Renal and Cardiovascular Effects of Exogenous Insulin in Healthy Volunteers

1991 ◽  
Vol 80 (3) ◽  
pp. 219-225 ◽  
Author(s):  
R. O. B. Gans ◽  
L. v.d. Toorn ◽  
H. J. G. Bilo ◽  
J. J. P. Nauta ◽  
R. J. Heine ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Analysis Of Variance ◽  
Sodium Excretion ◽  
Circadian Variation ◽  
Cardiovascular Effects ◽  
Insulin Dosage ◽  
Angiotensin I ◽  
Blood Pressure Elevation ◽  
Fractional Sodium Excretion

1. Renal and cardiovascular effects of three dosages of insulin [50 (Ins I), 300 (Ins II) and 500 (Ins III) m-units h−1 kg−1] were investigated in healthy males by using a euglycaemic clamp technique. On separate days, control experiments were carried out to correct for any circadian variation in the variables studied. 2. All three insulin dosages resulted in a marked decline in fractional sodium excretion (actual experiments: basal, 0.95 ± 0.15%, Ins I, 0.79 ± 0.10%, Ins II, 0.80 ± 0.12%, Ins III, 0.84 ± 0.08%; control experiments: basal, 0.96 ± 0.10%, Ins I, 1.20 ± 0.12%, Ins II, 1.53 ± 0.15%, Ins III, 1.43 ± 0.10%; means ± sem, P < 0.005, analysis of variance). With the highest insulin dosage, the reduction in fractional sodium excretion tended to be less striking. This coincided with a rise in heart rate, pulse pressure and pulse rate-systolic blood pressure product (double product). Although blood pressure itself did not change, systolic blood pressure also tended to increase (actual experiments: basal, 133 ± 5 mmHg, Ins I, 132 ± 5 mmHg, Ins II, 139 ± 5 mmHg, Ins III, 143 ± 4 mmHg; control experiments: basal, 128 ± 3 mmHg, Ins I, 129 ± 3 mmHg, Ins II, 130 ± 3 mmHg, Ins III, 133 ± 3 mmHg; means ± sem, P = 0.09, analysis of variance). There was a positive correlation between the change in fractional sodium excretion and the change in systolic blood pressure over control values (r = 0.696, P < 0.028). At a rise in systolic blood pressure of 18 mmHg, the sodium-retaining effect of insulin appeared to be offset. A shift of the pressure-natriuresis relation to the right is suggested. 3. Plasma catecholamines did not change. Plasma renin activity increased from 1.11 ± 0.17 (basal) to 2.13 ± 0.31 (Ins III) pmol of angiotensin I h−1 ml−1; on the control day, a decline from 1.28 ± 0.24 (basal) to 0.81 ± 0.13 (Ins III) pmol of angiotensin I h−1 ml−1 was noted (P < 0.001). Despite this rise no concomitant rise in plasma aldosterone occurred. 4. Chronic hyperinsulinaemia may lead to blood pressure elevation in the long-term if it is postulated that resistance to the glucose-lowering effect of insulin is absent for the effects of insulin on the kidney and the cardiovascular system.

scholarly journals Urinary sodium excretion and the risk of cardiovascular disease: A community-based cohort study in Taiwan

2021 ◽  
pp. 1-42
Author(s):  
Yi-Jie Wang ◽  
Kuo-Lioug Chien ◽  
Hsiu-Ching Hsu ◽  
Hung-Ju Lin ◽  
Ta-Chen Su ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Metabolic Syndrome ◽  
Systolic Blood Pressure ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Salt Sensitivity ◽  
Urinary Sodium ◽  
Mediating Effect ◽  
Cvd Risk ◽  
Media Thickness

Abstract Urinary sodium excretion is a potential risk factor for cardiovascular diseases (CVD). However, the underlying biological mechanisms and effects of salt sensitivity are unclear. The purpose of this study was to characterize the relative contribution of biological factors to the sodium-CVD association. A total of 2112 participants were enrolled in this study. Structured questionnaires and blood and urine samples were obtained. Twenty-four-hour sodium excretion was estimated using a single overnight urine sample. Hypertension, metabolic syndrome, and overweight status were considered to indicate salt sensitivity. Cox proportional hazard models were used to investigate the effects of salt sensitivity on urinary sodium excretion and CVD risk. The traditional mediation approach was used to calculate the proportion of mediation. The mean age (standard deviation) of the 2112 participants was 54.5 (12.2) years, and they were followed up for a mean of 14.1 [8.1] years. Compared with those in the lowest quartile, the highest baseline urinary sodium excretion (>4.2g/24 hours) was associated with a 43% higher CVD risk (hazard ratio, 1.43; 95% confidence interval, 1.02-1.99). Participants with high urinary sodium excretion, hypertension, or metabolic syndrome had a significantly high risk of CVD. The carotid intima-media thickness had the largest mediating effect (accounting for 35% of the sodium-CVD association), followed by systolic blood pressure (33%), left ventricular mass (28%), and diastolic blood pressure (14%). Higher urinary sodium excretion increased the risk of CVD, which was explained largely by carotid media-thickness and systolic blood pressure.

P1691Impact of dose and duration of dietary salt reduction on blood pressure levels: systematic review and meta-analysis of randomised trials

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
L Huang ◽  
K Trieu ◽  
S Yoshimura ◽  
M Woodward ◽  
N Campbell ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Diastolic Blood Pressure ◽  
Sodium Excretion ◽  
Salt Intake ◽  
Meta Analysis ◽  
Dietary Salt ◽  
Baseline Blood Pressure ◽  
Salt Reduction ◽  
The Impact

Abstract Background Authoritative medical and public health agencies in most countries advise to reduce population dietary salt intake to under 5–6 g/day as a strategy for preventing high blood pressure and cardiovascular disease. However, there is still dispute about whether salt reduction should be adopted by all populations. In addition, the effect of duration of dietary salt reduction has not been sufficiently investigated. Purpose To understand the effect of dietary salt reduction on blood pressure and the impact of intervention duration. Methods A systematic review and meta-analysis was conducted. Randomized controlled trials that allocated participants to low and high salt intake, without confounding from unequal concomitant interventions, were included. We excluded studies done in individuals younger than 18 years, pregnant women, individuals with renal disease or heart failure, and studies with sodium excretion estimated from spot urine. Random effect meta-analysis was used to generate pooled estimates of the effect on 24-hour urinary sodium excretion, systolic and diastolic blood pressure. Multivariate meta-regression was used to quantify the dose response effect of dietary salt on blood pressure change and to understand the impact of the intervention duration. Results 125 studies were included with 162 data points extracted. Ninety-nine data points (61%) had interventions under 4 weeks. Overall, 24-hour urinary sodium excretion changed by −141 mmol (95% CI: −156; −126), systolic blood pressure changed by −4.4 mm Hg (95% CI: −5.2; −3.7) and diastolic blood pressure changed by −2.4 mm Hg (95% CI: −2.9; −1.9). Sodium reduction resulted in a significant decrease of systolic blood pressure in all subgroups except in participants with low baseline sodium intake (<109 mmol) (Figure 1). Each 100 mmol reduction of sodium was associated with 2.7 mm Hg (95% CI: 1.0; 4.4; p=0.002) reduction of systolic blood pressure and 1.2 mm Hg (95% CI: 0.0; 2.4; p=0.046) reduction of diastolic blood pressure after adjusting for intervention duration, age, sex, race, baseline blood pressure, baseline sodium intake and interaction between age and baseline blood pressure. For the same amount of salt reduction, a 10 mm Hg higher baseline systolic blood pressure would result in 2.5 mm Hg greater reduction of systolic blood pressure. There is not enough evidence to show the impact of intervention duration. Figure 1 Conclusions Our meta-analysis showed that sodium reduction could reduce blood pressure in all adult populations regardless of age, sex and race. The effect of salt reduction on systolic blood pressure increases with higher baseline blood pressure. Further studies, designed to investigate the impact of intervention duration, are needed to understand the significance of the duration. Acknowledgement/Funding None

EFFECTS OF 9-ALPHA-FLUOROHYDROCORTISONE ON BLOOD PRESSURE, PLASMA VOLUME, AND SODIUM, POTASSIUM AND WATER BALANCE IN RATS

1974 ◽  
Vol 76 (3) ◽  
pp. 539-555 ◽  
Author(s):  
D. Haack ◽  
E. Hackenthal ◽  
E. Homsy ◽  
B. Möhring ◽  
J. Möhring
Keyword(s):  
Blood Pressure ◽  
Water Balance ◽  
Plasma Volume ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Sodium Concentration ◽  
Urinary Sodium ◽  
Blood Pressure Elevation ◽  
High Doses ◽  
Water And Sodium Excretion

ABSTRACT In normal rats on a standard sodium diet, the administration of 9-alpha-fluorohydrocortisone (9aFF) induced a rapid increase of blood pressure in parallel to an increase of plasma volume. Water and potassium balances became negative. Urinary sodium excretion remained unchanged or increased after high doses, whereas urinary sodium concentration and faecal sodium excretion were reduced. The diurnal rhythm of water and sodium excretion changed: during the night-period, renal water and sodium excretion were diminished, whereas during the day-period both were enhanced. Thus, some effects of 9aFF on electrolyte and water balance are similar to those of DOC, while other effects are similar to those of cortisone. It is postulated that a shift of fluid from intracellular to extracellular compartments, which increases plasma volume, is of critical importance for the 9aFF-induced blood pressure elevation in rats.

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