Effects of Glucose and Sodium Chloride on the Release of Vasopressin in Response to Angiotensin II from the Guinea Pig Hypothalamo-Neurohypophyseal Complex in Organ Culture

Ishikawa, San‐e; Saito, Toshikazu; Yoshida, Sho

doi:10.1159/000123104

Cited by 13 publications

(4 citation statements)

References 23 publications

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“…Robertson et al (12) and Zerbe & Robertson (15) reported that glucose inhibits the release of AVP from the neurohypophysis. We confirmed glucose inhibition of AVP release using the in vitro hypothalamo-neurohypophyseal complex in organ culture (16,17). How¬ ever, a recent report by Vokes et al (18) described that glucose is an effective osmotic stimulant ofAVP release under insulinopenic conditions.…”

Section: Discussionsupporting

confidence: 74%

Prompt recovery of plasma arginine vasopressin in diabetic coma after intravenous infusion of a small dose of insulin and a large amount of fluid

Ishikawa

Saito²,

Okada³

et al. 1990

Acta Endocrinologica

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We studied the changes in plasma arginine vasopressin in 5 patients with diabetic ketoacidosis and one patient with non-ketotic hyperosmolar coma who had marked hyperglycemia (36.6 \ m=+-\ 4.6 mmol/l, mean \ m=+-\ sem) and dehydration. Plasma osmolality (Posm) was 342.2 \ m=+-\ 11.4 mOsm/kg H2O, and hematocrit, serum protein, and blood urea nitrogen were also elevated at hospitalization. Circulating blood volume was decreased by approximately 21% as compared with that on day 7. Plasma AVP level was increased to 8.5 \m=+-\1.6 pmol/l at hospitalization. When hyperglycemia was improved by iv infusion of a small dose of insulin plus fluid administration, plasma AVP level promptly decreased to 2.4 \m=+-\0.4 pmol/l within six hours. When plasma AVP level had normalized, Posm was still as high as 305 mOsm/kg H2O, but the loss of circulating blood volume was only 4.2% of the control state. Plasma AVP level was positively correlated with change in hematocrit (plasma AVP = 3.58 + 0.45 \m=.\ hematocrit, r = 0.468, p < 0.01), serum protein (r = 0.487, p < 0.01), Posm (r = 0.388, p < 0.01), and blood glucose (r = 0.582, p < 0.01). Plasma AVP level was negatively correlated with the change in circulating blood volume (plasma AVP = 3.6 \p=n-\0.14 \ m=. \ change in circulating blood volume, r = \m=-\0.469, p <0.01). These results indicate that both non-osmotic and osmotic stimuli are involved in the mechanism for AVP release in patients with diabetic coma, and that the non-osmotic control of AVP may contribute to circulating homeostasis, protecting against severe blood volume depletion in diabetic patients suffering from hyperglycemia and dehydration.We have demonstrated that plasma arginine vaso¬ pressin increases in patients with non-insulin-de¬ pendent diabetes mellitus whose fasting blood glu¬ cose is moderately elevated (9.5-10.1 mmol/1, mean value) (1). Such an increase in plasma AVP normalized at the time of discharge, and it is closely related to the decrement in circulating blood volume.Marked elevation of blood glucose is common in ketotic and non-ketotic diabetic coma, accompa¬ nied by marked glucosuria and osmotic diuresis. The patients are thus suffering from serious dehy¬ dration. Such volume-depleted states usually in¬ crease plasma renin activity (PRA) and plasma aldosterone concentration (2). This has been ex¬ plained by the decrease in circulating blood volume, mediated through an activation of baroreceptors. Several reports have shown that plasma AVP is also elevated in diabetic ketoacidosis (3-6).Zerbe et al. noted the relative roles of osmotic and non-osmotic stimuli in AVP response (3). The phys¬ iological significance of elevated AVP and the mechanism for the increase in AVP release in con¬ ditions such as ketoacidosis are still unclear, how¬ ever.In the present study we determined whether plasma AVP increases in diabetic coma, and what mechanisms are involved in the increase in AVP release. Also, we investigated how fast the in¬ creased level of plasma AVP returns to the normal range after the start of in...

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Section: Discussionsupporting

confidence: 74%

Prompt recovery of plasma arginine vasopressin in diabetic coma after intravenous infusion of a small dose of insulin and a large amount of fluid

Ishikawa

Saito²,

Okada³

et al. 1990

Acta Endocrinologica

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“…At the same time, we continuously measured the SjvO 2 value and regional cerebral oxygenation using an analysis system (Explorer system, Baxter Healthcare Corp, Irvine, Calif) and found that there were no changes in the SjvO 2 and regional cerebral oxygenation values throughout the study. In our previous study, 2 we reported a close correlation between the oxygen saturation value measured by the optical catheter and the oxygen saturation value in sampled blood by the blood gas analyzer. Therefore we do not think that the change in Sjvo 2 would be observed if the value had been measured more frequently during cardiopulmonary bypass (CPB).…”

Section: Reply To the Editorsupporting

confidence: 59%

“…While discussing the mechanisms for arginine vasopressin deficiency, which may be multifactorial, the authors failed to mention that angiotensin II decreases arginine vasopressin release from the neurohypophysis. 2 This implies that the newer selective angiotensin II inhibitors like losartan may also cause vasodilatory shock.…”

Section: Vasodilatation After Cardiac Surgerymentioning

confidence: 99%

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Kadoi

Saito

2000

The Journal of Thoracic and Cardiovascular Surgery

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unlikely that the modest IABP-induced pulse pressure of only 24 ± 8 mm Hg would generate a dp/dt of 645 ± 64 mm Hg/s, particularly at the level of small cerebral arteries, and thus be enough to produce sufficient stretch to induce significant production of L-arginine in the small cerebral arteries. If the pulse pressure was not sufficient, then significant cerebral vasodilation would not be obtained to affect the SjvO 2 , and hence the IABP-induced pulsatility would be unable to ameliorate the impaired SjvO 2 . A similar study using a pulsatile system capable of producing a pulse pressure of 50 to 60 mm Hg 6 to mimic that produced by the natural heart would be needed to be able to definitely exclude or include the role played by pulsatility. The study only demonstrates that the modest IABP-induced pulsatility was not effective but by no means excludes the role pulsatility may have.3. It is widely known that during CPB the levels of circulating endogenous catecholamines including norepinephrine are increased. During systemic infusion of norepinephrine, increased electrical brain activity (consisting of increased low-voltage high-frequency waves and decreased high-voltage slow-frequency waves) suggestive of promotion of excitatory (N-methyl-D-aspartate?) receptor activation has been noted in nonischemic rabbits (unpublished observations of electroencephalograms concurrent to brain microdialysis studies), which may lead to Na + and Ca ++ influx. To maintain the normal Na + and Ca ++ transmembrane gradient, the demand for mechanisms to extrude them, which are highly oxygen consuming, will be increased. Therefore during late CPB the decreased SjvO 2 might be a manifestation of that increased oxygen extraction not counteracted by the anesthetics, pressures, or pulsatility used by the authors. The exact effect of increased circulating catecholamines during CPB on the cerebral vasculature is not known, but if it was equivalent to increased sympathetic activity, then vasoconstriction of small cerebral vessels would result with consequent decreased flow. 7 If both effects are operating, the development of decreased SjvO 2 over the first 20 minutes of perfusion and the return to normal after CPB, also in 20 or 30 minutes, are easily explainable.Norepinephrine determination with and without blockade in conjunction with metabolic studies across the brain in both groups might shed some light.

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“…On the other hand, vasopressin is also released when an giotensin is added to the bathing medium [33,34,61] which is to be expected since angiotensin can directly excite supraoptic neurones [50]. However, both angiotensin-and osmotically-stimulated hormone secretion are blocked by saralasin, an angiotensin antagonist [62].…”

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confidence: 99%

The Supraoptic Nucleus as an Osmoreceptor

Leng

Mason

Dyer³

1982

Neuroendocrinology

131

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This ‘Progress’ review is written to challenge the prevalent belief that neurones of the supraoptic nucleus are not involved in the reception of osmotic stimuli. Evidence is presented that these neurones are depolarised by physiological increases in the osmotic pressure of the extracellular fluid. However, generation of action potentials in these depolarised cells still requires the presence of synaptic input from currently unidentified neurones. We suggest that the osmoreceptor regulating vasopressin secretion is probably composed of more than one type of neurone and discuss this suggestion in the context of selected experiments previously cited as evidence that the supraoptic nucleus is not involved in osmoreception.

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Effects of Glucose and Sodium Chloride on the Release of Vasopressin in Response to Angiotensin II from the Guinea Pig Hypothalamo-Neurohypophyseal Complex in Organ Culture

Cited by 13 publications

References 23 publications

Prompt recovery of plasma arginine vasopressin in diabetic coma after intravenous infusion of a small dose of insulin and a large amount of fluid

Prompt recovery of plasma arginine vasopressin in diabetic coma after intravenous infusion of a small dose of insulin and a large amount of fluid

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The Supraoptic Nucleus as an Osmoreceptor

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