RGD Reference Report - AT-1 receptor and phospholipase C are involved in angiotensin III modulation of hypothalamic noradrenergic transmission. - Rat Genome Database

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AT-1 receptor and phospholipase C are involved in angiotensin III modulation of hypothalamic noradrenergic transmission.

Authors: Rodriguez-Campos, M  Kadarian, C  Rodano, V  Bianciotti, L  Fernandez, B  Vatta, M 
Citation: Rodriguez-Campos M, etal., Cell Mol Neurobiol. 2000 Dec;20(6):747-62.
RGD ID: 1582152
Pubmed: PMID:11100981   (View Abstract at PubMed)

1. We previously reported that angiotensin III modulates noradrenergic neurotransmission in the hypothalamus of the rat. In the present work we studied the effects of angiotensin III on norepinephrine release and tyrosine hydroxylase activity. We also investigated the receptors and intracellular pathways involved in angiotensin III modulation of noradrenergic transmission. 2. In rat hypothalamic tissue labeled with [3H]norepinephrine 1, 10, and 100 nM and 1 microM losartan (AT1 receptor antagonist) had no effect on basal neuronal norepinephrine release, whereas 10 and 100 nM and 1 microM losartan partially diminished norepinephrine secretion evoked by 25 mM KCl. The AT2 receptor antagonist PD 123319 showed no effect either on basal or evoked norepinephrine release. The increase in both basal and evoked norepinephrine output induced by 1 microM angiotensin III was blocked by 1 microM losartan, but not by 1 microM PD 123319. 3. The phospholipase C inhibitor 5 microM neomicin inhibited the increase in basal and evoked norepinephrine release produced by 1 microM angiotensin III. 4. Tyrosine hydroxylase activity was increased by 1 microM angiotensin III and this effect was blocked by 1 microM LST and 5 microM neomicin, but not by PD 123319. On the other hand, 1 microM angiotensin III enhanced phosphatidyl inositol hydrolysis that was blocked by 1 microM losartan and 5 microM neomicin. PD 123319 (1 microM) did not affect ANG III-induced phosphatidyl inositol hydrolysis enhancement. 5. Our results confirm that angiotensin III acts as a modulator of noradrenergic transmission at the hypothalamic level through the AT1-phospholipase C pathway. This enhancement of hypothalamic noradrenergic activity suggests that angiotensin III may act as a central modulator of several biological processes regulated at this level by catecholamines, such as cardiovascular, endocrine, and autonomic functions as well as water and saline homeostasis.

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
activation of phospholipase C activity  IMP 1582152 RGD 
positive regulation of catalytic activity  IMP 1582152 RGD 
regulation of norepinephrine secretion  IMP 1582152 RGD 

Molecular Pathway Annotations    Click to see Annotation Detail View

RGD Manual Annotations

Objects Annotated

Genes (Rattus norvegicus)
Agt  (angiotensinogen)
Agtr1a  (angiotensin II receptor, type 1a)
Agtr1b  (angiotensin II receptor, type 1b)

Genes (Mus musculus)
Agt  (angiotensinogen)
Agtr1a  (angiotensin II receptor, type 1a)
Agtr1b  (angiotensin II receptor, type 1b)

Genes (Homo sapiens)
AGT  (angiotensinogen)
AGTR1  (angiotensin II receptor type 1)


Additional Information