Effects of the Biguanide Metformin on Splanchnic Blood Flow in Rats: Preferential and Dose-Dependent Increase in Islet Blood Flow

Pharmacology ◽  
1995 ◽  
Vol 51 (1) ◽  
pp. 43-47 ◽  
Author(s):  
Leif Jansson
Keyword(s):  
Blood Flow ◽  
Splanchnic Blood Flow ◽  
Islet Blood Flow ◽  
Dose Dependent Increase ◽  
Dose Dependent

Dose-Dependent Effects of Meclofenamate on Peripheral Vasculature of Conscious Rabbits

1983 ◽  
Vol 64 (5) ◽  
pp. 471-474 ◽  
Author(s):  
R. A. Banks ◽  
L. J. Beilin ◽  
J. Soltys
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Organ Blood Flow ◽  
Hepatic Circulation ◽  
Peripheral Vasculature ◽  
Conscious Rabbits ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
The Brain ◽  
Intravenous Sodium

1. Changes in systemic haemodynamics and organ blood flow were measured in conscious rabbits after various doses of intravenous sodium meclofenamate, an inhibitor of prostaglandin cyclo-oxygenase. 2. Meclofenamate had no effect on arterial pressure or cardiac output but caused a dose-dependent fall in renal blood flow. 3. Meclofenamate also reduced adrenal perfusion but, in contrast, caused a dose-dependent increase in blood flow to the brain, bronchial and hepatic circulation and to the testis. No effect was demonstrated on other organs studied. 4. The effect on the cerebral circulation was observed at the lowest dose of meclofenamate (0.75 mg/kg). Higher total doses were necessary for an effect on the renal and bronchial (3 mg/kg) and testicular and hepatic arteries (6 mg/kg). 5. The results suggest a variety of local vasomotor influences of renal and non-renal prostaglandins in conscious rabbits.

Effects of intrarenal adenosine on renal function and medullary blood flow in the rat

1988 ◽  
Vol 255 (6) ◽  
pp. F1230-F1234 ◽  
Author(s):  
M. Miyamoto ◽  
Y. Yagil ◽  
T. Larson ◽  
C. Robertson ◽  
R. L. Jamison
Keyword(s):  
Blood Flow ◽  
Sodium Excretion ◽  
Systemic Circulation ◽  
Urinary Flow ◽  
Medullary Blood Flow ◽  
Vasa Recta ◽  
Potent Vasodilator ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Higher Doses

Adenosine is a potent vasodilator of the systemic circulation. Infusion of adenosine into the aorta causes water and sodium retention and a fall in glomerular filtration rate and renal blood flow. The effect of adenosine on medullary blood flow is unknown. Because systemic vasodilatory effects may confound its renal actions, adenosine was infused into the renal artery of anesthetized Munich-Wistar rats at doses of 2, 6, and 15 micrograms/min. A marked dose-dependent increase in urinary flow and sodium excretion was observed. Inulin and p-aminohippuric acid clearance did not change significantly. Blood flow in vasa recta in the exposed renal papilla, as determined by fluorescence videomicroscopy, increased significantly only with the highest dose of adenosine. In control animals infused with the vehicle only, there was no change in any of the above variables. These results indicate that direct intrarenal infusion of adenosine in the rat increases urinary flow and sodium excretion and at higher doses also increases vasa recta blood flow. The effects on urinary flow and sodium excretion were therefore mediated by a mechanism other than an increase in vasa recta blood flow.

Dopamine stimulates cAMP production in canine afferent arterioles via DA1 receptors

1989 ◽  
Vol 256 (3) ◽  
pp. H626-H629
Author(s):  
T. Tamaki ◽  
C. E. Hura ◽  
R. T. Kunau
Keyword(s):  
Blood Flow ◽  
Sch 23390 ◽  
Fold Increase ◽  
Camp Accumulation ◽  
Afferent Arteriole ◽  
Camp Production ◽  
Receptor Stimulation ◽  
Afferent Arterioles ◽  
Dose Dependent Increase ◽  
Dose Dependent

Dopamine increases renal blood flow and dilates isolated afferent and efferent arterioles preconstricted with norepinephrine via dopamine 1 (DA1) receptors. DA1-receptor stimulation also results in dopamine-induced elevation of adenosine 3'5'-cyclic monophosphate (cAMP) in dog and rat renal arteries. The present study was undertaken to determine the effects of dopamine on cAMP accumulation in isolated canine superficial cortical afferent arterioles. The effect of Sch 23390, a specific DA1-receptor antagonist, on dopamine-stimulated cAMP accumulation was also examined. Forskolin (10(-5) M), a potent stimulator of adenylate cyclase, produced a greater than 11-fold increase in cAMP production compared with control. Dopamine produced a dose-dependent increase in cAMP accumulation in afferent arterioles at concentrations of 10(-4) M and 10(-6) M, Sch 23390 (2 x 10(-4) M) abolished dopamine (10(-4) M)-stimulated cAMP accumulation in afferent arterioles. The dopamine-induced increase in arteriolar cAMP accumulation was unaffected by propranolol (10(-4) M). Our results suggest that dopamine increases cAMP production in afferent arterioles via the DA1 receptor. Increased cAMP production may be responsible for dopamine-induced vasodilation in the afferent arteriole.

Loss of vasomotor responsiveness to the μ-opioid receptor ligand endomorphin-1 in adjuvant monoarthritic rat knee joints

2004 ◽  
Vol 286 (4) ◽  
pp. R634-R641 ◽  
Author(s):  
Jason J. McDougall ◽  
A. Kursat Barin ◽  
Chelsea M. McDougall
Keyword(s):  
Blood Flow ◽  
Opioid Receptor ◽  
Opioid Receptors ◽  
Immunohistochemical Analysis ◽  
Knee Joints ◽  
Μ Opioid Receptor ◽  
Arthritic Joints ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Μ Opioid Receptors

Endomorphin-1 is a short-chain neuropeptide with a high affinity for the μ-opioid receptor and has recently been localized in acutely inflamed knee joints where it was found to reduce inflammation. The present study examined the propensity of endomorphin-1 to modulate synovial blood flow in normal and adjuvant-inflamed rat knee joints. Under deep urethane anesthesia, endomorphin-1 was topically applied to exposed normal and 1 wk adjuvant monoarthritic knee joints (0.1 ml bolus; 10-12-10-9 mol). Relative changes in articular blood flow were measured by laser Doppler perfusion imaging and vascular resistances in response to the opioid were calculated. In normal knees, endomorphin-1 caused a dose-dependent increase in synovial vascular resistance and this effect was significantly inhibited by the specific μ-opioid receptor antagonist d-Phe-Cys-Tyr-d-Trp-Orn-Thr-Pen-Thr amide (CTOP) ( P < 0.0001, 2-factor ANOVA, n = 5-7). One week after adjuvant inflammation, the hypoaemic effect of endormophin-1 was completely abolished ( P < 0.0001, 2-factor ANOVA, n = 5-7). Immunohistochemical analysis of normal and adjuvant-inflamed joints showed a ninefold increase in endomorphin-1 levels in the monoarthritic knee compared with normal control. Western blotting and immunohistochemistry revealed a moderate number of μ-opioid receptors in normal knees; however, μ-opioid receptors were almost undetectable in arthritic joints. These findings demonstrate that peripheral administration of endomorphin-1 reduces knee joint blood flow and this effect is not sustainable during advanced inflammation. The loss of this hypoaemic response appears to be due to downregulation of μ-opioid receptors as a consequence of endomorphin-1 accumulation within the arthritic joint.

Effect of isoproterenol on phosphorylase activation in the hyperthyroid rat heart

1979 ◽  
Vol 57 (6) ◽  
pp. 567-573 ◽  
Author(s):  
Penelope A. Longhurst ◽  
John H. McNeill
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Time Dependent ◽  
Force Of Contraction ◽  
Phosphorylase Activity ◽  
Isolated Atria ◽  
Langendorff Hearts ◽  
The Right ◽  
Dose Dependent Increase ◽  
Dose Dependent

Pretreatment of rats for 3 days with triiodothyronine produced an increase in rate in the right atrium and a decrease in force of contraction in the right ventricle and Langendorff heart.Isoproterenol administration produced a time-dependent increase in rate and tension. The increase in rate was consistently greater in atria from hyperthyroid rats, and the increase in tension consistently greater in tissues from euthyroid rats. Isoproterenol also produced a time- and dose-dependent increase in phosphorylase a activity. In the isolated atria and ventricles enzyme activity was similar in the two groups. In the Langendorff hearts, however, there was an enhancement of the isoproterenol-induced increase in phosphorylase activity in hearts from hyperthyroid rats. Reduction of the coronary blood flow to the level found in euthyroid animals did not reduce the potentiation of phosphorylase activation found in hearts from hyperthyroid rats.It is concluded that the potentiation of phosphorylase activation in hearts from hyperthyroid rats is not due to the increase in coronary blood flow.

DOSE DEPENDENT INCREASE OF CEREBRAL BLOOD FLOW WITH ENDOTHELIN-1 DURING ADVANCED CARDIAC LIFE SUPPORT IN PIGS

1999 ◽  
Vol 27 (Supplement) ◽  
pp. 108A
Author(s):  
Michael Holzer ◽  
Wilhelm Behringer ◽  
Fritz Sterz ◽  
Elisabeth Oschatz ◽  
Julia Kofler ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Life Support ◽  
Advanced Cardiac Life Support ◽  
Endothelin 1 ◽  
Dose Dependent Increase ◽  
Dose Dependent

Ethanol-induced increase in portal blood flow: role of adenosine

1988 ◽  
Vol 254 (4) ◽  
pp. G495-G501 ◽  
Author(s):  
H. Orrego ◽  
F. J. Carmichael ◽  
V. Saldivia ◽  
H. G. Giles ◽  
S. Sandrin ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Portal Vein ◽  
Portal Blood Flow ◽  
Portal Blood ◽  
Maximal Effect ◽  
Dependent Manner ◽  
Dose Dependent Increase ◽  
Dose Dependent

The mechanism by which ethanol induces an increase in portal vein blood flow was studied in rats using radiolabeled microspheres. Ethanol (2 g/kg) by gavage resulted in an increase of 50-70% in portal vein blood flow. The ethanol-induced increase in portal blood flow was suppressed by the adenosine receptor blocker 8-phenyltheophylline [ethanol, 61.8 +/- 4.1 ml.kg-1.min-1; ethanol + 8-phenyltheophylline (0.2 mg.kg-1.min-1), 44.2 +/- 2.0 ml.kg-1.min-1; P less than 0.05]. By itself, 8-phenyltheophylline (0.2 mg.kg-1.min-1) was without effect on cardiac output or portal blood flow. Adenosine infusion resulted in a dose-dependent increase in portal blood flow with a maximal effect at a dose of 0.17 mg.kg-1.min-1 (control, 41.3 +/- 2.3; adenosine, 81.7 +/- 8.0 ml.kg-1.min-1; P less than 0.05). This adenosine-induced increase in portal blood flow was inhibited by 8-phenyltheophylline in a dose-dependent manner [adenosine, 81.7 +/- 8.0 ml.kg-1.min-1; adenosine + 8-phenyltheophylline (0.2 mg.kg-1.min-1), 49.8 +/- 6.6 ml.kg-1.min; P less than 0.05]. Both alcohol and adenosine significantly reduced preportal vascular resistance by 40% (P less than 0.02) and 60% (P less than 0.01), respectively. These effects were fully suppressed by 8-phenyltheophylline. It is concluded that adenosine is a likely candidate to mediate the ethanol-induced increase in portal vein blood flow. It is suggested that an increase in circulating acetate and liver hypoxia may mediate the effects of alcohol by increasing tissue and interstitial adenosine levels.

Effect of Prostaglandins A1, A2, B1, E2 and F2α on Forearm Arterial Bed and Superficial Hand Veins in Man

1973 ◽  
Vol 44 (4) ◽  
pp. 367-376 ◽  
Author(s):  
B. F. Robinson ◽  
J. G. Collier ◽  
S. M. M. Karim ◽  
K. Somers
Keyword(s):  
Blood Flow ◽  
Blood Vessels ◽  
Brachial Artery ◽  
Peripheral Blood ◽  
Forearm Blood Flow ◽  
The Other ◽  
Dose Dependent Increase ◽  
Dose Dependent

1. The effects of local infusions of prostaglandins (PG) A1, A2, B1, E2 and F2α have been studied in the forearm arterial bed and superficial hand veins of man. 2. Prostaglandins A1, A2, B1, E2 and F2α all gave rise to a dose-dependent increase in forearm blood flow when infused into the brachial artery. At dosages just below the dilator range, PGF2α caused a transient fall in forearm flow, but this was not seen with any of the other prostaglandins. 3. Prostaglandins A1, A2 and E2 had no effect when infused locally into relaxed veins but caused dose-dependent dilatation when given into veins preconstricted with either noradrenaline or 5-hydroxytryptamine. Prostaglandins B1 and F2α caused dose-dependent constriction when given into relaxed veins and had no dilator effect when infused into preconstricted veins. 4. The results suggest that there are at least two types of receptors mediating responses to prostaglandins in peripheral blood vessels.

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