Effect of chronic renal medullary nitric oxide inhibition on blood pressure

1994 ◽  
Vol 266 (5) ◽  
pp. H1918-H1926 ◽  
Author(s):  
D. L. Mattson ◽  
S. Lu ◽  
K. Nakanishi ◽  
P. E. Papanek ◽  
A. W. Cowley
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Blood Flow ◽  
Renal Medulla ◽  
Sodium Balance ◽  
Sprague Dawley ◽  
Nitric Oxide Inhibition ◽  
Medullary Blood Flow ◽  
Nitric Oxide Inhibitor ◽  
Oxide Inhibition

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.

Role of renal medullary blood flow in the development of L-NAME hypertension in rats

1995 ◽  
Vol 268 (2) ◽  
pp. R317-R323 ◽  
Author(s):  
K. Nakanishi ◽  
D. L. Mattson ◽  
A. W. Cowley
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Flow Distribution ◽  
Renal Medulla ◽  
Sodium Balance ◽  
Cortical Blood Flow ◽  
Medullary Blood Flow ◽  
Intrarenal Blood Flow ◽  
Renal Medullary Blood Flow ◽  
Renal Cortical Blood Flow

The effect of chronic intravenous infusion of the nitric oxide inhibitor NG-nitro-L-arginine methyl ester (L-NAME; 8.6 mg.kg-1.day-1) on blood pressure, intrarenal blood flow distribution, and sodium and water balance was studied in conscious rats. On the 1st day of intravenous L-NAME infusion, renal medullary blood flow was reduced by 22%, renal cortical blood flow was unaltered, approximately 1 meq of sodium and 12 ml of water were retained, and blood pressure increased from 96 +/- 2 to 118 +/- 2 mmHg. Medullary blood flow was maintained at this decreased level, sodium continued to be retained, body weight continued to increase, and blood pressure remained elevated for the 5 days of L-NAME infusion. During the postcontrol period, blood flow in the renal medulla returned to levels not significantly different from control; the animals went into negative sodium balance and stopped gaining weight, and blood pressure returned to control. The present experiments indicate that decreased renal medullary blood flow and retention of sodium and water play an important role in the development of hypertension during chronic systemic L-NAME administration despite no measurable changes in renal cortical blood flow.

scholarly journals The effect of chronic nitric oxide inhibition on vascular reactivity and blood pressure in pregnant rats

1999 ◽  
Vol 117 (5) ◽  
pp. 197-204 ◽  
Author(s):  
Nilton Hideto Takiuti ◽  
Maria Helena Cetelli Carvalho ◽  
Soubhi Kahhale ◽  
Dorothy Nigro ◽  
Hermes Vieira Barbeiro ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Vascular Reactivity ◽  
Unit Weight ◽  
Control Group ◽  
Pregnant Rats ◽  
Nitric Oxide Inhibition ◽  
Female Wistar Rats ◽  
Main Component ◽  
Oxide Inhibition

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.

20-HETE-mediated vasoconstriction by hemoglobin-O2 carrier in Sprague-Dawley but not Wistar rats

2005 ◽  
Vol 98 (3) ◽  
pp. 772-779 ◽  
Author(s):  
Andrew D. Baines ◽  
Patrick Ho
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Blood Flow ◽  
Wistar Rats ◽  
Filtration Rate ◽  
Blood Substitutes ◽  
Sprague Dawley ◽  
Ringer Lactate ◽  
Sd Rats ◽  
Renal Vascular

Hypothetically either decreased nitric oxide (NO) or increased O2 could initiate 20-HETE-mediated vasoconstriction associated with hemoglobin-based blood substitutes (HBOC). To test this hypothesis, we infused Tm-Hb, an HBOC with low O2 affinity, into isoflurane-anesthetized Wistar (W) and Sprague-Dawley (SD) rats after exchanging 20% of their blood with Ringer lactate. For comparison we infused an equal amount of BSA or BSA with NG-nitro-l-arginine methyl ester (BSA+NAME). Tm-Hb increased blood pressure (BP) and renal vascular resistance (RVR) equally in W and SD rats. Renal blood flow (RBF; Doppler ultrasound) decreased. BSA decreased RVR and raised glomerular filtration rate. BSA+NAME raised BP, RVR, and GFR. HET0016, an inhibitor of 20-HETE production, blunted BP and RVR responses to Tm-Hb and BSA+NAME in SD but not W rats. Arterial O2 content with BSA was lower than with Tm-Hb but O2 delivery was 60% higher with BSA because of higher RBF. BSA raised Po2 (Oxylite) in cortex and medulla and reduced RVR. Tm-Hb decreased Po2 and increased RVR. Switching rats from breathing air to 100% O2 raised intrarenal Po2 two- to threefold and increased BP and RVR. HET0016 did not alter hyperoxic responses. In conclusion, 20-HETE contributes to vasoconstriction by Tm-Hb in SD but not in W rats, and increased 20-HETE activity results primarily from decreased NO.

scholarly journals Nitric Oxide Inhibition Impairs Blood Flow During Exercise in Hearts With a Collateral-Dependent Myocardial Region

1998 ◽  
Vol 31 (1) ◽  
pp. 67-74 ◽  
Author(s):  
Jay H Traverse ◽  
James W Kinn ◽  
Christopher Klassen ◽  
Dirk J Duncker ◽  
Robert J Bache
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Nitric Oxide Inhibition ◽  
Oxide Inhibition

scholarly journals Reactive oxygen species as important determinants of medullary flow, sodium excretion, and hypertension

2015 ◽  
Vol 308 (3) ◽  
pp. F179-F197 ◽  
Author(s):  
Allen W. Cowley ◽  
Michiaki Abe ◽  
Takefumi Mori ◽  
Paul M. O'Connor ◽  
Yusuke Ohsaki ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Hydrogen Peroxide ◽  
Blood Flow ◽  
Reactive Oxygen ◽  
Selective Reduction ◽  
Renal Medulla ◽  
Thick Ascending Limb ◽  
Oxygen Species ◽  
Medullary Blood Flow

The physiological evidence linking the production of superoxide, hydrogen peroxide, and nitric oxide in the renal medullary thick ascending limb of Henle (mTAL) to regulation of medullary blood flow, sodium homeostasis, and long-term control of blood pressure is summarized in this review. Data obtained largely from rats indicate that experimentally induced elevations of either superoxide or hydrogen peroxide in the renal medulla result in reduction of medullary blood flow, enhanced Na+ reabsorption, and hypertension. A shift in the redox balance between nitric oxide and reactive oxygen species (ROS) is found to occur naturally in the Dahl salt-sensitive (SS) rat model, where selective reduction of ROS production in the renal medulla reduces salt-induced hypertension. Excess medullary production of ROS in SS rats emanates from the medullary thick ascending limbs of Henle [from both the mitochondria and membrane NAD(P)H oxidases] in response to increased delivery and reabsorption of excess sodium and water. There is evidence that ROS and perhaps other mediators such as ATP diffuse from the mTAL to surrounding vasa recta capillaries, resulting in medullary ischemia, which thereby contributes to hypertension.

NITRIC OXIDE INHIBITION IN SPRAGUE DAWLEY RATS CAUSES SEVERE HYPERTENSION AND RENAL INSUFFICIENCY

2004 ◽  
Vol 22 (Suppl. 2) ◽  
pp. S282
Author(s):  
F. Therrien ◽  
P. Lavoie ◽  
M. Agharazzi ◽  
M. Lebel ◽  
R. Larivière
Keyword(s):  
Nitric Oxide ◽  
Renal Insufficiency ◽  
Severe Hypertension ◽  
Sprague Dawley ◽  
Nitric Oxide Inhibition ◽  
Sprague Dawley Rats ◽  
Oxide Inhibition

scholarly journals Increased activity and expression of Ca2+-dependent NOS in renal cortex of ANG II-infused hypertensive rats

1999 ◽  
Vol 277 (5) ◽  
pp. F797-F804 ◽  
Author(s):  
So Yeon Chin ◽  
Kailash N. Pandey ◽  
Shang-Jin Shi ◽  
Hiroyuki Kobori ◽  
Carol Moreno ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Renal Cortex ◽  
Renal Medulla ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Differential Distribution ◽  
Cortical Blood Flow ◽  
Renal Cortical Blood Flow

We have previously demonstrated that nitric oxide (NO) exerts a greater modulatory influence on renal cortical blood flow in ANG II-infused hypertensive rats compared with normotensive rats. In the present study, we determined nitric oxide synthase (NOS) activities and protein levels in the renal cortex and medulla of normotensive and ANG II-infused hypertensive rats. Enzyme activity was determined by measuring the rate of formation ofl-[14C]citrulline froml-[14C]arginine. Western blot analysis was performed to determine the regional expression of endothelial (eNOS), neuronal (nNOS), and inducible (iNOS) isoforms in the renal cortex and medulla of control and ANG II-infused rats. Male Sprague-Dawley rats were prepared by the infusion of ANG II at a rate of 65 ng/min via osmotic minipumps implanted subcutaneously for 13 days and compared with sham-operated rats. Systolic arterial pressures were 127 ± 2 and 182 ± 3 mmHg in control ( n = 13) and ANG II-infused rats ( n = 13), respectively. The Ca2+-dependent NOS activity, expressed as picomoles of citrulline formed per minute per gram wet weight, was higher in the renal cortex of ANG II-infused rats (91 ± 11) than in control rats (42 ± 12). Likewise, both eNOS and nNOS were markedly elevated in the renal cortex of the ANG II-treated rats. In both groups of rats, Ca2+-dependent NOS activity was higher in the renal medulla than in the cortex; however, no differences in medullary NOS activity were observed between the groups. Also, no differences in medullary eNOS levels were observed between the groups; however, medullary nNOS was decreased by 45% in the ANG II-infused rats. For the Ca2+-independent NOS activities, the renal cortex exhibited a greater activity in the control rats (174 ± 23) than in ANG II-infused rats (101 ± 10). Similarly, cortical iNOS was greater by 47% in the control rats than in ANG II-treated rats. No differences in the activity were found for the renal medulla between the groups. There was no detectable signal for iNOS in the renal medulla for both groups. These data indicate that there is a differential distribution of NOS activity, with the Ca2+-dependent activity and protein expression higher in the renal cortex of ANG II-infused rats compared with control rats, and support the hypothesis that increased constitutive NOS activity exerts a protective effect in ANG II-induced hypertension to maintain adequate renal cortical blood flow.

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