Role of nitric oxide in the arterial pressure and renal adaptations to long-term changes in sodium intake

1997 ◽  
Vol 272 (4) ◽  
pp. R1162-R1169 ◽  
Author(s):  
R. D. Manning ◽  
L. Hu ◽  
J. F. Reckelhoff
Keyword(s):  
Nitric Oxide ◽  
Arterial Pressure ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Urinary Sodium Excretion ◽  
Control Group ◽  
High Sodium ◽  
Sodium Sensitivity ◽  
High Sodium Intake

The goals of this study were to determine whether long-term nitric oxide (NO) synthesis inhibition in dogs results in an increase in the sodium sensitivity of arterial pressure and whether changes in plasma renin activity or the plasma concentrations of arginine vasopressin (AVP) and aldosterone play an important role in this hypertension. Studies were conducted in a control group and groups that received NO inhibition with N(G)-nitro-L-arginine methyl ester (L-NAME) at 10 or 25 microg x kg(-1) x min(-1). Each group was challenged with normal, low, and high sodium intake for periods of 5 days each. Urinary nitrate + nitrite excretion (UNOx) more than doubled in the control group during high sodium intake. In both L-NAME groups, UNOx decreased significantly, there was a hypertensive shift in the relation between urinary sodium excretion and arterial pressure, and urinary sodium excretion remained normal even in the high-sodium intake period. L-NAME infusion did not change the sodium sensitivity of arterial pressure or plasma renin activity, plasma aldosterone, and plasma AVP. In conclusion, the data suggest that, in dogs, increases in NO synthesis are not necessary to excrete a chronic sodium load, and decreases in NO do not increase the sodium sensitivity of arterial pressure.

scholarly journals Contribution of Nitric Oxide to Arterial Pressure and Heart Rate Variability in Rats Submitted to High-Sodium Intake

Hypertension ◽  
2001 ◽  
Vol 38 (3) ◽  
pp. 326-331 ◽  
Author(s):  
Silvia Lacchini ◽  
Elton L. Ferlin ◽  
Ruy S. Moraes ◽  
Jorge P. Ribeiro ◽  
Maria Claudia Irigoyen
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Arterial Pressure ◽  
Sodium Intake ◽  
High Sodium ◽  
High Sodium Intake

Chronic effects of a physiological dose of ANP on arterial pressure and renin release

1990 ◽  
Vol 258 (5) ◽  
pp. H1491-H1497
Author(s):  
S. D. Kivlighn ◽  
T. E. Lohmeier ◽  
H. M. Yang ◽  
Y. Shin
Keyword(s):  
Arterial Pressure ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Urinary Sodium Excretion ◽  
Renal Perfusion ◽  
Renin Release ◽  
Long Term Effects ◽  
Chronic Effects ◽  
Physiological Dose

To determine the long-term effects of a physiological dose of atrial natriuretic peptide (ANP) on renin release, the renin response to reductions in renal arterial pressure (RAP) was studied during 1) control conditions and 2) acute and 3) chronic (5 days) intravenous infusion (5 ng.kg-1.min-1) of alpha-human ANP in conscious dogs maintained on a normal sodium intake. Renal perfusion pressure was servo controlled at reduced levels with an inflatable occluder placed around the abdominal aorta just above the renal arteries. Under control conditions, reducing RAP by 30 and 40 mmHg increased plasma renin activity (PRA) 4- to 5- and 9- to 10-fold, respectively. Acute ANP infusion had no significant effect on either basal levels of PRA or the PRA response to reduced RAP. During chronic ANP infusion there was a two- to threefold increment in plasma ANP concentration and approximately a twofold increase in urinary sodium excretion on day 1; however, there were no significant long-term changes in mean arterial pressure, basal PRA, or the levels of PRA achieved during reductions in RAP. These findings indicate that the changes in plasma ANP concentration that occur under normal physiological conditions do not appreciably alter either basal PRA or renin release in response to renal hypotension in conscious sodium-replete dogs studied under resting conditions.

Renal and cardiac oxidative/nitrosative stress in salt-loaded pregnant rat

2007 ◽  
Vol 293 (4) ◽  
pp. R1657-R1665 ◽  
Author(s):  
Annie Beauséjour ◽  
Véronique Houde ◽  
Karine Bibeau ◽  
Rébecca Gaudet ◽  
Jean St-Louis ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Nitrosative Stress ◽  
Gestational Hypertension ◽  
Sodium Intake ◽  
Pregnant Rats ◽  
High Sodium ◽  
High Sodium Intake ◽  
Arterial Blood ◽  
Cardiac Ventricle

Sodium supplementation given for 1 wk to nonpregnant rats induces changes that are adequate to maintain renal and circulatory homeostasis as well as arterial blood pressure. However, in pregnant rats, proteinuria, fetal growth restriction, and placental oxidative stress are observed. Moreover, the decrease in blood pressure and expansion of circulatory volume, normally associated with pregnancy, are prevented by high-sodium intake. We hypothesized that, in these pregnant rats, a loss of the balance between prooxidation and antioxidation, particularly in kidneys and heart, disturbs the normal course of pregnancy and leads to manifestations such as gestational hypertension. We thus investigated the presence of oxidative/nitrosative stress in heart and kidneys following high-sodium intake in pregnant rats. Markers of this stress [8-isoprostaglandin F2α (8-iso-PGF2α) and nitrotyrosine], producer of nitric oxide [nitric oxide synthases (NOSs)], and antioxidants [superoxide dismutase (SOD) and catalase] were measured. Then, molecules (Na+-K+-ATPase and aconitase) or process [apoptosis (Bax and Bcl-2), inflammation (monocyte chemoattractant protein-1, connective tissue growth factor, and TNF-α)] susceptible to free radicals was determined. In kidneys from pregnant rats on 1.8% NaCl-water, NOSs, apoptotic index, and nitrotyrosine expression were increased, whereas Na+-K+-ATPase mRNA and activity were decreased. In the left cardiac ventricle of these rats, heightened nitrotyrosine, 8-iso-PGF2α, and catalase activity together with reduced endothelial NOS protein expression and SOD and aconitase activities were observed. These findings suggest that oxidative/nitrosative stress in kidney and left cardiac ventricle destabilizes the normal course of pregnancy and could lead to gestational hypertension.

Effects of Nifedipine during Low, Normal and High Intakes of Sodium in Patients with Essential Hypertension

1982 ◽  
Vol 63 (s8) ◽  
pp. 447s-450s ◽  
Author(s):  
Gloria Valdés ◽  
M. Eugenia Soto ◽  
Hector R. Croxatto ◽  
Teresa Bellolio ◽  
Ramón Corbalán ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Hypotensive Effect ◽  
Sodium Balance ◽  
Hypotensive Action ◽  
High Sodium ◽  
High Sodium Intake ◽  
Low Sodium Diet

1. Nifedipine (20 mg) was given by mouth to seven patients with moderate essential hypertension receiving a low, normal or high sodium intake. The drug produced an important hypotensive effect. Normal sodium intake enhanced the hypotensive action of the drug compared with that during the low and high sodium regimens. Blood pressure remained significantly lower 3 h after drug ingestion. 2. Increases in heart rate and plasma renin activity under all conditions reflected enhanced adrenergic activity. 3. A short-term natriuresis followed nifedipine ingestion in spite of increased aldosterone excretion during the low sodium diet and a decrease in urinary kallikrein during the low and high sodium diets. 4. Nifedipine increased urinary volume only during the high sodium intake. 5. Apart from vasodilatation, nifedipine induces important changes in neurogenic, renal and adrenal mechanisms that regulate blood pressure homoeostasis. Different conditions of sodium balance modulate most of these effects.

Superoxide Formation and Interaction with Nitric Oxide Modulate Systemic Arterial Pressure and Renal Function in Salt-Depleted Dogs

2006 ◽  
Vol 231 (3) ◽  
pp. 269-276 ◽  
Author(s):  
Utpal K. Dutta ◽  
Jason Lane ◽  
L. Jackson Roberts ◽  
Dewan S. A. Majid
Keyword(s):  
Nitric Oxide ◽  
Arterial Pressure ◽  
Salt Intake ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Urinary Sodium Excretion ◽  
Systemic Arterial Pressure ◽  
Nitric Oxide Synthase Inhibitor ◽  
Basal Plasma ◽  
Synthase Inhibitor

To determine the role of superoxide (O2–) formation in the kidney during alterations in the renin-angiotensin system, we evaluated responses to the intra-arterial infusion of an O2–-scavenging agent, tempol, in the denervated kidney of anesthetized salt-depleted (SD, n = 6) dogs and salt-replete (SR, n = 6) dogs. As expected, basal plasma renin activity was higher in SD than in SR dogs (8.4 ± 1.0 vs. 2.3 ± 0.6 ng angiotensin 1/ml/hr). Interestingly, the basal level of urinary F2-isoprostanes excretion (marker for endogenous O2– activity) relative to creatinine (Cr) excretion was also significantly higher in SD compared to SR dogs (9.1 ± 2.8 vs. 1.6 ± 0.4 ng F2-isoprostanes/mg of Cr). There was a significant increase in renal blood flow (4.3 ± 0.5 to 4.9 ± 0.6 ml/min/g) and decreases in renal vascular resistance (38.2 ± 5.8 to 33.2 ± 4.7 mm Hg/ml/min/g) and mean systemic arterial pressure (148 ± 6 to 112 ± 10 mm Hg) in SD dogs but not in SR dogs during infusion of tempol at 1 mg/kg/min for 30 mins. Glomerular filtration rate and urinary sodium excretion (UNaV) did not change significantly during tempol infusion in both groups of dogs. Administration of the nitric oxide synthase inhibitor nitro-L-arginine (50 μg/kg/min) during tempol infusion caused a reduction in UNaV in SR dogs (47% ± 12%) but did not cause a decrease in SD dogs. These data show that low salt intake enhances O2– activity that influences renal and systemic hemodynamics and thus may contribute to the regulation of arterial pressure in the salt-restricted state.

Suppression of plasma renin and aldosterone in stress-salt hypertension in dogs

1986 ◽  
Vol 251 (1) ◽  
pp. R181-R186 ◽  
Author(s):  
D. E. Anderson ◽  
C. Gomez-Sanchez ◽  
J. R. Dietz
Keyword(s):  
Arterial Pressure ◽  
Avoidance Conditioning ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Saline Infusion ◽  
Base Line ◽  
Angiotensin I ◽  
High Sodium ◽  
Salt Hypertension ◽  
Hormone Sensitive

Plasma renin activity (PRA) and plasma aldosterone concentrations (PAC) of 12 intact chronically instrumented dogs were measured at midday after 1) 7-12 days of normal sodium intake and no behavioral stress, 2) 7-12 days of continuous saline infusion (1.34 l/day) only, and/or 3) 7-12 days of saline infusion and avoidance-conditioning sessions. The saline infusion procedure did not significantly change arterial pressure or heart rate relative to base line but was associated with a consistent decrease in PRA (-0.90 +/- 0.38 ng angiotensin I . ml-1 . h-1) and PAC (-3.6 +/- 1.1 ng/dl). The combination of saline infusion and avoidance conditioning resulted in significant elevations in arterial pressure, but, again, both PRA (-1.46 +/- 0.16 ng angiotensin I . ml-1 . h-1) and PAC (-3.7 +/- 1.1 ng/dl) were significantly decreased. These results show that high sodium intake decreased aldosterone via suppression of renin release but do not rule out a possible hypertensinogenic role for stress-induced adrenocorticotrophic hormone-sensitive corticoids.

Effect of sodium intake on insulin sensitivity

1993 ◽  
Vol 264 (5) ◽  
pp. E730-E734 ◽  
Author(s):  
D. S. Donovan ◽  
C. G. Solomon ◽  
E. W. Seely ◽  
G. H. Williams ◽  
D. C. Simonson
Keyword(s):  
Insulin Sensitivity ◽  
Sodium Intake ◽  
Random Order ◽  
Urinary Sodium Excretion ◽  
High Sodium ◽  
High Sodium Intake ◽  
Disease States ◽  
Low Sodium Diet ◽  
White Males ◽  
Highly Correlated

To examine the effects of sodium intake on insulin sensitivity, we performed euglycemic insulin clamp studies (40 mU.m-2.min-1) in eight healthy normotensive nondiabetic white males (age = 36 +/- 5 yr; wt = 66 +/- 3 kg) after 5 days on high (200 meq/day)- and low (10 meq/day)-sodium diets administered in random order. High sodium intake was associated with significantly greater urinary sodium excretion (160 +/- 7 vs. 8 +/- 2 meq/day; P < 0.0001), suppression of plasma aldosterone (7 +/- 3 vs. 38 +/- 6 ng/dl; P < 0.001) and renin (1.5 +/- 0.2 vs. 6.0 +/- 0.9 ng.ml-1.h-1; P < 0.005) levels, but no change in blood pressure (116 +/- 3/63 +/- 2 vs. 114 +/- 3/64 +/- 2 mmHg; P = not significant). The rate of glucose infusion during the clamp was significantly reduced during the high- vs. low-sodium diet (279 +/- 19 vs. 334 +/- 24 mg.m-2.min-1; P < 0.01). This impairment in insulin sensitivity was not related to changes in serum potassium, epinephrine, norepinephrine, cortisol, or growth hormone but was highly correlated with an increment in circulating free fatty acid levels during high sodium intake (r = 0.82, P < 0.05). These data suggest that 1) high sodium intake may exacerbate insulin resistance by increasing circulating free fatty acids, and 2) differences in sodium intake may influence measures of insulin sensitivity in other disease states.

Sign in / Sign up

Export Citation Format

Share Document