scholarly journals KATP Channels and Pancreatic Islet Blood Flow in Anesthetized Rats: Increased Blood Flow Induced by Potassium Channel Openers

Diabetes ◽  
2003 ◽  
Vol 52 (8) ◽  
pp. 2043-2048 ◽  
Author(s):  
L. Jansson ◽  
M. Kullin ◽  
F. A. Karlsson ◽  
B. Bodin ◽  
J. B. Hansen ◽  
...  
Keyword(s):  
Blood Flow ◽  
Potassium Channel ◽  
Pancreatic Islet ◽  
Katp Channels ◽  
Potassium Channel Openers ◽  
Islet Blood Flow ◽  
Anesthetized Rats ◽  
Increased Blood Flow

Pancreatic islet blood flow in conscious rats during hyperglycemia and hypoglycemia

2001 ◽  
Vol 280 (6) ◽  
pp. R1601-R1605 ◽  
Author(s):  
M. Iwase ◽  
K. Tashiro ◽  
Y. Uchizono ◽  
D. Goto ◽  
M. Yoshinari
Keyword(s):  
Blood Flow ◽  
Pancreatic Islet ◽  
Organ Perfusion ◽  
Pancreatic Blood Flow ◽  
Pentobarbital Sodium ◽  
Time Points ◽  
Conscious Rats ◽  
Colored Microspheres ◽  
Islet Blood Flow ◽  
Anesthetized Rats

Anesthesia affects general hemodynamics and regulation of organ perfusion. We used colored microspheres to measure pancreatic islet blood flow in conscious rats at two time points, during either hyperglycemia or hypoglycemia. This method, using black and green microspheres, was validated by comparison with previous microsphere experiments and by lack of effect of a nonmetabolizable glucose analog, 3- O-methylglucose, on islet perfusion. Basal and glucose-stimulated islet blood flow levels were similar in pentobarbital sodium-anesthetized and conscious rats. However, the basal distribution of pancreatic blood flow was altered by anesthesia (fractional islet blood flow 5.8 ± 0.4% in conscious rats, 7.9 ± 0.8% in pentobarbital-anesthetized rats, P < 0.05). Insulin-induced hypoglycemia significantly increased whole pancreatic blood flow in conscious rats, whereas islet blood flow remained unchanged and fractional islet blood flow was decreased (5.8 ± 0.5% in the basal state, 4.2 ± 0.4% during hypoglycemia, P < 0.001). Methylatropine pretreatment significantly increased islet blood flow during hypoglycemia by 181%. This result suggests that prevention of hypoglycemia-induced increase in islet perfusion may be mediated, at least in part, by a cholinergic, vagal muscarinic mechanism.

Blood lipids affect rat islet blood flow regulation through β3-adrenoceptors

2014 ◽  
Vol 307 (8) ◽  
pp. E653-E663 ◽  
Author(s):  
Enyin Lai ◽  
Ulrika Pettersson ◽  
Alberto Delgado Verdugo ◽  
Per-Ola Carlsson ◽  
Birgitta Bodin ◽  
...  
Keyword(s):  
Blood Flow ◽  
Pancreatic Islet ◽  
Blood Lipids ◽  
Parasympathetic Nervous System ◽  
Serum Insulin ◽  
Insulin Response ◽  
Simultaneous Increase ◽  
Acute Administration ◽  
Islet Blood Flow ◽  
Anesthetized Rats

Pancreatic islet blood perfusion varies according to the needs for insulin secretion. We examined the effects of blood lipids on pancreatic islet blood flow in anesthetized rats. Acute administration of Intralipid to anesthetized rats increased both triglycerides and free fatty acids, associated with a simultaneous increase in total pancreatic and islet blood flow. A preceding abdominal vagotomy markedly potentiated this and led acutely to a 10-fold increase in islet blood flow associated with a similar increase in serum insulin concentrations. The islet blood flow and serum insulin response could be largely prevented by pretreatment with propranolol and the selective β3-adrenergic inhibitor SR-59230A. The nitric oxide synthase inhibitor NG-nitro-l-arginine methyl ester prevented the blood flow increase but was less effective in reducing serum insulin. Increased islet blood flow after Intralipid administration was also seen in islet and whole pancreas transplanted rats, i.e., models with different degrees of chronic islet denervation, but the effect was not as pronounced. In isolated vascularly perfused single islets Intralipid dilated islet arterioles, but this was not affected by SR-59230A. Both the sympathetic and parasympathetic nervous system are important for the coordination of islet blood flow and insulin release during hyperlipidemia, with a previously unknown role for β3-adrenoceptors.

A specific β3-adrenoceptor agonist induces increased pancreatic islet blood flow and insulin secretion in rats

1996 ◽  
Vol 298 (3) ◽  
pp. 287-292 ◽  
Author(s):  
Nadia Atef ◽  
Max Lafontan ◽  
Alexandre Double ◽  
Christophe Hélary ◽  
Alain Ktorza ◽  
...  
Keyword(s):  
Blood Flow ◽  
Insulin Secretion ◽  
Pancreatic Islet ◽  
Islet Blood Flow ◽  
Adrenoceptor Agonist

Endothelin-1 and pancreatic islet vasculature: studies in vivo and on isolated, vascularly perfused pancreatic islets

2007 ◽  
Vol 292 (6) ◽  
pp. E1616-E1623 ◽  
Author(s):  
En Yin Lai ◽  
A. Erik G. Persson ◽  
Birgitta Bodin ◽  
Örjan Källskog ◽  
Arne Andersson ◽  
...  
Keyword(s):  
Blood Flow ◽  
Pancreatic Islet ◽  
Vascular Reactivity ◽  
Blood Perfusion ◽  
Receptor Subtype ◽  
Endothelin 1 ◽  
Islet Blood Flow ◽  
Endothelin B

Endothelin-1 (ET-1) is a potent endothelium-derived vasoconstrictor, which also stimulates insulin release. The aim of the present study was to evaluate whether exogenously administered ET-1 affected pancreatic islet blood flow in vivo in rats and the islet arteriolar reactivity in vitro in mice. Furthermore, we aimed to determine the ET-receptor subtype that was involved in such responses. When applying a microsphere technique for measurements of islet blood perfusion in vivo, we found that ET-1 (5 nmol/kg) consistently and markedly decreased total pancreatic and especially islet blood flow, despite having only minor effects on blood pressure. Neither endothelin A (ETA) receptor (BQ-123) nor endothelin-B (ETB) receptor (BQ-788) antagonists, alone or in combination, could prevent this reduction in blood flow. To avoid confounding interactions in vivo, we also examined the arteriolar vascular reactivity in isolated, perfused mouse islets. In the latter preparation, we demonstrated a dose-dependent constriction in response to ET-1. Administration of BQ-123 prevented this, whereas BQ-788 induced a right shift in the response. In conclusion, the pancreatic islet vasculature is highly sensitive to exogenous ET-1, which mediates its effect mainly through ETA receptors.

scholarly journals Duct ligation and pancreatic islet blood flow in rats: physiological growth of islets does not affect islet blood perfusion

2005 ◽  
Vol 153 (2) ◽  
pp. 345-351 ◽  
Author(s):  
Leif Jansson ◽  
Birgitta Bodin ◽  
Örjan Källskog ◽  
Arne Andersson
Keyword(s):  
Blood Flow ◽  
Pancreatic Islet ◽  
Serum Insulin ◽  
Blood Perfusion ◽  
Islet Function ◽  
Sprague Dawley ◽  
Islet Mass ◽  
Islet Blood Flow ◽  
Sprague Dawley Rats ◽  
Duct Ligation

Objectives: The aim of this study was to evaluate islet blood-flow changes during stimulated growth of the islet organ without any associated functional impairment of islet function. Design: A duct ligation encompassing the distal two-thirds of the pancreas was performed in adult, male Sprague–Dawley rats. Methods: Pancreatic islet blood flow was measured in duct-ligated and sham-operated rats 1, 2 or 4 weeks after surgery. In some animals studied 4 weeks after surgery, islet blood flow was also measured also during hyperglycaemic conditions. Results: A marked atrophy of the exocrine pancreas was seen in all duct-ligated rats. Blood glucose and serum insulin concentrations were normal. An increased islet mass was only seen 4 weeks after surgery. No differences in islet blood perfusion were noted at any time point after duct ligation. In both sham-operated and duct-ligated rats islet blood flow was increased during hyperglycaemia; the response was, however, slightly more pronounced in the duct-ligated part of the gland. Conclusions: Normal, physiological islet growth does not cause any major changes in the islet blood perfusion or its regulation. This is in contrast to findings during increased functional demands on the islets or during deteriorated islet function, when increased islet blood flow is consistently seen.

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