High Sodium Sensitivity Implicates Nocturnal Hypertension in Essential Hypertension

Hypertension ◽  
1996 ◽  
Vol 28 (1) ◽  
pp. 139-142 ◽  
Author(s):  
Takashi Uzu ◽  
Frida S. Kazembe ◽  
Kazuhiko Ishikawa ◽  
Satoko Nakamura ◽  
Takashi Inenaga ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Nocturnal Hypertension ◽  
High Sodium ◽  
Sodium Sensitivity

Sodium sensitivity of blood pressure and baroreceptor reflex function in patients with essential hypertension

1988 ◽  
Vol 6 (4) ◽  
pp. S209-212 ◽  
Author(s):  
Akira Sakaguchi ◽  
Toshihiro Saito ◽  
Kazutoshi Yamamoto ◽  
Jiro Iwata ◽  
Masahide Tonooka ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Baroreceptor Reflex ◽  
Sodium Sensitivity

scholarly journals Sodium Sensitivity, Sodium Resistance, and Incidence of Hypertension

Hypertension ◽  
2021 ◽  
Author(s):  
Jiang He ◽  
Jian-Feng Huang ◽  
Changwei Li ◽  
Jing Chen ◽  
Xiangfeng Lu ◽  
...  
Keyword(s):  
Sodium Intake ◽  
Experimental Studies ◽  
Dietary Sodium ◽  
Cross Sectional ◽  
Incident Hypertension ◽  
High Sodium ◽  
Sodium Sensitivity ◽  
Sodium Diet ◽  
Low Sodium ◽  
Increased Risk

Cross-sectional studies have reported that high sodium sensitivity is more common among individuals with hypertension. Experimental studies have also reported various animal models with sodium-resistant hypertension. It is unknown, however, whether sodium sensitivity and resistance precede the development of hypertension. We conducted a feeding study, including a 7-day low-sodium diet (1180 mg/day) followed by a 7-day high-sodium diet (7081 mg/day), among 1718 Chinese adults with blood pressure (BP) <140/90 mm Hg. We longitudinally followed them over an average of 7.4 years. Three BP measurements and 24-hour urinary sodium excretion were obtained on each of 3 days during baseline observation, low-sodium and high-sodium interventions, and 2 follow-up studies. Three trajectories of BP responses to dietary sodium intake were identified using latent trajectory analysis. Mean (SD) changes in systolic BP were −13.7 (5.5), −4.9 (3.0), and 2.4 (3.0) mm Hg during the low-sodium intervention and 11.2 (5.3), 4.4 (4.1), and −0.2 (4.1) mm Hg during the high-sodium intervention ( P <0.001 for group differences) in high sodium-sensitive, moderate sodium-sensitive, and sodium-resistant groups, respectively. Compared with individuals with moderate sodium sensitivity, multiple-adjusted odds ratios (95% CIs) for incident hypertension were 1.43 (1.03–1.98) for those with high sodium sensitivity and 1.43 (1.03–1.99) for those with sodium resistance ( P =0.006 for nonlinear trend). Furthermore, a J-shaped association between systolic BP responses to sodium intake and incident hypertension was identified ( P <0.001). Similar results were observed for diastolic BP. Our study indicates that individuals with either high sodium sensitivity or sodium resistance are at an increased risk for developing hypertension.

Alterations in Cerebrospinal Fluid Angiotensin II by Sodium Intake in Patients with Essential Hypertension

1989 ◽  
Vol 77 (4) ◽  
pp. 389-394 ◽  
Author(s):  
Minoru Kawamura ◽  
Yuhei Kawano ◽  
Kaoru Yoshida ◽  
Masahito Imanishi ◽  
Satoshi Akabane ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Essential Hypertension ◽  
Sodium Intake ◽  
Ang Ii ◽  
Sodium Depletion ◽  
High Sodium ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium

1. Angiotensin (ANG) levels were measured in the cerebrospinal fluid of 15 patients with essential hypertension on a high sodium diet for 1 week and on a low sodium diet for a further week. ANGs were determined using a system of extraction by Sep-Pak cartridges followed by h.p.l.c. combined with radioimmunoassay. 2. Sodium depletion resulted in increases of ANG II in the cerebrospinal fluid from 1.16 ± 0.38 (sem) to 1.83 ± 0.43 fmol/ml (P < 0.01) and of ANG III from 0.65 ± 0.11 to 0.86 ± 0.15 fmol/ml (P < 0.01). 3. The ANG II level in the cerebrospinal fluid was found to be unchanged and recovery of added ANG II was approximately 90%, even after incubation for 3 h, on both diets. Thus, it is unlikely that ANG II is produced or degraded in the cerebrospinal fluid in vitro. 4. There was no significant correlation between the cerebrospinal fluid and the plasma ANG II concentration on the low sodium diet. 5. These results suggest that the cerebrospinal fluid ANG II level increases with sodium depletion, and that the effect of the level of ANG II on the activity of the angiotensin-forming system in the central nervous system may be assessed by determination of ANG II in the cerebrospinal fluid in patients with essential hypertension.

Plasma Progesterone in Normal Subjects and Patients with Benign Essential Hypertension on Normal, Low, and High Sodium Intake1

1972 ◽  
Vol 34 (4) ◽  
pp. 650-660 ◽  
Author(s):  
C. SASAKI ◽  
W. NOWACZYNSKI ◽  
O. KUCHEL ◽  
C. CHAVEZ ◽  
F. LEDOUX ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Normal Subjects ◽  
Plasma Progesterone ◽  
High Sodium

Relation of obesity, high sodium intake, and eccentric left ventricular hypertrophy to left ventricular exercise dysfunction in essential hypertension

1990 ◽  
Vol 88 (5) ◽  
pp. 477-485 ◽  
Author(s):  
James Blake ◽  
Richard B. Devereux ◽  
Jeffrey S. Borer ◽  
Massimiliano Szulc ◽  
Thomas W. Pappas ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Sodium Intake ◽  
Left Ventricular ◽  
High Sodium ◽  
High Sodium Intake

Reversed Diurnal Blood Pressure Rhythm in Hypertensive Pregnancies

1976 ◽  
Vol 51 (s3) ◽  
pp. 687s-689s ◽  
Author(s):  
C. W. G. Redman ◽  
L. J. Beilin ◽  
J. Bonnar
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Severe Hypertension ◽  
Practical Importance ◽  
Theoretical Interest ◽  
Hypotensive Drug ◽  
Pressure Pattern ◽  
Nocturnal Hypertension ◽  
Hypertension In Pregnancy ◽  
In Pregnancy

1. Reversal of the normal diurnal blood pressure pattern has been demonstrated in women with severe hypertension and renal impairment in pregnancy (pre-eclampsia). 2. Maximum arterial pressure occurred at night in these women. The phenomenon was not due to hypotensive drug therapy or posture. Patients with uncomplicated essential hypertension in pregnancy retained a normal diurnal blood pressure pattern. 3. Nocturnal hypertension in pre-eclampsia is of theoretical interest and practical importance.

Abstract 058: High Sodium Intake Induces a Catabolic State via Glomerular Hyperfiltration and Enhanced Glomerulotubular Balance in Essential Hypertension

Hypertension ◽  
2019 ◽  
Vol 74 (Suppl_1) ◽  
Author(s):  
Giacomo Rossitto ◽  
Giuseppe Maiolino ◽  
Silvia Lerco ◽  
Giulio Ceolotto ◽  
Gavin Blackburn ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Sodium Intake ◽  
Glomerular Hyperfiltration ◽  
High Sodium ◽  
High Sodium Intake ◽  
Catabolic State ◽  
Glomerulotubular Balance

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.

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