Effect of Angiotensin II and ACTH on Adrenal Blood Flow in the Male Rat Adrenal Gland In Vivo

Autor: William B. Campbell, Tamas Kriska, Abdul Jabbar Shah, John R. Falck, Kathryn M. Gauthier
Rok vydání: 2017
Předmět:
Male
medicine.medical_specialty
Miconazole
Indomethacin
030209 endocrinology & metabolism
Adrenocorticotropic hormone
030204 cardiovascular system & hematology
Nitric Oxide
Epoxyeicosatrienoic acid
Receptor
Angiotensin
Type 2

Nitric oxide
Rats
Sprague-Dawley

03 medical and health sciences
chemistry.chemical_compound
8
11
14-Eicosatrienoic Acid

0302 clinical medicine
Endocrinology
Adrenocorticotropic Hormone
Internal medicine
Adrenal Glands
Renin–angiotensin system
medicine
Animals
Cytochrome P-450 Enzyme Inhibitors
Cyclooxygenase Inhibitors
Enzyme Inhibitors
Research Articles
Aldosterone
biology
Chemistry
Angiotensin II
Nitric oxide synthase
NG-Nitroarginine Methyl Ester
medicine.anatomical_structure
Receptors
Corticotropin

Regional Blood Flow
Zona glomerulosa
Injections
Intravenous

biology.protein
Eicosanoids
Endothelium
Vascular

Nitric Oxide Synthase
hormones
hormone substitutes
and hormone antagonists

Signal Transduction
Zdroj: Endocrinology. 159:217-226
ISSN: 1945-7170
DOI: 10.1210/en.2016-1594
Popis: Angiotensin II (Ang II) and adrenocorticotropic hormone (ACTH) regulate adrenal vascular tone in vitro through endothelial and zona glomerulosa cell–derived mediators. The role of these mediators in regulating adrenal blood flow (ABF) and mean arterial pressure (MAP) was examined in anesthetized rats. Ang II (0.01 to 100 ng/kg) increased ABF [maximal increase of 97.2 ± 6.9 perfusion units (PUs) at 100 ng/kg] and MAP (basal, 115 ± 7 mm Hg; Ang II, 163 ± 5 mm Hg). ACTH (0.1 to 1000 ng/kg) also increased ABF (maximum increase of 91.4 ± 10.7 PU) without changing MAP. ABF increase by Ang II was partially inhibited by the nitric oxide (NO) synthase inhibitor N-nitro-l-arginine methyl ester (L-NAME) (maximum increase of 72.9 ± 4.2 PU), the cytochrome P450 inhibitor miconazole (maximum increase of 39.1 ± 6.8 PU) and the epoxyeicosatrienoic acid (EET) antagonist 14,15-epoxyeicosa-5(Z)-enoic acid (14,15-EEZE) (maximum increase of 56.0 ± 13.7 PU) alone, whereas combined administration of miconazole and L-NAME (maximum increase of 16.40 ± 8.98 PU) ablated it. These treatments had no effect on MAP. Indomethacin did not affect the increase in ABF or MAP induced by Ang II. The ABF increase by ACTH was partially ablated by miconazole and 14,15-EEZE but not by L-NAME. Steroidogenic stimuli such as Ang II and ACTH increase ABF to promote oxygen and cholesterol delivery for steroidogenesis and aldosterone transport to its target tissues. The increases in ABF induced by Ang II are mediated by release of NO and EETs, whereas ABF increases with ACTH are mediated by EETs only.
Databáze: OpenAIRE