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Biomedical subjects

T Sakaguchi

Publications and source records attributed to T Sakaguchi.

At least 343 records · Page 19Linked to original sources
PubMed1982

Alterations in gastric acid secretion following hepatic portal injections of D-glucose and its anomers.

Changes in acid outputs from the stomach were examined after portal injections of D-glucose and its optical anomers in the bilaterally adrenalectomized rats with insulin hypoglycaemia. Significant decrease in gastric acid outputs was noted after portal injections of alpha-D-glucose, optically equilibrated D-glucose (OEDG) consisting of 36% alpha-anomer and 64% beta-anomer and beta-D-glucose. The effect of beta-D-glucose was most potent in reducing the acid outputs and the inhibitory response was entirely prevented by prior vagotomy at the hepatic level. The injections of isotonic NaCl solution, however, produced no change in the acid outputs. Results suggest that changes in glucose levels in the portal vein may modulate gastric acid secretion through hepatic vagal afferents and gastric vagal efferents and suggest that activation of hepatic glucosensitive mechanisms may be dependent on the anomeric stereospecificity of D-glucose in the blood.

Afferent Pathways↗
PubMed1982

Central role of angiotensin in the hyperosmolality- and hypovolaemia-induced vasopressin release in conscious rats.

To evaluate a central role of angiotensin in vasopressin (ADH) release in response to hyperosmolality or hypovolaemia, we examined in conscious rats the effects of intraperitoneal (ip) injections of 2 ml/100 g body weight of hypertonic saline or polyethylene glycol (PEG; 250 mg/ml of 145 mM NaCl) on plasma ADH and angiotensin II (AII) levels and of intracerebroventricular (icv) administrations of Sar1-Ala8-AII (a competitive receptor blocker for AII) on the plasma ADH responses to the ip injections. Thirty min after ip injections of 900 mM NaCl, plasma ADH, osmolality and sodium increased with unchanged plasma AII and with reduced haematocrit. Two h after ip administrations of PEG, plasma ADH, AII and haematocrit were augmented with unaltered plasma osmolality and sodium. The responses of plasma ADH to ip injections of 900 mM NaCl and PEG were significantly inhibited (P less than 0.05) by 1 microgram of Sar1-Ala8-AII injected icv 5 min before blood samplings which had no appreciable effect on plasma osmolality, electrolytes and haematocrit. Based on these results, we concluded that angiotensin may participate in both the hyperosmolality- and hypovolaemia-induced ADH secretion by acting on the central nervous system.

Angiotensin II↗
PubMed1981

Effect of nephrectomy on angiotensin II concentrations in plasma and hypothalamus of the dehydrated rat.

Bilateral nephrectomy in the rats deprived of water for 46 h markedly reduced plasma angiotensin II concentrations (P less than 0.001), but it was without effect on extremely low levels of the hormone in the hypothalamic tissue. These results may suggest that the activity of a possible intrinsic brain renin-angiotensin system is not influenced by that of the kidney-plasma renin-angiotensin system.

Angiotensin II↗
PubMed1981

Adrenergic mechanisms in the hyperglycaemia and hyperinsulinaemia of diabetic KK mice.

Simultaneous occurrence of hyperglycaemia (up to 300 mg/100 ml) and hyperinsulinaemia (up to 1200 mu U/ml) was evident in the fed state in genetically diabetic KK mice, indicating insulin resistance. The hyperinsulinaemia was enhanced by alpha-adrenergic blockade and alleviated by B-blockade. Epinephrine-induced hyperglycaemia and isoproterenol-induced hyperinsulinaemia, both of which could be blocked by beta-adrenergic antagonists, were more marked in KK mice than in ICR mice. A possible significance of adrenergic mechanisms is discussed with respect to the aetiology of the metabolic disturbances characteristic of KK mice.

Animals↗
PubMed1981

Turnover rate of blood glucose in diabetic KK mice.

Metabolic rate constants for blood glucose turnover were estimated based on the decay of [U-14C, 6-3H]glucose injected intravenously in genetically diabetic KK mice. Comparison was made with the rate constants similarly obtained with non-diabetic and streptozotocin-induced diabetic ICR mice. Recycling of blood glucose via the Cori cycle, as estimated from the difference in the decay rate between 14C and 3H, was more active in KK mice than in non-diabetic and diabetic ICR mice. The Cori cycle activity was reduced by beta-adrenergic blockade in KK mice and was enhanced by alpha-blockade in ICR mice. It is concluded that predominance of beta-adrenergic functions in KK mice is responsible for activation of the Cori cycle as one of the mechanisms for metabolic resistance to endogenous insulin.

Animals↗
PubMed1980

Effects of intraventricular injection of Sar1-Ala8-angiotensin II on plasma vasopressin level increased by angiotensin II and by water deprivation in conscious rats.

The effects of intraventricular injection of Sar1-Ala8-angiotensin II (A specific antagonist of angiotensin II) on the plasma vasopressin level increased by intraventricular injection of angiotensin II and by water deprivation (46 h) were examined in conscious male rats with an indwelling cannula in the third cerebral ventricle. Blood samplings were made by decapitation and the plasma level of vasopressin was determined by radioimmunoassay. Twenty-five, 50 or 100 ng of angiotensin II produced significant (P less than 0.05) increase in plasma vasopressin level 90 sec after the injection. The effect of 50 ng of angiotensin II was inhibited significantly (P less than 0.05) at least with 100 ng of Sar1-Ala8-angiotensin II given 2 min before the injection of angiotensin II. The dehydrated rats to which 1000 ng of Sar1-Ala8-angiotensin II was given 5 min before the decapitation showed the significantly (P less than 0.05) lower median plasma vasopressin level than that of the dehydrated controls. No significant difference in plasma osmolality was noted between them. These results suggest that the plasma vasopressin response to intraventricular angiotensin II is produced via angiotensin II receptors in the brain and that Sar1-Ala8-angiotensin II inhibits the effect of endogenous angiotensin II on plasma vasopressin level under dehydration.

Angiotensin II↗
PubMed1980

Effects of vagal stimulation, vagotomy and adrenalectomy on release of insulin in the rat.

To evaluate the physiological role of the vagus nerve in the secretion of insulin in the rat, changes in plasma levels of insulin and sugar were examined after vagotomy with and without adrenalectomy. Male rats, fasted for 22 h, weighing about 300 g and anaesthetized with pentobarbitone sodium were used. Thirty minutes after unilateral or bilateral adrenalectomy, the first blood sample was taken just before pancreatic vagotomy and a second sample was taken 15 min after vagotomy. Pancreatic vagotomy significantly decreased levels of plasma insulin in bilaterally adrenalectomized rats. It was also confirmed that electrical stimulation of the pancreatic vagus nerve provoked an increase in levels of insulin associated with a reduction of carbohydrates in the blood. These observations support the theory that there is a vagal mechanism which modulates the secretion of insulin and suggest that the vagal mechanism is a potent factor although such a mechanism may be masked by the activity of the adrenal gland.

Adrenalectomy↗