In Vivo Cardiac Measurements in the Conscious Rat

1. The influence of urine pH on the urinary excretion of prostaglandin (PG) F2α and the PGE2/PGF2α ratio has been examined in the conscious rat. 2. The basal urinary PGF2α excretion rate of 3.9 pmol/h (n = 23) did not vary with urine pH. In marked contrast, PGE2 excretion increased as the urine became more alkaline. The PGE2/PGF2α ratio therefore progressively increased from 1.5 to 22 as the pH of the urine changed from pH 5.8 to pH 7.8. 3. The independence of PGF2α excretion from urine pH: (a) excludes cyclo-oxygenase as a potential site of action for the pH-dependence of urinary PGE2 excretion; (b) suggests that the urinary PGE2/PGF2α ratio measured in alkaline urine may be a more accurate reflection of the kidneys, ability to synthesize these two prostaglandins in vivo; (c) suggests that control of urine pH is required before the urinary PGE2/PGF2α ratio can be employed as an index of PGE2 9-ketoreductase (EC 1.1.1.189) activity in vivo.

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Short-term K+ deprivation provokes insulin resistance of cellular K+ uptake revealed with the K+ clamp

AJP Renal Physiology ◽

10.1152/ajprenal.2001.280.1.f95 ◽

2001 ◽

Vol 280 (1) ◽

pp. F95-F102 ◽

Cited By ~ 35

Author(s):

Cheol S. Choi ◽

Curtis B. Thompson ◽

Patrick K. K. Leong ◽

Alicia A. McDonough ◽

Jang H. Youn

Keyword(s):

Insulin Resistance ◽

Atpase Activity ◽

Infusion Rate ◽

Insulin Action ◽

Insulin Dose ◽

Short Term ◽

Conscious Rat ◽

Physiological Concentration ◽

Glucose Clearance

We aimed to test the feasibility of quantifying insulin action on cellular K+ uptake in vivo in the conscious rat by measuring the exogenous K+ infusion rate needed to maintain constant plasma K+ concentration ([K+]) during insulin infusion. In this “K+ clamp” the K+ infusion rate required to clamp plasma [K+] is a measure of insulin action to increase net plasma K+ disappearance. K+ infusion rate required to clamp plasma [K+] was insulin dose dependent. Renal K+ excretion was not significantly affected by insulin at a physiological concentration (∼90 μU/ml, P > 0.05), indicating that most of insulin-mediated plasma K+ disappearance was due to K+ uptake by extrarenal tissues. In rats deprived of K+ for 2 days, plasma [K+] fell from 4.2 to 3.8 mM, insulin-mediated plasma glucose clearance was normal, but insulin-mediated plasma K+ disappearance decreased to 20% of control, even though there was no change in muscle Na-K-ATPase activity or expression, which is believed to be the main K+ uptake route. After 10 days K+ deprivation, plasma [K+] fell to 2.9 mM, insulin-mediated K+ disappearance decreased to 6% of control (glucose clearance normal), and there were 50% decreases in Na-K-ATPase activity and α2-subunit levels. In conclusion, the present study proves the feasibility of the K+ clamp technique and demonstrates that short-term K+ deprivation leads to a near complete insulin resistance of cellular K+uptake that precedes changes in muscle sodium pump expression.

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In vivo insulin sensitivity in the rat determined by euglycemic clamp

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1983.245.1.e1 ◽

1983 ◽

Vol 245 (1) ◽

pp. E1-E7 ◽

Cited By ~ 21

Author(s):

E. W. Kraegen ◽

D. E. James ◽

S. P. Bennett ◽

D. J. Chisholm

Keyword(s):

Insulin Sensitivity ◽

Hepatic Glucose Production ◽

Glucose Production ◽

Porcine Insulin ◽

Metabolic Clearance ◽

Conscious Rat ◽

Insulin Levels ◽

In Vivo Measurement ◽

Plasma Insulin Levels

Our aim was to develop the glucose clamp (GC) technique in the conscious rat for assessment of in vivo insulin sensitivity. A 2-h euglycemic GC could be performed in chronically cannulated rats using 625 microliter blood. Overnight-fasted rats were infused with porcine insulin (1.67 mU . kg-1 . h-1). Insulin levels of 41 +/- 2 (SE) mU/liter were produced in rats aged 91 +/- 4 days with a 60- to 120-min glucose infusion rate (GIR60-120) of 10.6 +/- 0.6 mg . kg-1 . min-1 (n = 9) during euglycemia. GIR60-120 was significantly (P less than 0.025) reduced in rats aged greater than 130 days (mean, 169 +/- 16 days) to 7.7 +/- 1.2 mg . kg-1 . min-1 (n = 7). Metabolic clearance rate of porcine insulin (46 +/- 3 ml . kg-1 . min-1) and GIR60-120 compared with plateau plasma insulin levels are higher than values reported in humans. The latter may be due to suppression of a higher basal hepatic glucose production or increased potency of porcine compared with native insulin. We conclude that the GC can be accomplished in the rat. When combined with tracer administration and subsequent killing, it should provide a quantitative in vivo measurement of insulin sensitivity in individual tissues.

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Baroreflex buffering of pressor response to vasopressin is mediated by V1, not V2, receptors in conscious rats

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1993.264.2.r345 ◽

1993 ◽

Vol 264 (2) ◽

pp. R345-R349

Author(s):

K. Shimizu ◽

J. Schwartz ◽

B. P. McGrath

Keyword(s):

Heart Rate ◽

Receptor Agonist ◽

Pressor Response ◽

Conscious Rat ◽

Conscious Rats ◽

Pressor Responses ◽

Autonomic Blockade ◽

V2 Receptor ◽

Intact Rats

Arginine vasopressin (AVP) enhances reflex buffering of its own pressor response, thus attenuating its vasoconstrictor potential in vivo. To investigate the extent to which this effect of AVP is mediated by V1 or V2 receptors, mean arterial pressure (MAP) and heart rate (HR) changes were examined in response to graded injections of AVP or [Phe2,Orn8]oxytocin, a potent, selective V1-receptor agonist, in the absence and presence of infusion of [Val4,D-Arg8]VP, a selective V2-receptor agonist. Responses were compared in intact and autonomically blocked conscious rats. During autonomic blockade with methscopolamine and hexamethonium, the pressor sensitivities to AVP and [Phe2,Orn8]oxytocin were similarly increased. Infusion of the V2-receptor agonist had no effect by itself on MAP or HR in conscious intact rats. It also did not alter the pressor responses to the V1 agonist, in either intact or autonomically blocked rats. In the presence of the V2 agonist, the decrease in heart rate induced by the V1 agonist was enhanced. These results indicate that reflex buffering of the pressor response to AVP in the conscious rat is mediated by V1 and not V2 receptors. However, V2 receptors may be involved in modulating the heart rate response to AVP.

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Effects of withdrawal from neuroleptic treatment on dopamine and gaba release in dorsolateral striatum of the conscious rat. An in vivo microdialysis study

Schizophrenia Research ◽

10.1016/0920-9964(93)90553-u ◽

1993 ◽

Vol 9 (2-3) ◽

pp. 246

Author(s):

W.T. O'Connor ◽

S. Lillrank ◽

K. Kramlinger ◽

R. Schwarcz ◽

U. Ungerstedt

Keyword(s):

Gaba Release ◽

In Vivo Microdialysis ◽

Neuroleptic Treatment ◽

Conscious Rat ◽

Dorsolateral Striatum ◽

Microdialysis Study

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Effects of chronic coffee consumption on glucose kinetics in the conscious rat

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y07-070 ◽

2007 ◽

Vol 85 (8) ◽

pp. 823-830 ◽

Cited By ~ 35

Author(s):

J. Shearer ◽

E.A. Sellars ◽

A. Farah ◽

T.E. Graham ◽

D.H. Wasserman

Keyword(s):

Coffee Consumption ◽

Epidemiological Studies ◽

Whole Body ◽

Metabolic Clearance ◽

Sprague Dawley ◽

Glucose Kinetics ◽

Conscious Rat ◽

Beneficial Effects ◽

Decaffeinated Coffee

Epidemiological studies indicate that regular coffee consumption reduces the risk of developing type 2 diabetes. Despite these findings, the biological mechanisms by which coffee consumption exerts these effects are unknown. The aim of this study was twofold: to develop a rat model that would further delineate the effects of regular coffee consumption on glucose kinetics, and to determine whether coffee, with or without caffeine, alters the actions of insulin on glucose kinetics in vivo. Male Sprague–Dawley rats were fed a high-fat diet for 4 weeks in combination with one of the following: (i) drinking water as placebo (PL), (ii) decaffeinated coffee (2 g/100 mL) (DC), or (iii) alkaloid caffeine (20 mg/100 mL) added to decaffeinated coffee (2 g/100 mL) (CAF). Catheters were chronically implanted in a carotid artery and jugular vein for sampling and infusions, respectively. Recovered animals (5 days postoperative) were fasted for 5 h before hyperinsulinemic-euglycemic clamps (2 mU·kg–1·min–1). Glucose was clamped at 6 mmol/L and isotopes (2-deoxy-[14C]glucose and [3-3H]glucose) were administered to obtain indices of whole-body and tissue-specific glucose kinetics. Glucose infusion rates and measures of whole-body metabolic clearance were greater in DC than in PL or CAF, indicating increased whole-body insulin sensitivity. As the only difference between DC and CAF was the addition of alkaloid caffeine, it can be concluded that caffeine antagonizes the beneficial effects of DC. Given these findings, decaffeinated coffee may represent a nutritional means of combating insulin resistance.

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