Nitric Oxide Inhibition in the Rat Improves Blood Pressure and Renal Function During Hypovolemic Shock.

1991 ◽  
Author(s):  
Wilfred Lieberthal ◽  
Amy E. McGarry ◽  
James Sheils ◽  
C. R. Valeri
1999 ◽  
Vol 117 (5) ◽  
pp. 197-204 ◽  
Author(s):  
Nilton Hideto Takiuti ◽  
Maria Helena Cetelli Carvalho ◽  
Soubhi Kahhale ◽  
Dorothy Nigro ◽  
Hermes Vieira Barbeiro ◽  
...  

CONTEXT: The exact mechanism involved in changes in blood pressure and peripheral vascular resistance during pregnancy is unknown. OBJECTIVE:To evaluate the importance of endothelium-derivated relaxing factor (EDRF) and its main component, nitric oxide, in blood pressure and vascular reactivity in pregnant rats. DESIGN: Clinical trial in experimentation animals. SETTING: University laboratory of Pharmacology. SAMPLE: Female Wistar rats with normal blood pressure, weight (152 to 227 grams) and age (90 to 116 days). INTERVENTION: The rats were divided in to four groups: pregnant rats treated with L-NAME (13 rats); pregnant control rats (8 rats); virgin rats treated with L-NAME (10 rats); virgin control rats (12 rats). The vascular preparations and caudal blood pressure were obtained at the end of pregnancy, or after the administration of L-NAME in virgin rats. MAIN MEASUREMENTS: The caudal blood pressure and the vascular response to acetylcholine in pre-contracted aortic rings, both with and without endothelium, and the effect of nitric oxide inhibition, Nw-L-nitro-arginine methyl-ester (L-NAME), in pregnant and virgin rats. The L-NAME was administered in the drinking water over a 10-day period. RESULTS: The blood pressure decreased in pregnancy. Aortic rings of pregnant rats were more sensitive to acetylcholine than those of virgin rats. After L-NAME treatment, the blood pressure increased and relaxation was blocked in both groups. The fetal-placental unit weight of the L-NAME group was lower than that of the control group. CONCLUSION: Acetylcholine-induced vasorelaxation sensitivity was greater in pregnant rats and that blood pressure increased after L-NAME administration while the acetylcholine-induced vasorelaxation response was blocked.


1994 ◽  
Vol 22 (1) ◽  
pp. A123 ◽  
Author(s):  
Werner Lingnau ◽  
Roy McGuire ◽  
Lillian D Traber ◽  
Naoki Matsumoto ◽  
Daniel L Traber

Physiology ◽  
1994 ◽  
Vol 9 (6) ◽  
pp. 268-271
Author(s):  
V Lahera ◽  
AA Khraibi

In normotensive rats, natriuresis and diuresis resulting from a pressor dose of nitric oxide (NO) inhibitors are primarily due to a pressure-natriuresis phenomenon. In the Okamoto spontaneously hypertensive rat, administration of the same dose of NO inhibitor does not increase blood pressure but produces exaggerated natriuresis and diuresis.


2003 ◽  
Vol 21 (7) ◽  
pp. 1339-1346 ◽  
Author(s):  
Angelo Scuteri ◽  
Markus C Stuehlinger ◽  
John P Cooke ◽  
Jeanette G Wright ◽  
Edward G Lakatta ◽  
...  

1994 ◽  
Vol 266 (5) ◽  
pp. H1918-H1926 ◽  
Author(s):  
D. L. Mattson ◽  
S. Lu ◽  
K. Nakanishi ◽  
P. E. Papanek ◽  
A. W. Cowley

The effects of chronic nitric oxide inhibition in the renal medulla on renal cortical and medullary blood flow, sodium balance, and blood pressure were evaluated in conscious uninephrectomized Sprague-Dawley rats. During a 5-day renal medullary interstitial infusion of the nitric oxide inhibitor NG-nitro-L-arginine methyl ester (L-NAME, 120 micrograms/h) in saline (0.5 ml/min), renal medullary blood flow was selectively decreased by 30% after 2 h and was maintained at that level for the entire infusion. The decrease in medullary blood flow was associated with sodium retention and increased blood pressure. After the cessation of L-NAME infusion, medullary blood flow returned to control, and the sodium balance became negative as blood pressure returned to baseline. These data indicate that renal medullary nitric oxide plays an important role in the regulation of renal blood flow, sodium excretion, and blood pressure.


1994 ◽  
Vol 1 ◽  
pp. 276
Author(s):  
Y. Konishi ◽  
M. Okamura ◽  
M. Nishimura ◽  
N. Negoro ◽  
T. Inoue ◽  
...  

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