus paraventricularis and nucleus supraopticus, nor in other relevant areas for osmoregulation, e.g. the circumventricular organs of the hypothalamus. Furthermore, no sex difference in angiotensin II binding was observed.

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

Cited by 35 publications

References 38 publications

AT₁ and glutamatergic receptors in paraventricular nucleus support blood pressure during water deprivation

AT₁ and glutamatergic receptors in paraventricular nucleus support blood pressure during water deprivation

Angiotensin depolarizes parvocellular neurons in paraventricular nucleus through modulation of putative nonselective cationic and potassium conductances

Angiotensin II-binding sites in chicken brain and pituitary: autoradiographic localization

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

Cited by 35 publications

References 38 publications

AT1 and glutamatergic receptors in paraventricular nucleus support blood pressure during water deprivation

AT1 and glutamatergic receptors in paraventricular nucleus support blood pressure during water deprivation

Angiotensin depolarizes parvocellular neurons in paraventricular nucleus through modulation of putative nonselective cationic and potassium conductances

Angiotensin II-binding sites in chicken brain and pituitary: autoradiographic localization

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AT₁ and glutamatergic receptors in paraventricular nucleus support blood pressure during water deprivation

AT₁ and glutamatergic receptors in paraventricular nucleus support blood pressure during water deprivation