Effects of standard oral glucose loading on the renin-angiotensin-aldosterone system and its relationship to circulating insulin

Beretta-Piccoli, C; Weidmann, P; Glück, Z.; Bachmann, C.

doi:10.1007/bf01476801

Cited by 5 publications

(3 citation statements)

References 34 publications

(37 reference statements)

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“…The present study confirmed the previous data that the oral glucose loading caused suppression of plasma aldosterone and stimulation of plasma renin activity, with concomitant fall in serum potassium level {Beretta- Piccoli et al 1980). Further, we demonstrated that the renal patients exhibited the glucose-associated renin-angiotensin-aldosterone system different from that in normal subjects.…”

Section: Discussionsupporting

confidence: 91%

“…Oral glucose loading is known to suppress plasma aldosterone and stimulate plasma renin activity (PRA) in normal subjects (Beretta-Piccoli, Weidmann, Flammer, Gliick and Bachmann 1980). Because glucose-induced hyperinsulinemia causes hypokalemia by facilitating the transfer of excess potassium into intracellular compartment (Hiatt, Yamakawa and Davidson 1974), the fall in serum potassium level during glucose loading was regarded to be responsible for aldosterone suppression from the adrenal gland (Beretta-Piccoli et al 1980). In the meantime, potassium administration and its deprivation in human were significantly associated with decrease and increase of plasma renin activity, respectively (Brunner, Baer, Sealey, Ledingham and Laragh 1970).…”

Section: Introductionmentioning

confidence: 99%

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Acute Effects of Oral Glucose Loading on the Renin-Angiotensin-Aldosterone System in Patients with Chronic Renal Disease

Uemasu¹,

Fujihara²,

Matsumoto³

et al. 1993

Horm Metab Res

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To determine the changes of the glucose-induced renin-angiotensin-aldosterone system in chronic renal disease, a standard oral glucose loading test (75g) was performed in patients with chronic glomerulonephritis (CGN) (n = 12) and compared with control subjects (10). Glucose loading resulted in a significant decrease of serum aldosterone as well as increases of blood glucose and insulin similarly in both CGN and C. However, the suppression of aldosterone was statistically milder in CGN than in C (p < 0.05). In contrast, significant elevations of plasma renin activity were observed in CGN at 60 and 120 min, but not in C after glucose loading. Urinary sodium excretion after glucose ingestion was lower in CGN than in C. These data demonstrated that the glucose-induced renin-angiotensin-aldosterone system in patients with chronic renal disease differed from that in healthy subjects.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Acute Effects of Oral Glucose Loading on the Renin-Angiotensin-Aldosterone System in Patients with Chronic Renal Disease

Uemasu¹,

Fujihara²,

Matsumoto³

et al. 1993

Horm Metab Res

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“…Earlier studies using the OGTT have shown that glucose-induced hyperinsulinemia decreases sodium excretion. 23 These studies, however, were performed under conditions of marked extracellular volume expansion without acute sodium administration. In our protocol, 30 mmol of sodium were given intravenously over 4 hours without previous volume expansion; this maneuver may have masked any insulin-induced antinatriuresis.…”

Section: Figure 4 Scatterplots Show Relation Between Insulin-stimulamentioning

confidence: 99%

Effects of chronic angiotensin converting enzyme inhibition on glucose tolerance and insulin sensitivity in essential hypertension.

et al. 1992

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Hie relation between the renin-angiotensin-aldosterone (RAA) system and carbohydrate metabolism and insulin sensitivity in essential hypertension has not been investigated systematically. Twenty nondiabetic patients (age, 49±1 years; body mass index (BM1), 26.1 ±0.4 kg/m 2 ) with essential hypertension (blood pressure, 155±3/105±l mm Hg) received an oral glucose tolerance test (OGTT) at the end of a 1-month placebo period and again monthly during 3 months of angiotensin converting enzyme (ACE) inhibition (cilazapril, 5 mg/day). Furthermore, a two-step eughycemic insulin clamp was performed after placebo and again at the end of treatment Blood pressure fell by 7±4/10±3 mm Hg (p<0.001), while BMI remained stable. On the euglycemic clamp, insulin-mediated (plasma insulin, 470 pM) whole body glucose use averaged 42.5±1.6 /unol • min" 1 • kg" 1 before and 43.6±1.9 after ACE inhibition (p=NS). Substrate concentrations and oxidative rates and energy expenditure (as estimated by indirect calorimetry) were not altered by ACE inhibition, either in the fasting state or in response to insulin. In contrast, oral glucose tolerance was significantly (p<0.05) improved after treatment (area under OGTT curve (AUC), 240±24 versus 282±23 mmol 2 hr • 1"'). The latter change was associated with enhanced (+16%,p<0.05) insulin responsiveness to glucose (estimated as the insulin AUC divided by the glucose AUC) throughout the 3 months of ACE inhibition. At baseline, both the OGTT and the clamp had a marked hypokalemic effect (mean decrements in plasma potassium of 0.75±0.05 and 0.92±0.05 ramol/l, respectively) in association with plasma aldosterone reductions of 30% and 50%. Chronic ACE inhibition caused a further 20% (p<0.03) lowering of plasma aldosterone concentrations but attenuated insulin-induced hypokalemia. Plasma sodium, which was unaltered by the pretreatment tests, fell during the posttreatment tests (by 3 mmol/1, p<0.001). In the urine, the ratio of the fractional excretion of potassium to that of sodium was decreased by both oral glucose (-22%, p<0.01) and ACE inhibition (-21%, p<0.001). Higher plasma potassium levels before treatment predicted a better blood pressure response to ACE inhibition (r=0.60, /?< 0.005). In conclusion, in essential hypertension 1) chronic ACE inhibition does not interfere with insulin's effect on glucose uptake, substrate oxidation, or thennogenesis, but causes resistance to the potassium-lowering action of insulin; 2) this electrolyte change is associated with heightened insulin secretory response to glucose stimulation and improved oral glucose tolerance; and 3) higher plasma potassium levels predict a better blood pressure response to ACE inhibition. The salient features of the insulin resistance of essential hypertension are that it involves mostly the peripheral tissues (i.e., skeletal muscle 6 ) and that it is apparently pathway-specific (lipid and protein metabolism being unaffected 4 ). Its origin remains, however, obscure.The renin-angiotensin-aldosterone (RAA) system is involved in bloo...

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Studies on acute glucose-induced aldosterone suppression: Role of renin-angiotensin system

et al. 1984

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Glucose loading is known to cause acute suppression of plasma aldosterone and stimulation of plasma renin activity. The relative contribution of variations in circulating angiotensin II to the regulation of aldosterone secretion following glucose loading was assessed in ten normal subjects. The effects of a standard oral glucose loading test (100 g) on plasma concentrations of glucose, insulin, potassium, aldosterone, renin activity and cortisol were studied (a) under basal conditions, and (b) after inhibition of angiotensin II with the converting enzyme inhibitor captopril (50 mg t.i.d. during 3 days). Under basal conditions the acute increase in plasma glucose and insulin after glucose loading was accompanied by a significant decrease (P less than 0.01) in plasma cortisol and aldosterone and by a significant increase in plasma renin activity (P less than 0.01); plasma potassium was decreased slightly but not significantly. Following captopril treatment preloading plasma renin activity was increased significantly, most probably reflecting an effective reduction of angiotensin II. Glucose loading caused a similar suppression of plasma aldosterone, as observed under basal conditions. This observation suggests that renin activation does not substantially contribute to the acute regulation of plasma aldosterone after an oral glucose load.

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Effects of standard oral glucose loading on the renin-angiotensin-aldosterone system and its relationship to circulating insulin

Cited by 5 publications

References 34 publications

Acute Effects of Oral Glucose Loading on the Renin-Angiotensin-Aldosterone System in Patients with Chronic Renal Disease

Acute Effects of Oral Glucose Loading on the Renin-Angiotensin-Aldosterone System in Patients with Chronic Renal Disease

Effects of chronic angiotensin converting enzyme inhibition on glucose tolerance and insulin sensitivity in essential hypertension.

Studies on acute glucose-induced aldosterone suppression: Role of renin-angiotensin system

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