Relationship between Insulin Release, Antinatriuresis and Hypokalaemia after Glucose Ingestion in Normal and Hypertensive Man

1993 ◽  
Vol 85 (3) ◽  
pp. 327-335 ◽  
Author(s):  
Andrea Natali ◽  
Alfredo Quiñones Galvan ◽  
Donatella Santoro ◽  
Neda Pecori ◽  
Stefano Taddei ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Potassium Concentration ◽  
Plasma Potassium ◽  
Oral Glucose ◽  
Plasma Insulin Concentration ◽  
Hypertensive Patients ◽  
Insulin Resistant ◽  
Glucose Ingestion ◽  
Before And After ◽  
Tightly Coupled

1. Insulin simultaneously causes hypokalaemia and antinatriuresis, and it has been suggested that the two effects are tightly coupled. Whether these actions are preserved in patients with essential hypertension is not known. 2. Eight hypertensive patients and eight normotensive control subjects were studied before and after the ingestion of 75 g of glucose. Despite similar glycaemic profiles, the patients showed a hyperinsulinaemic response incremental area 49 ±8 versus 27 ± 6 nmoll−1 3h, P <0.04) but a blunted hypokalemic response (−7±1 versus −16±1%, P <0.001). Both absolute and fractional urinary excretion of sodium and potassium were significantly decreased during glucose-induced hyperinsulinaemia in hypertensive patients as well as in normotensive subjects (P <0.05 for all changes). 3. To test whether hypokalaemia is required for insulin-induced antinatriuresis, each hypertensive patient received another oral glucose load during which enough potassium chloride was given to clamp the plasma potassium concentration at baseline. Under these conditions, significant insulin-induced antinatriuresis still occurred. In addition, whereas the glycaemic profile was superimposable, the response of the plasma insulin concentration was significantly greater with than without maintenance of the plasma potassium concentration (total area 79 ± 14 versus 63 ± 8 nmoll−1 3h, P <0.04). 4. We conclude that (a) insulin causes antinatriuresis, antikaliuresis and hypokalaemia under physiological conditions; (b) in hyperinsulinaemic (insulin-resistant) patients with essential hypertension, the anti-natriuretic action of insulin is quantitatively preserved; and (c) clamping plasma potassium levels prevents insulin-induced antikaliuresis but not anti-natriuresis, and potentiates the insulin secretory response to glucose.

Assessment of red blood cell glutathione status in insulin resistance

2012 ◽  
Vol 37 (5) ◽  
pp. 997-1002
Author(s):  
Jose E. Galgani ◽  
Karla Vasquez ◽  
Giannella Leonelli ◽  
Alejandra Espinosa ◽  
Hector Araya ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Blood Cell ◽  
Red Blood Cell ◽  
Postprandial Glucose ◽  
Serum Glucose ◽  
Oral Glucose ◽  
Glucose Response ◽  
Insulin Resistant ◽  
Glucose Ingestion ◽  
Before And After

The aim of this study was to assess red blood cell glutathione from insulin-sensitive and insulin-resistant individuals before and after an oral glucose dose. Fifteen healthy, young (24 ± 5 years), nonobese (23 ± 2 kg·m–2), insulin-sensitive (ISI composite = 6.0 ± 1.2) individuals and 14 healthy, young (22 ± 2 years), nonobese (24 ± 2 kg·m–2), insulin-resistant (ISI composite = 2.7 ± 1.1) individuals received a 75 g oral glucose dose. Blood samples were drawn before and for 2 h after glucose ingestion for red blood cell glutathione and serum glucose and insulin concentrations. Glycemia before and after glucose ingestion was similar between groups (p = 0.17), which suggest that hyperinsulinemia compensated impaired insulin sensitivity. Red blood cell total (p = 0.81), reduced (p = 0.79), and oxidized (p = 0.88) glutathione concentrations were similar between groups under fasting and postprandial conditions. However, in response to glucose, increases in total and reduced glutathione concentrations were found at the end of the 2 h assessment period in both groups (p < 0.05). Direct associations between postprandial glucose response and red blood cell total (r = 0.52; p < 0.05) and oxidized (r = 0.61; p = 0.02) glutathione concentrations were observed only in insulin-sensitive subjects. In conclusion, healthy individuals differing in their degree of insulin resistance showed similar red blood cell glutathione concentrations under non-glucose- and glucose-stimulated conditions.

Relation of Arterial Pressure with Body Sodium, Body Potassium and Plasma Potassium in Essential Hypertension

1982 ◽  
Vol 63 (3) ◽  
pp. 257-270 ◽  
Author(s):  
C. Beretta-Piccoli ◽  
D. L. Davies ◽  
K. Boddy ◽  
J. J. Brown ◽  
A. M. M. Cumming ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Arterial Pressure ◽  
Potassium Concentration ◽  
Plasma Potassium ◽  
Normal Subjects ◽  
Total Body Potassium ◽  
Hypertensive Patients ◽  
Body Sodium ◽  
Low Renin Hypertension ◽  
Total Body

1. Exchangeable sodium (NaE), plasma electrolytes and arterial pressure were measured in 121 normal subjects and 91 patients with untreated essential hypertension (diastolic >100 mmHg), 21 of whom had low-renin hypertension. Plasma concentrations of renin, angiotensin II and aldosterone were measured in all hypertensive patients, total body sodium, total body potassium and exchangeable potassium (KE) in some patients. 2. Mean NaE was not different in normal and hypertensive subjects provided the two groups were matched for leanness index. In the subgroup of young hypertensive patients aged 35 years or less mean NaE was below normal. NaE was not related to arterial pressure in normal subjects but in hypertensive patients there were positive and significant correlations of arterial pressure with NaE and with total body sodium. 3. NaE and total body sodium increased with age in hypertensive but not in normal subjects. Partial regression analysis suggested that the correlation of NaE with arterial pressure was not explained by an influence of age. 4. Mean NaE was not increased and mean KE was not decreased in patients with low-renin hypertension. 5. Plasma potassium concentration, KE and total body potassium correlated inversely and significantly with blood pressure in hypertensive patients. These correlations were more marked in young than in old patients. 6. Multiple regression analysis showed that the combination of NaE and plasma potassium concentration ‘explained’ more of the variation of systolic blood pressure in hypertensive patients than it did in normal subjects. Plasma potassium concentration ‘explained’ more of the variation in young hypertensives and NaE ‘explained’ more in older patients. 7. Our findings suggest that changes of plasma and body potassium are important in the earlier stages of essential hypertension and that changes of body sodium become important later.

Normalization of carbohydrate-induced thermogenesis by fructose in insulin-resistant states

1988 ◽  
Vol 254 (2) ◽  
pp. E201-E207 ◽  
Author(s):  
D. C. Simonson ◽  
L. Tappy ◽  
E. Jequier ◽  
J. P. Felber ◽  
R. A. DeFronzo
Keyword(s):  
Energy Expenditure ◽  
Carbohydrate Oxidation ◽  
Cellular Mechanisms ◽  
Primary Defect ◽  
Plasma Insulin Concentration ◽  
Insulin Resistant ◽  
Obesity And Diabetes ◽  
Glucose Ingestion ◽  
Intracellular Metabolism ◽  
Insulin Dependent Diabetic

To examine whether defects in carbohydrate oxidation and thermogenesis in aging, obesity, and diabetes are secondary to impaired insulin action or to a primary defect in intracellular metabolism, we compared substrate oxidation and energy expenditure in 9 younger, 9 older, 9 obese, and 10 non-insulin-dependent diabetic subjects after the ingestion of 75 g of glucose or fructose (a monosaccharide whose transport into the cell and subsequent metabolism are independent of insulin). In young control subjects fructose produced a significantly greater increase in carbohydrate oxidation and energy expenditure than glucose despite significantly lower plasma glucose and insulin levels. In aged, obese, and diabetic individuals the increments in carbohydrate oxidation and energy expenditure after glucose ingestion were significantly imparied versus the younger controls. After fructose ingestion the increase in carbohydrate oxidation in the three insulin-resistant groups remained below that observed in the younger volunteers, whereas carbohydrate-induced thermogenesis was enhanced to levels that were comparable with those seen in the younger group. These data suggest that 1) the stimulation of thermogenesis after fructose ingestion is related to an augmentation of intracellular metabolism rather than an increase in the plasma insulin concentration per se, 2) the insulin resistance of aging, obesity, and diabetes is associated with a defect in intracellular carbohydrate oxidation, and 3) the cellular mechanisms involved in carbohydrate-induced thermogenesis are not primarily impaired in insulin-resistant states.

Proximal and Distal Tubular Reabsorption during Isotonic Volume Expansion in Patients with Essential Hypertension as Estimated by Means of Combined Lithium and 51Cr-Labelled EDTA Clearance

1982 ◽  
Vol 63 (s8) ◽  
pp. 219s-221s ◽  
Author(s):  
N.-H. Holstein-Rathlou ◽  
U. G. Svendsen ◽  
P. P. Leyssac
Keyword(s):  
Essential Hypertension ◽  
Significant Rise ◽  
Tubular Reabsorption ◽  
Sodium Reabsorption ◽  
Absolute Rate ◽  
Hypertensive Patients ◽  
Volume Load ◽  
Before And After ◽  
Normotensive Subjects ◽  
Normotensive Control

1. Ten patients with essential hypertension and ten normotensive control subjects were investigated before and after an isotonic volume load. 2. The increases in the clearances of lithium and of sodium were greater in the hypertensive than in the normotensive subjects (P < 0.05). The fractional increases showed a positive correlation (rs = 0.68, P < 0.05) in the hypertensive patients. 3. An increase in glomerular filtration rate in the hypertensive patients correlated positively with the increase in proximal output (rs = 0.70, P < 0.05), but did not correlate with the change in sodium excretion. 4. The exaggerated natriuresis was accompanied by a significant rise in the absolute rate of sodium reabsorption in the distal segments, but distal fractional reabsorption decreased. 5. It is concluded that the exaggerated natriuresis can be accounted for by an increase in the proximal output of sodium and water.

The Relation of Arterial Pressure with Plasma and Body Electrolytes is Similar in Conn's Syndrome and Essential Hypertension

1982 ◽  
Vol 63 (s8) ◽  
pp. 89s-92s ◽  
Author(s):  
C. Beretta-Piccoli ◽  
D. L. Davies ◽  
J. J. Brown ◽  
J. B. Ferriss ◽  
R. Fraser ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Arterial Pressure ◽  
Potassium Concentration ◽  
Young Patients ◽  
Plasma Potassium ◽  
Surgical Removal ◽  
Exchangeable Sodium ◽  
Plasma Urea ◽  
Conn’S Syndrome

1. Arterial pressure, exchangeable sodium (NaE), exchangeable potassium (KE) and plasma concentrations of sodium, potassium, urea, angiotension II and aldosterone were measured in 34 patients with untreated Conn's syndrome before surgical removal of their adenoma. The study was repeated in 23 patients between 3 and 12 months after the operation. 2. Plasma aldosterone, NaE and plasma sodium concentration were higher and KE and plasma potassium concentration were lower than predicted normal. Surgery corrected these abnormalities, also reducing blood pressure from an average of 183/112 to 138/86 mmHg. 3. Systolic blood pressure was positively correlated with plasma and exchangeable sodium and negatively correlated with plasma potassium concentration. The relation of NaE and arterial pressure was closer in old than in young patients. None of these correlations was significant after operation. Before operation plasma urea was insignificantly related to arterial pressure but after operation a significant and positive correlation emerged. 4. A relation between arterial pressure and NaE is to be expected in a state of mineralocorticoid excess but the different correlation in old and young patients was not expected. A similar difference exists in patients with essential hypertension.

Potassium dynamics are attenuated in hyperkalemia and a determinant of QT adaptation in exercising hemodialysis patients

2013 ◽  
Vol 115 (4) ◽  
pp. 498-504 ◽  
Author(s):  
Cao Thach Tran ◽  
Henning Bundgaard ◽  
Søren Daustrand Ladefoged ◽  
Stig Haunsø ◽  
Keld Kjeldsen
Keyword(s):  
Qt Interval ◽  
Potassium Concentration ◽  
Plasma Potassium ◽  
Work Load ◽  
Hemodialysis Patients ◽  
Cycle Ergometer ◽  
Potassium Dynamics ◽  
Before And After ◽  
Stage Renal Disease ◽  
End Stage

Disturbances in plasma potassium concentration (pK) are well known risk factors for the development of cardiac arrhythmia. The aims of the present study were to evaluate the effect of hemodialysis on exercise pK dynamics and QT hysteresis, and whether QT hysteresis is associated with the pK decrease following exercise. Twenty-two end-stage renal disease patients exercised on a cycle ergometer with incremental work load before and after hemodialysis. ECG was recorded and pK was measured during exercise and recovery. During exercise, pK increased from 5.1 ± 0.2 to 6.1 ± 0.2 mM (mean ± SE; P < 0.0001) before hemodialysis and from 3.8 ± 0.1 to 5.1 ± 0.1 mM ( P < 0.0001) after hemodialysis. After 2 min of recovery, pK had decreased to 5.0 ± 0.2 mM and 4.1 ± 0.1 mM ( P < 0.0001) before and after hemodialysis, respectively. pK increase during exercise was accentuated after hemodialysis. The pK increase was negatively linearly correlated with pK before exercise (β = −0.21, R2 = 0.23, P = 0.001). QT hysteresis was negatively linearly correlated with the decrease in pK during recovery (β = −28 ms/mM, R2 = 0.36, P = 0.006). Thus, during recovery, low pK was associated with relatively longer QT interval. In conclusion, new major findings are an accentuated increase in pK during exercise after hemodialysis, an attenuated increase in pK in hyperkalemia, and an association between pK and QT interval adaptation during recovery. The acute pK shift after exercise may modulate QT interval adaptation and trigger cardiac arrhythmias.

Suppression of Post-Glucose Hyperinsulinaemia Does Not Affect Blood Pressure in Either Normotensive or Hypertensive Subjects

1998 ◽  
Vol 94 (6) ◽  
pp. 609-614
Author(s):  
Mark W. Savage ◽  
Vidya Mohamed-Ali ◽  
Gareth Williams
Keyword(s):  
Blood Pressure ◽  
Insulin Response ◽  
Control Group ◽  
Oral Glucose ◽  
Short Term ◽  
Hypertensive Patients ◽  
Hypertensive Group ◽  
Glucose Ingestion ◽  
Regulation Of Blood Pressure ◽  
Noradrenaline Levels

1. Hyperinsulinaemia and insulin resistance are thought to be intimately involved in the development of hypertension, but controversy remains as to whether hyperinsulinaemia is a consequence or a cause of hypertension per se, and whether it plays a role in the short-term regulation of blood pressure. 2. We studied six hypertensive patients [blood pressure 161(9)/101(2) mmHg] and seven normotensive control subjects [blood pressure 122(6)/76(4) mmHg], (P < 0.005) using two oral glucose tolerance tests of 3 h duration. In one of these tests the endogenous insulin response was inhibited with subcutaneous octreotide. 3. After placebo, hypertensive patients had slightly but significantly higher blood glucose levels than controls (P < 0.0001), but comparable insulin concentrations (P > 0.5). Plasma noradrenaline levels were consistently lower in the hypertensive group (P < 0.001). Blood pressure did not change in either group during the 3 h after glucose ingestion. 4. Octreotide completely abolished the immediate insulin response to glucose in all subjects (both P < 0.0001) and caused a delayed and significantly increased glycaemic response in born groups (P < 0.0001). There were no significant differences in plasma glucose responses between groups; however, after octreotide, the hypertensive subjects had a greater insulin suppression than the controls (P < 0.02). Octreotide suppressed noradrenaline levels in the normotensive group (P < 0.001); they were also suppressed in the hypertensive group, but just failed to reach significance (P = 0.056). Throughout the study the hypertensive group's noradrenaline levels remained generally lower than those in the control group (P < 0.0001). 5. In this study there were no differences between hypertensive and normotensive subjects in fasting or post-glucose insulin levels, nor any significant change in blood pressure in either group when post-glucose hyperinsulinaemia was suppressed. This argues against insulin playing a direct role in the short-term regulation of blood pressure.

scholarly journals Normal erythrocyte calpain I activity on membrane proteins under near-physiological conditions in patients with essential hypertension

2002 ◽  
Vol 120 (1) ◽  
pp. 05-08
Author(s):  
Tereza Maria Dantas de Medeiros ◽  
Katia Coelho Ortega ◽  
Décio Mion Júnior ◽  
Kimiyo Nonoyama ◽  
Orlando Cesar de Oliveira Barretto
Keyword(s):  
Essential Hypertension ◽  
Membrane Proteins ◽  
Protective Factor ◽  
Polyacrylamide Gel Electrophoresis ◽  
Cell Activity ◽  
Red Cell ◽  
Red Cell Membrane ◽  
Activity Increase ◽  
Hypertensive Patients ◽  
Before And After

CONTEXT: It has been reported that the equilibrium between the erythrocyte protease calpain I and its physiological inhibitor calpastatin is disrupted in patients with essential hypertension. OBJECTIVE: To investigate the activity of non-purified calpain I in hemolysates against the erythrocytic membrane proteins, rather than against other substrates. DESIGN: Evaluation of calpain I red cell activity upon its own physiological substrates in hypertensive patients, in a near-physiological environment. SETTING: LIM-23 and LIM-40 of Hospital das Clinicas of the Faculty of Medicine of USP. SAMPLE: Patients with moderate primary hypertension over 21 years of age who were given amlodipine (n:10) and captopril (n:10) for 8 weeks, plus normal controls (n:10). MAIN MEASUREMENTS: Red cell membrane proteins were incubated with and without protease inhibitors and with and without calcium chloride and underwent polyacrylamide gel electrophoresis. RESULTS: Digestion of bands 2.1 and 4.1 was observed, indicating calpain I acitivity. No statistical differences regarding bands 2.1 and 4.1 were observed before treatment, between the controls and the hypertensive patients, either in ghosts prepared without calcium or with increasing concentrations of calcium. Nor were statistical differences observed after treatment, between the controls and the patients treated with amlodipine and captopril, or between the patients before and after treatment with both drugs. CONCLUSION: The final activity of non-purified calpain I upon its own physiological substrate, which was the approach utilized in this study, may more adequately reflect what happens in red cells. Under such conditions no imbalance favoring calpain I activity increase was observed. The protective factor provided by calpastatin against calpain I activity may diminish under hypertension.

Effect of standard oral glucose loading on aldosterone secretion in primary hyperaldosteronism

1982 ◽  
Vol 101 (1) ◽  
pp. 66-71 ◽  
Author(s):  
C. Beretta-Piccoli ◽  
P. Weidmann ◽  
J. J. Brown ◽  
R. Fraser ◽  
A. F. Lever ◽  
...  
Keyword(s):  
Plasma Glucose ◽  
Plasma Insulin ◽  
Plasma Potassium ◽  
Normal Subjects ◽  
Plasma Aldosterone ◽  
Primary Hyperaldosteronism ◽  
Oral Glucose ◽  
Aldosterone Secretion ◽  
Glucose Loading ◽  
Glucose Ingestion

Abstract. The effects of mild acute decreases in plasma potassium induced by standard oral glucose loading (100 g) on plasma aldosterone and renin levels were assessed in 10 patients with primary hyperaldosteronism as compared with 10 normal subjects. Following overnight fast, mean plasma glucose was identical in both groups; plasma insulin, potassium and renin levels were lower and plasma aldosterone higher in patients than in controls. Glucose loading significantly increased plasma glucose and insulin concentrations and decreased plasma potassium and aldosterone levels in both groups. The increases in plasma insulin and the decreases in plasma potassium or aldosterone tended to be blunted in primary hyperaldosteronism. Glucose-induced changes in plasma aldosterone correlated significantly (P < 0.025) with those in plasma potassium in the patients and with variations in plasma renin activity in the normal subjects. These findings suggest that the metabolic changes induced by glucose ingestion are capable of modifying aldosterone secretion in primary hyperaldosteronism. However, the glucose-induced decreases in plasma aldosterone are blunted in this disorder; this could be related to the impaired insulin response to glucose loading.

Effects of hyperglycemia on glucose metabolism before and after oral glucose ingestion in normal men

2006 ◽  
Vol 290 (6) ◽  
pp. E1198-E1204 ◽  
Author(s):  
Vincent Rigalleau ◽  
Marie-Christine Beauvieux ◽  
Jean-Louis Gallis ◽  
Henri Gin ◽  
Phillippe Schneiter ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Plasma Glucose ◽  
Glucose Disposal ◽  
Oral Glucose ◽  
Oral Glucose Load ◽  
Glucose Load ◽  
Glucose Ingestion ◽  
Before And After ◽  
Endogenous Glucose ◽  
Normal Men

The plasma glucose excursion may influence the metabolic responses after oral glucose ingestion. Although previous studies adressed the effects of hyperglycemia in conditions of hyperinsulinemia, it has not been evaluated whether the route of glucose administration (oral vs. intravenous) plays a role. Our aim was to determine the effects of moderately controlled hyperglycemia on glucose metabolism before and after oral glucose ingestion. Eight normal men underwent two oral glucose clamps at 6 and 10 mmol/l plasma glucose. Glucose turnover and cycling rates were measured by infusion of [2H7]glucose. The oral glucose load was labeled by d-[6,6-2H2]glucose to monitor exogenous glucose appearance, and respiratory exchanges were measured by indirect calorimetry. Sixty percent of the oral glucose load appeared in the systemic circulation during both the 6 and 10 mmol/l plasma glucose tests, although less endogenous glucose appeared during the 10 mmol/l tests before glucose ingestion ( P < 0.05). This inhibitory effect of hyperglycemia was not detectable after oral glucose ingestion, although glucose utilization was increased (+28%, P < 0.05) due to increased nonoxidative glucose disposal [10 vs. 6 mmol/l: +20%, not significant (NS) before oral glucose ingestion; +40%, P < 0.05 after oral glucose ingestion]. Glucose cycling rates were increased by hyperglycemia (+13% before oral glucose ingestion, P < 0.001; +31% after oral glucose ingestion, P < 0.05) and oral glucose ingestion during both the 6 (+10%, P < 0.05) and 10 mmol/l (+26%, P < 0.005) tests. A moderate hyperglycemia inhibits endogenous glucose production and contributes to glucose tolerance by enhancing nonoxidative glucose disposal. Hyperglycemia and oral glucose ingestion both stimulate glucose cycling.

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