Renal and endocrine changes in rats with inherited stress-induced arterial hypertension (ISIAH).
Hypertensive inbred rats (ISIAH; inherited stress-induced arterial hypertension) present with baseline hypertension (>170 mmHg in adult rats), but attain substantially higher values upon mild emotional stress. We aimed to characterize key parameters related to hypertension in ISIAH. Kidneys, adrenals, and systemic endocrine parameters were studied in ISIAH of different ages and compared to normotensive Wistar albino Glaxo (WAG) rats. Native organs were obtained for Western and PCR analysis. Perfusion-fixed organs were prepared for histopathology and quantitative histochemistry. Plasma renin and adrenal hormones were measured. Renal morphology was unaltered in ISIAH. The hypothalamic-pituitary-adrenocortical (HPA) axis was constitutively upregulated with enlarged adrenal cortices and enhanced plasma corticosterone levels. Plasma renin activity was not different between groups, whereas aldosterone levels were in part reduced. Juxtaglomerular NO synthase type 1, cyclooxygenase type 2, and renin expression were significantly reduced, whereas tubular gene products related to sodium transport (bumetanide-sensitive Na, K, 2Cl cotransporter type 2; thiazide-sensitive Na, Cl cotransporter; epithelial Na channel-alpha; 11beta-hydroxysteroid dehydrogenase type 2) were increased. These data suggest enhanced volume conservation by the kidney. Our data define ISIAH as an attractive model for the renal components determining salt and water homeostasis in hypertension. The specific condition of a basally stimulated HPA axis is highlighted, including the option to study effects superimposed by emotional stress.
Amstislavsky
Sergej
S
Institute of Cytology and Genetics, Lavrentyev Avenue 10, 630090, Novosibirsk, Russia.
Welker
Pia
P
Frühauf
Jan-Henning
JH
Maslova
Larissa
L
Ivanova
Ludmila
L
Jensen
Boye
B
Markel
Arkady L
AL
Bachmann
Sebastian
S
D000818:Animals; D001794:Blood Pressure; D051546:Cyclooxygenase 2 / Q000032:analysis / Q000378:metabolism; D004195:Disease Models, Animal; D053503:Epithelial Sodium Channels / Q000032:analysis / Q000235:genetics / Q000378:metabolism; D015870:Gene Expression; D006706:Homeostasis; D006973:Hypertension / Q000209:etiology / Q000235:genetics / Q000503:physiopathology*; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology*; D007668:Kidney / Q000737:chemistry / Q000473:pathology / Q000503:physiopathology*; D019001:Nitric Oxide Synthase / Q000032:analysis / Q000378:metabolism; D052248:Nitric Oxide Synthase Type I; D010913:Pituitary-Adrenal System / Q000503:physiopathology*; D051381:Rats / Q000378:metabolism*; D011919:Rats, Inbred Strains; D012083:Renin / Q000097:blood; D049992:Sodium Chloride Symporters / Q000032:analysis / Q000235:genetics / Q000378:metabolism; D028021:Sodium-Potassium-Chloride Symporters / Q000032:analysis / Q000235:genetics / Q000378:metabolism; D064466:Solute Carrier Family 12, Member 1; D013315:Stress, Psychological / Q000150:complications*; D014867:Water / Q000378:metabolism
D053503:Epithelial Sodium Channels; C578716:Slc12a1 protein, rat; D049992:Sodium Chloride Symporters; D028021:Sodium-Potassium-Chloride Symporters; D064466:Solute Carrier Family 12, Member 1; D014867:Water; D019001:Nitric Oxide Synthase; D052248:Nitric Oxide Synthase Type I; C496322:Nos1 protein, rat; D051546:Cyclooxygenase 2; D012083:Renin