Arginine hydrochloride stimulation of serum potassium and aldosterone is enhanced by somatostatin-28

Abstract. Potassium, aldosterone and insulin responses to arginine infusion were compared in 5 normal men during infusions of somatostatin-14 (SS-14), somatostatin-28 (SS-28) and a control infusion. SS-14 and SS-28 were infused continuously at a rate of 8.6 pmol/min/kg and arginine (0.5 g/kg) was infused from 30–60 min. Following the control infusion with arginine hydrochloride, serum aldosterone and potassium levels increased slightly. The rise in potassium appears to be due to an exchange of cellular potassium for the proton from the arginine hydrochloride. SS-14 had no significant effect on serum potassium or aldosterone but an equimolar dose of SS-28 significantly enhanced the rise in potassium and aldosterone. SS-28 completely inhibited the arginine-stimulated insulin increase while SS-14 only partially inhibited the insulin increase. Since insulin opposes the increase in serum potassium by stimulating cellular uptake of this cation, the enhanced rise in serum potassium in response to arginine hydrochloride during the SS-28 infusion is likely due to the potent insulin suppressing effect of SS-28. The rise in serum aldosterone is directly related to the degree of elevation of serum potassium. These findings caution against the infusion of SS-28 during an arginine stimulation test.

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Serum potassium: values in normal men in Shanghai vs those in men from Shanghai living abroad

Clinical Chemistry ◽

10.1093/clinchem/40.2.340 ◽

1994 ◽

Vol 40 (2) ◽

pp. 340-340 ◽

Cited By ~ 4

Author(s):

Z P Gu ◽

S Segal ◽

M M Reidenberg

Keyword(s):

Serum Potassium ◽

Normal Men

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Effects of Secretin on Insulin Secretion and Glucose Tolerance

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y75-155 ◽

1975 ◽

Vol 53 (6) ◽

pp. 1115-1121 ◽

Cited By ~ 8

Author(s):

J. Dupré ◽

D. J. Chisholm ◽

T. J. McDonald ◽

A. Rabinovitch

Keyword(s):

Insulin Secretion ◽

Glucose Tolerance ◽

Glucose Production ◽

High Rate ◽

Immunoreactive Insulin ◽

Continuous Administration ◽

Normal Men ◽

Mean Glucose ◽

Insulin Responses ◽

Infusion Period

Effects of intravenous (IV) infusion of secretin during IV infusion of glucose were examined in normal men. Secretin was administered according to three schedules: with each schedule a comparable priming dose was delivered in the first minute, but this was followed by a maintained (120 min) infusion of secretin at a relatively high rate, or by maintained infusion at one-third that rate, or by brief (15 min) infusion at the lower rate. The lower infusion rate produced increments in secretin in the blood within the range attainable during endogenous secretion. By comparison with effects of glucose alone each secretin infusion enhanced the increments of immunoreactive insulin in the blood. Enhancement of the early release (0–5 min) of insulin was similar with each type of secretin infusion, but the integrated changes in insulin levels through the total infusion period were related to the total doses of secretin. With each dose of secretin glucose tolerance was improved but the three mean glucose curves observed during infusions of secretin were not distinguishable from one another in spite of widely different integrated insulin responses. Secretin did not modify suppression of immunoreactive glucagon or free fatty acids in the blood during hyperglycemia. The results suggest that the effect of continuous administration of secretin on glucose tolerance is not simply related to its integrated insulinotropic action. It is suggested that the effect may be highly dependent on enhancement of insulin secretion early in the response to glycemia, or that it may be due to effects of secretin on glucose production or disposal which are not mediated by insulin.

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Acid-Activated Renin Responses to Hydrochlorothiazide, Propranolol and Indomethacin

Clinical Science ◽

10.1042/cs055151s ◽

1978 ◽

Vol 55 (s4) ◽

pp. 151s-153s ◽

Cited By ~ 1

Author(s):

J. K. McKenzie ◽

E. Reisin

Keyword(s):

Blood Pressure ◽

Serum Potassium ◽

Potassium Concentration ◽

Hypertensive Patients ◽

Serum Potassium Concentration ◽

Active Renin ◽

Serum Aldosterone ◽

Low Salt ◽

Inactive Renin ◽

Marked Suppression

1. Six essential hypertensive patients (five with low renin) were treated in successive weeks with placebo; hydrochlorothiazide 100 mg (382 μmol)/day; hydrochlorothiazide and 50 mmol of sodium/day diet; hydrochlorothiazide, 50 mmol of sodium diet and propranolol 160 mg (544 μmol)/day; and hydrochlorothiazide, 50 mmol of sodium and indomethacin 100 mg (287 μmol)/day. 2. Although blood pressure remained unchanged and serum potassium fell on diuretic with or without low salt, there was a marked increase of active renin and a lesser increase of inactive renin, resulting in an increased proportion of active to total renin. 3. Propranolol decreased both active and inactive renin, but not significantly. 4. Indomethacin produced a marked suppression of active renin, a smaller reduction in inactive renin, and a reduction of the ratio of active to total renin almost to placebo values. 5. Blood pressure rose to control values on indomethacin despite the fall in renin whereas it fell with propranolol with little change in renin. 6. Serum aldosterone rose with stimulation but remained elevated despite effective renin suppression with indomethacin and continuing reduced serum potassium concentration.

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THE PANCREATIC ALPHA AND BETA CELLS RESPONSES TO 1-ARGININE AND INSULIN-INDUCED HYPOGLYCAEMIA IN HYPERTHYROIDISM

Acta Endocrinologica ◽

10.1530/acta.0.0830114 ◽

1976 ◽

Vol 83 (1) ◽

pp. 114-122 ◽

Cited By ~ 5

Author(s):

K. Shima ◽

N. Sawazaki ◽

R. Tanaka ◽

S. Morishila ◽

S. Tarui ◽

...

Keyword(s):

Beta Cells ◽

Normal Subjects ◽

Insulin Injection ◽

Plasma Glucagon ◽

Arginine Infusion ◽

Significant Difference ◽

Functional Defect ◽

Plasma Insulin Levels ◽

Glucagon And Insulin ◽

Insulin Responses

ABSTRACT In order to assess the secretory capacity of the pancreatic alpha and beta cells in patients with hyperthyroidism, the plasma glucagon and insulin responses to 1-arginine and insulin-induced hypoglycaemia in 12 patients were compared with those in 6 normal subjects. The response of beta cell to hypoglycaemia was evaluated by measuring the decrease in plasma C-peptide immunoreactivity (CPR) level. There was a negligible rise in blood glucose and plasma insulin levels in the patients, whereas a significant increase occurred in normal subjects during the arginine infusion. Although no difference in the fasting plasma glucagon concentration between the two groups was found, 30 min after the beginning of the arginine infusion, the plasma glucagon levels rose to a peak of 252 ± 35 pg/ml in the patients, a value significantly lower than 387 ± 53 pg/ml in the normal subjects. The insulin-induced hypoglycaemia caused no significant difference in the peak values of plasma glucagon between the two groups. There was a significant fall in plasma CPR after the insulin injection in both groups but the per cent decrement was rather greater in the patients than in the normal subjects. These results suggest that the pancreatic alpha and beta cells in hyperthyroidism have a functional defect in response to 1-arginine but not to insulin-induced hypoglycaemia. The mechanism involved in these disorders is discussed.

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The Effects of Cardioselective and Non-Selective β-Adrenoceptor Blockade on the Hypokalaemic and Cardiovascular Responses to Adrenomedullary Hormones in Man

Clinical Science ◽

10.1042/cs0650143 ◽

1983 ◽

Vol 65 (2) ◽

pp. 143-147 ◽

Cited By ~ 87

Author(s):

A. D. Struthers ◽

J. L. Reid ◽

R. Whitesmith ◽

J. C. Rodger

Keyword(s):

Heart Rate ◽

Serum Potassium ◽

Qt Interval ◽

Diastolic Pressure ◽

Plasma Concentrations ◽

Systolic Pressure ◽

Cardiovascular Responses ◽

Potassium Influx ◽

Adrenomedullary Hormones ◽

Stimulation Of

1. Adrenaline was infused intravenously in nine normal volunteers to plasma concentrations similar to those found after myocardial infarction. This study was undertaken on three occasions after 5 days' treatment with placebo or the β-adrenoceptor antagonists, atenolol or timolol. 2. Adrenaline increased the systolic pressure by 11 mmHg, decreased the diastolic pressure by 14 mmHg, and increased the heart rate by 7 beats/min. These changes were prevented by atenolol. However, after timolol the diastolic pressure rose (+19 mmHg) and heart rate fell (− 8 beats/min). 3. Adrenaline caused the corrected QT interval (QTc) to lengthen (0.36 ± 0.02 s to 0.41 ± 0.06 s). No significant changes were found in the QTc when subjects were pretreated with atenolol or timolol. 4. The serum potassium fell from 4.06 to 3.22 mmol/l after adrenaline. Serum potassium fell to a lesser extent to 3.67 mmol/l after atenolol and actually increased to 4.25 mmol/l after timolol. Adrenaline-mediated hypokalaemia appears to result from the stimulation of a β2-adrenoceptor linked to membrane Na+/K+-ATPase causing potassium influx.

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Dexamethasone-induced insulin resistance enhances B cell responsiveness to glucose level in normal men

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1984.247.5.e592 ◽

1984 ◽

Vol 247 (5) ◽

pp. E592-E596 ◽

Cited By ~ 7

Author(s):

J. C. Beard ◽

J. B. Halter ◽

J. D. Best ◽

M. A. Pfeifer ◽

D. Porte

Keyword(s):

Insulin Resistance ◽

B Cell ◽

Glucose Level ◽

Cell Function ◽

Insulin Level ◽

Glucose Levels ◽

B Cell Function ◽

Normal Men ◽

Insulin Responses ◽

Effect Of Glucose

To determine whether islet adaptation during insulin resistance involves increased responsiveness to the level of plasma glucose, insulin resistance was induced in nine normal men by giving dexamethasone (Dex) (3 mg twice daily for 2 days). Plasma insulin and acute insulin responses (AIR) to isoproterenol were measured at three different glucose levels under control and Dex conditions. During Dex there were elevations above control levels of basal glucose (104 +/- 2 vs. 94 +/- 3 mg/dl) and insulin (21 +/- 3 vs. 13 +/- 2 microU/ml, both P less than 0.03). When glucose levels were raised stepwise by matching amounts using glucose clamps, AIR to isoproterenol rose as a linear function of glucose level under both conditions but rose more steeply during Dex. That is, the potentiating effect of glucose (delta AIR/delta glucose) was greater during Dex: 1.3 +/- 0.2 vs. 0.8 +/- 0.2 (P less than 0.01). Similarly, matched increments in glucose level produced greater increments in prestimulus insulin level during Dex (P less than 0.03). We conclude that 48 h of Dex raises the "gain" of the potentiating effect of glucose. Because the direct effect of glucocorticoids on B cell function has been reported to be inhibitory, the observed stimulation is likely to be a result of the insulin resistance caused by Dex.

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Haemodynamic and Biochemical Responses to l-Arginine and l-Lysine Infusions in Normal Subjects: l-Arginine-Induced Vasodilatation Cannot be Explained by Non-Specific Effects of Cationic Amino Acids

Clinical Science ◽

10.1042/cs0920367 ◽

1997 ◽

Vol 92 (4) ◽

pp. 367-374 ◽

Cited By ~ 23

Author(s):

R. A. Smulders ◽

M. Aarsen ◽

T. Teerlink ◽

P. M. J. M. De Vries ◽

G. J. Van Kamp ◽

...

Keyword(s):

Blood Pressure ◽

Cyclic Gmp ◽

Extracellular Fluid ◽

Normal Subjects ◽

No Production ◽

Plasma Volume Expansion ◽

Arginine Infusion ◽

Specific Effects ◽

Cationic Amino Acids ◽

Stimulation Of

1. Pharmacological stimulation of the synthesis of nitric oxide (NO) may be important in the prevention or treatment of cardiovascular diseases. 2. There is much discussion as to whether the precursor of NO, l-arginine, is able to stimulate basal endothelial NO production. l-Arginine is known to have vasodilating effects. However, it is not clear whether l-arginine-induced vasodilatation is attributable to an increase in NO production or to other systemic effects of l-arginine. 3. To investigate further the mechanisms of the l-arginine-induced vasodilatation, we compared the responses to l-arginine with those to saline and l-lysine in healthy subjects. l-Lysine is not a substrate for NO synthesis, but shares many of l-arginine's other properties. 4. During l-arginine infusion, blood pressure decreased [systolic blood pressure from 120.2 (SD 8.8) to 117.3 (12.1) mmHg (P = 0.05); diastolic blood pressure from 65.3 (5.9) to 61.6 (7.9) mmHg (P < 0.01)], and heart rate and extracellular fluid volume increased. The total peripheral vascular resistance decreased during l-arginine infusion by 18.0 (11.4)% (P ≤ 0.05 compared with baseline and compared with l-lysine infusion). These results indicate vasodilatation. No changes were observed during l-lysine and saline infusion. 5. Plasma cyclic GMP (the second messenger for NO) increased during l-arginine but also during l-lysine infusion [from 5.7 (1.2) to 6.8 (1.7) nmol/l (P < 0.01), and from 5.8 (1.8) to 7.0 (2.9) nmol/l (P < 0.05) respectively]. Plasma l-citrulline (a by-product of NO synthesis from l-arginine) increased during l-arginine infusion from 30.6 (7.5) to 47.1 (9.9) μmol/l (P < 0.001), but also during l-lysine infusion from 32.7 (6.5) to 42.0 (8.3) μmol/l (P < 0.001). 6. Plasma electrolytes and atrial natriuretic peptide concentrations responded similarly to l-arginine and l-lysine infusion, indicating similar effects on osmolality, plasma volume expansion and potassium distribution. 7. In conclusion, although l-lysine infusion had effects that were similar to those of l-arginine infusion, no vasodilatation was observed. Therefore, these effects cannot account for the l-arginine-induced vasodilatation. This finding indirectly supports the hypothesis that the vasodilatation during l-arginine infusion might be mediated by an increase in NO synthesis. If so, our data suggest that the presumed markers for NO synthesis, plasma cyclic GMP and l-citrulline concentrations, do not accurately reflect this increase. Instead, the rise in plasma cyclic GMP may be related to the rise in ANP. The rise in l-citrulline may be related to competition with l-arginine for the same cell membrane transport mechanism and to stimulation of the urea cycle.

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Stimulation of arginine vasopressin secretion by a small increase in blood ionized calcium in normal men

European Journal of Clinical Investigation ◽

10.1046/j.1365-2362.1997.1450694.x ◽

1997 ◽

Vol 27 (7) ◽

pp. 575-578 ◽

Cited By ~ 1

Author(s):

P. CHIODERA ◽

R. VOLPI ◽

L. CAPRETTI ◽

G. CAFFARRI ◽

S. PILLA ◽

...

Keyword(s):

Arginine Vasopressin ◽

Ionized Calcium ◽

Vasopressin Secretion ◽

Normal Men ◽

Stimulation Of

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Impact of hydrocortisone and of CRH infusion on the hypothalamus-pituitary-adrenocortical axis of septic male mice

Endocrinology ◽

10.1210/endocr/bqab222 ◽

2021 ◽

Author(s):

Arno Téblick ◽

Lauren De Bruyn ◽

Tim Van Oudenhove ◽

Sarah Vander Perre ◽

Lies Pauwels ◽

...

Keyword(s):

Adrenal Cortex ◽

Plasma Cortisol ◽

Adrenocorticotropic Hormone ◽

Ex Vivo ◽

High Plasma ◽

Plasma Acth ◽

Markers Of Inflammation ◽

Equimolar Dose ◽

And Function ◽

Stimulation Of

Abstract Purpose Sepsis is hallmarked by high plasma cortisol/corticosterone (CORT), low adrenocorticotropic hormone (ACTH) and high pro-opiomelanocortin (POMC). While corticotropin-releasing hormone-(CRH) and arginine-vasopressin-(AVP) driven pituitary POMC expression remains active, POMC processing into ACTH becomes impaired. Low ACTH is accompanied by loss of adrenocortical structure, although steroidogenic enzymes remain expressed. We hypothesized that treatment of sepsis with hydrocortisone (HC) aggravates this phenotype whereas CRH infusion safeguards ACTH-driven adrenocortical structure. Methods In a fluid-resuscitated, antibiotics-treated mouse model of prolonged sepsis, we compared the effects of HC and CRH infusion with placebo, on plasma ACTH, POMC and CORT and on markers of hypothalamic CRH and AVP signaling and pituitary POMC processing, and on the adrenocortical structure and markers of steroidogenesis. In adrenal explants, we studied the steroidogenic capacity of POMC. Results During sepsis, HC further suppressed plasma ACTH, but not POMC, predominantly by suppressing sepsis-activated CRH/AVP-signaling pathways. In contrast, in CRH-treated sepsis, plasma ACTH was normalized following restoration of pituitary POMC processing. The sepsis-induced rise in markers of adrenocortical steroidogenesis was unaltered by CRH and suppressed partially by HC which also increased adrenal markers of inflammation. Ex vivo stimulation of adrenal explants with POMC increased CORT as effectively as an equimolar dose of ACTH. Conclusions Treatment of sepsis with HC impaired integrity and function of the HPA axis at the level of the pituitary and the adrenal cortex while CRH restored pituitary POMC processing without affecting the adrenal cortex. Sepsis-induced high circulating POMC may be responsible for ongoing adrenocortical steroidogenesis despite low ACTH.

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