The role of the kidney in the development of hypertension a transplantation study in the prague hypertensive rat

1993 ◽  
Vol 425 (3-4) ◽  
pp. 208-212 ◽  
Author(s):  
Jiři Heller ◽  
Gisela Schubert ◽  
Jana Havlíčkova ◽  
Klaus Thurau
Keyword(s):  
Hypertensive Rat ◽  
Transplantation Study ◽  
Prague Hypertensive Rat

scholarly journals The Role of Mammalian Target of Rapamycin in Hypertensive Rat Atria

2011 ◽  
Vol 27 (Supplement) ◽  
pp. OP04_2
Author(s):  
Koichi Nagashima ◽  
Takeshi Yamashita ◽  
Akiko Sekiguchi ◽  
Ichiro Watanabe ◽  
Atsushi Hirayama
Keyword(s):  
Mammalian Target Of Rapamycin ◽  
Target Of Rapamycin ◽  
Rat Atria ◽  
Hypertensive Rat

EDHF-mediated vasodilation involves different mechanisms in normotensive and hypertensive rat lungs

2003 ◽  
Vol 284 (5) ◽  
pp. H1762-H1770 ◽  
Author(s):  
Yoshiteru Morio ◽  
Ethan P. Carter ◽  
Masahiko Oka ◽  
Ivan F. McMurtry
Keyword(s):  
Gap Junction ◽  
Vascular Tone ◽  
Pulmonary Vasodilation ◽  
Hypertensive Rat ◽  
Rat Lungs ◽  
Hypoxic Vasoconstriction ◽  
Gap Junction Intercellular Communication ◽  
Oxide Synthase ◽  
Cytochrome P 450

The role of endothelium-derived hyperpolarizing factor (EDHF) in regulating the pulmonary circulation and the participation of cytochrome P-450 (CYP450) activity and gap junction intercellular communication in EDHF-mediated pulmonary vasodilation are unclear. We tested whether tonic EDHF activity regulated pulmonary vascular tone and examined the mechanism of EDHF-mediated pulmonary vasodilation induced by thapsigargin in salt solution-perfused normotensive and hypoxia-induced hypertensive rat lungs. After blockade of both cyclooxygenase and nitric oxide synthase, inhibition of EDHF with charybdotoxin plus apamin did not affect either normotensive or hypertensive vascular tone or acute hypoxic vasoconstriction but abolished thapsigargin vasodilation in both groups of lungs. The CYP450 inhibitors 7-ethoxyresorufin and sulfaphenazole and the gap junction inhibitor palmitoleic acid, but not 18α-glycyrrhetinic acid, inhibited thapsigargin vasodilation in normotensive lungs. None of these agents inhibited the vasodilation in hypertensive lungs. Thus tonic EDHF activity does not regulate either normotensive or hypertensive pulmonary vascular tone or acute hypoxic vasoconstriction. Whereas thapsigargin-induced EDHF-mediated vasodilation in normotensive rat lungs involves CYP450 activity and might act through gap junctions, the mechanism of vasodilation is apparently different in hypertensive lungs.

scholarly journals Distribution and role of angiotensin II receptor in the brain of spontaneously hypertensive rat.

1980 ◽  
Vol 44 (5) ◽  
pp. 403-408 ◽  
Author(s):  
KENJI MIZUNO ◽  
SHUICHI SHIGETOMI ◽  
JUN-ICHIROH MATSUI ◽  
SOITSU FUKUSHI
Keyword(s):  
Angiotensin Ii ◽  
Spontaneously Hypertensive Rat ◽  
Angiotensin Ii Receptor ◽  
Spontaneously Hypertensive ◽  
Hypertensive Rat ◽  
The Brain

Enhanced depressor effect of bromocriptine in the DOCA/NaCl hypertensive rat

1985 ◽  
Vol 249 (1) ◽  
pp. H64-H70 ◽  
Author(s):  
S. Nagahama ◽  
Y. F. Chen ◽  
S. Oparil
Keyword(s):  
Adrenal Medulla ◽  
Dopaminergic System ◽  
Plasma Norepinephrine ◽  
Depressor Response ◽  
Hypertensive Rat ◽  
Basal Plasma ◽  
Plasma Prl ◽  
Depressor Effect ◽  
Dose Dependent

To elucidate the role of the dopaminergic system in the maintenance of hypertension in the deoxycorticosterone acetate (DOCA)/NaCl hypertensive rat, the responses of mean arterial pressure (MAP), plasma norepinephrine (NE), epinephrine (E), and prolactin (PRL) to intravenous (iv) administration of bromocriptine, a dopamine agonist, and hexamethonium bromide, a ganglion blocker, were examined in conscious, unrestrained 4-wk DOCA/NaCl hypertensive rats. Bromocriptine was administered to adrenomedullectomized (ADMX) rats to assess the role of the adrenal medulla in its depressor effect. Bromocriptine (50, 250, and 500 micrograms/kg) and hexamethonium (3 and 30 mg/kg) caused dose-dependent decreases in MAP that were greater in DOCA/NaCl rats than in uninephrectomized controls. Basal plasma NE, E, and PRL were significantly higher in DOCA/NaCl rats than in controls. Bromocriptine (500 micrograms/kg iv) decreased plasma PRL to undetectable levels and increased plasma E significantly without changing NE levels in DOCA/NaCl and uninephrectomized control rats. In ADMX rats bromocriptine (500 micrograms/kg iv) decreased MAP, PRL, and NE without affecting E levels. These results suggest that the depressor response to bromocriptine could be related to inhibition of sympathetic outflow without participation of the adrenal medulla. The hyperprolactinemia and enhanced depressor response to bromocriptine observed in DOCA/NaCl animals suggest that the dopaminergic system might be altered in this model of hypertension.

The renal endothelin system in the Prague hypertensive rat, a new model of spontaneous hypertension

1999 ◽  
Vol 97 (1) ◽  
pp. 91 ◽  
Author(s):  
Volker VOGEL ◽  
Angela BÄCKER ◽  
Jiri HELLER ◽  
Herbert J. KRAMER
Keyword(s):  
Spontaneous Hypertension ◽  
New Model ◽  
Hypertensive Rat ◽  
Endothelin System ◽  
Prague Hypertensive Rat
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