Blockade of renal effects of dopamine in the dog by the DA1 antagonist SCH 23390

1985 ◽  
Vol 249 (2) ◽  
pp. F236-F240 ◽  
Author(s):  
E. D. Frederickson ◽  
T. Bradley ◽  
L. I. Goldberg
Keyword(s):  
Blood Flow ◽  
Renal Artery ◽  
Renal Blood Flow ◽  
Intravenous Infusion ◽  
Sch 23390 ◽  
Receptor Subtypes ◽  
Base Line ◽  
Electrolyte Excretion ◽  
Pentobarbital Sodium ◽  
Before And After

Dopamine (DA) acts on two receptor subtypes, DA1 and DA2. The purpose of this study was to determine which subtype is involved in the increments in renal blood flow (RBF) and electrolyte excretion produced by DA. Mongrel dogs were anesthetized with pentobarbital sodium. Phenoxybenzamine (10 mg X kg-1 ia) and propranolol (5 mg X kg-1 iv) were administered to exclude effects mediated by alpha- and beta-adrenoceptors. DA was infused into the renal artery before and after administration of either the selective DA1 antagonist SCH 23390 or the selective DA2 antagonist domperidone. With DA alone, RBF increased by 52 +/- 7%, Na+ excretion increased by 35 +/- 8%, and K+ excretion increased by 35 +/- 5%. Infusion of SCH 23390 (0.5 micrograms X kg-1 X min-1) completely blocked DA-induced increase in RBF and electrolyte excretion. Intravenous infusion of domperidone (1 microgram X kg-1 X min-1) did not attenuate the responses to DA. Neither SCH 23390 nor domperidone affected base-line RBF or electrolyte excretion, suggesting that in these experiments endogenous DA was not active. In conclusion, these data indicate that the effects of DA to increase RBF and electrolyte excretion are the result of action on DA1 receptors.

Plasma dopamine in regulation of canine renal blood flow

1988 ◽  
Vol 255 (3) ◽  
pp. R379-R387 ◽  
Author(s):  
D. R. Kapusta ◽  
N. W. Robie
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Sch 23390 ◽  
Renal Perfusion ◽  
Receptor Activation ◽  
Renal Autoregulation ◽  
Alpha Adrenoceptor ◽  
Before And After ◽  
Anesthetized Dogs ◽  
Control Infusion

Studies were performed in pentobarbital-anesthetized dogs to determine whether circulating plasma dopamine (DA) is involved in renal blood flow (RBF) regulation. During graded reductions in renal perfusion pressure (RPP), total renal venous (RV) DA content significantly increased at RPPs below the autoregulatory range. The RBF response to decrements in RPP was also examined during control, infusion of DA (1.2 micrograms.kg(-1).min(-1)ia), and after DA receptor blockade by SCH 23390 (30 micrograms/kg iv). During DA infusion, autoregulation was still evident over the same RPPs, although at higher flow rates. At pressures below the autoregulatory range, RBF decreased linearly and the autoregulatory curve merged with control at 50 mmHg. After SCH 23390, autoregulation ceased at a higher RPP than during control, and RBF was significantly less than control rates at pressures of 80 mmHg and below. To elucidate reasons for this latter response, reductions in RPP were repeated before and after administration of both prazosin (0.1 mg/kg iv) and SCH 23390. The results indicated that RBF rates were not different from control at any RPP. Further, prazosin alone did not alter renal autoregulation but significantly increased RBF at RPP below the autoregulatory range. Thus these results indicate that dopamine does not participate in RBF control at pressures above the inflection point for the lowest limit of RBF autoregulation but may be released at lower RPP to act as a vasodilator agent to oppose alpha-adrenoceptor-mediated reductions in RBF. Moreover, tonic DA receptor activation may influence the setting of the lower limit of canine RBF autoregulation.

Characterization of the postocclusive response of renal blood flow in the cat

1978 ◽  
Vol 235 (4) ◽  
pp. F286-F290 ◽  
Author(s):  
W. S. Spielman ◽  
H. Osswald
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Artery ◽  
Renal Blood Flow ◽  
Artery Occlusion ◽  
Renal Nerves ◽  
Vasoconstrictor Response ◽  
Renal Artery Occlusion ◽  
Chronic Denervation

In contrast to the postocclusive hyperemia of brain, heart, and skeletal muscle, the hemodynamic response of the kidney following renal artery occlusion is highly variable in that both hyperemia and ischemia have been reported. The present study evaluates the factors influencing the renal response to complete renal artery occlusion (5-60 s) in the anesthetized cat. Marked postocclusive vasoconstriction could only be domonstrated in meclofenamate-treated (10 mg/kg) cats. The delta% renal blood flow (RBF) (30-s occlusion) was 16 +/- 4 in controls and 54 +/- 4 after meclofenamate (n= 10; P less than 0.001). Chronic denervation of the kidney, alpha-adrenergic receptor blockade, or infusion of [Sar1, Ile8]angiotensin II(2 microgram/min per kg) did not affect the postocclusive reduction of RBF, indicating that the vasoconstriction was independent of renal nerves, catecholamines, and circulating angiotesin II. Adenosine injected into the renal artery of five cats caused a dose-dependent transient fall of RBF. A dose of 100 nmol adenosine reduced RBF by 44 +/- 6% whereas after meclofenamate only 1 nmol produced the same degree of vasoconstriction. In summary, this study demonstrates a marked potentiation of the postocclusive vasoconstrictor response and the vasoconstrictive action of adenosine by meclofenamate in the anesthetized animal. No evidence was obtained to support a role for the sympathetic nervous system or circulating angiotensin II in mediating the postocclusive vasoconstriction.

Human renal response to meat meal

1986 ◽  
Vol 250 (4) ◽  
pp. F613-F618 ◽  
Author(s):  
T. H. Hostetter
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Renal Plasma Flow ◽  
Statistical Significance ◽  
Prostaglandin E ◽  
Base Line ◽  
Meat Meal ◽  
Time Period ◽  
Beef Steak ◽  
Renal Vascular

Glomerular filtration rate (GFR) increases after a meat meal in several species. The mechanism of this phenomenon is unknown and the excretory and metabolic responses largely unexplored. We examined in humans the nature of the hemodynamic response to a meat meal, the role of salt and water load in this response, and the associated renal excretory responses. Ten normal volunteers were studied after eating an average of 3.5 g/kg body wt of lean cooked beef steak and, on a separate day, after ingesting an amount of sodium and water equivalent to that in the steak. Average GFR increased by 28% for the entire 3 h after the meat meal compared with the same time period after the control salt solution (90 +/- 8 vs. 114 +/- 6 ml X min-1 X 1.73 M-2, mean +/- SE, P less than 0.05) and by 15% compared with the base-line periods, although this difference was not of statistical significance. However, not all subjects demonstrated an increase, and in those eight who did the degree was variable from 5 to 46% for the 3-h mean above the basal value. During the hour of peak GFR, the increment was associated with a nearly proportional increase in renal plasma flow and renal blood flow (all P less than 0.05). The increase in renal blood flow was entirely due to a significant fall in renal vascular resistance. The vasodilation was not accompanied by any change in prostaglandin E excretion.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Results of Surgical Repair of Hilar Renal Artery Aneurysm to Preserve Renal Blood Flow

2020 ◽  
Vol 13 (3) ◽  
pp. 281-285
Author(s):  
Takumi Kawase ◽  
Yosuke Inoue ◽  
Jiro Matsuo ◽  
Atsushi Omura ◽  
Yoshimasa Seike ◽  
...  
Keyword(s):  
Blood Flow ◽  
Renal Artery ◽  
Renal Blood Flow ◽  
Surgical Repair ◽  
Artery Aneurysm ◽  
Renal Artery Aneurysm

Abstract 1785: Renal Artery Angioplasty Improves Diastolic Cardiac Function In Patients With heart failure Possessing Renal Artery Stenosis.

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Eisei Yamamoto ◽  
Hitoshi Takano ◽  
Hiroyuki Tajima ◽  
Jun Tanabe ◽  
Hidekazu Kawanaka ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Function ◽  
Renal Artery ◽  
Renal Blood Flow ◽  
Renal Artery Stenosis ◽  
Arterial Blood Pressure ◽  
Arterial Blood ◽  
Diastolic Cardiac Function

Background: Renal artery stenosis (RAS) often plays an important role not only in malignant hypertension but also in sudden development of heart failure (HF) so called ‘flash pulmonary edema’ or chronic HF refractory to medical treatment. One of the possible mechanisms whereby RAS affects these unique conditions of HF is suppression of LV compliance through the complex interaction between neurohormonal systems originating from the reduction of renal blood flow. Renal artery angioplasty is expected to be an effective treatment for restoring renal blood flow in patients with RAS. The aim of the present study was whether the angioplasty can improve the impaired neurohormonal systems and diastolic cardiac function in patients with RAS. Methods: A prospective analysis was performed in 18 HF patients with RAS (age: 72±6, 3 females, NYHA I/II/III: 5/9/4) who underwent renal artery angioplasty between 2005 and 2007. Four patients with significant bilateral RAS and 3 patients with unilateral RAS in the vessel supplying a functional solitary kidney were included. We monitored the changes of biochemical and neurohormonal markers and blood pressure. Cardiac function was evaluated by tissue Doppler echocardiogram before and 3 months after the procedure. Results: Technical success was achieved in all interventions. The results are shown in table . Systolic arterial blood pressure significantly decreased by renal angioplasty. B-type natriuretic peptide (BNP) was significantly reduced 3 months after the angioplasty, whereas the change of sCr or angiotensinII was not statistically significant. Myocardial early diastolic velocity (Em), a parameter of diastolic LV function, was significantly improved compared with that measured before the procedure. Conclusions: In patients with either overt or latent HF possessing RAS, renal artery angioplasty not only decreases arterial blood pressure but also improves diastolic cardiac function in parallel with the reduction of BNP level.

Renal vascular and excretory responses to prostaglandin endoperoxides in the dog

1979 ◽  
Vol 236 (3) ◽  
pp. H427-H433
Author(s):  
J. A. Oliver ◽  
R. R. Sciacca ◽  
P. J. Cannon
Keyword(s):  
Blood Flow ◽  
Renal Artery ◽  
Renal Blood Flow ◽  
Biologically Active ◽  
Direct Effects ◽  
Cortical Areas ◽  
Anesthetized Dogs ◽  
Renal Vascular ◽  
Higher Doses

To determine whether the prostaglandin endoperoxides PGG2 and PGH2 have direct effects in the kidney, PGG2 and PGH2 were administered into the renal artery of anesthetized dogs and their effects were compared to those of PGE2. Like PGE2, PGG2 and PGH2 induced a dose-related renal vasodilation. A 50% increase in the renal blood flow was observed with 0.05 microgram/kg body wt of PGE2 and with four- and sixfold higher doses of PGH2 and PGG2, respectively. Infusion of all three compounds at doses inducing a 50% increase in the renal blood flow resulted in 1) increases in blood flow to all cortical areas, with the greatest increase occurring in the juxtamedullary area, 2) diuresis with no change in the glomerular filtration rate, and 3) natriuresis and kaliuresis. In vitro incubation of PGH2, a maneuver known to result in its conversion to other prostaglandins, had no influence on its renal effects. The data indicate that PGH2 and PGG2 are biologically active when infused into the renal artery of the anesthetized dog and suggest that the endoperoxides exert their effects after bioconversion to other prostaglandins.

Enhanced adrenergic constriction of iliac artery with removal of endothelium in conscious dogs

1986 ◽  
Vol 250 (5) ◽  
pp. H892-H897 ◽  
Author(s):  
M. A. Young ◽  
S. F. Vatner
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Iliac Artery ◽  
Conscious Dogs ◽  
Base Line ◽  
Adrenergic Agonists ◽  
Arterial Infusion ◽  
Iliac Arteries ◽  
Acetyl Choline ◽  
Before And After

We studied, in conscious dogs, the effects of removal of endothelium on the responses of iliac artery diameter and iliac blood flow to intra-arterial infusions of adrenergic agonists. With endothelium intact, iliac diameter increased with intra-arterial infusion of nitroglycerin (4.7 +/- 0.4%), acetylcholine (4.2 +/- 0.6%), and epinephrine (4.5 +/- 1.3%), and decreased with norepinephrine (-7.5 +/- 1.7%), phenylephrine (-6.6 +/- 1.0%), and B-HT 920 (-2.1 +/- 0.6%). One- to-five days following removal of endothelium with a balloon-tipped catheter, base-line iliac diameter was unchanged, and still increased with nitroglycerin (4.6 +/- 0.5%), but not with acetyl-choline, and epinephrine actually decreased diameter (-3.5 +/- 1.3%). Removal of the endothelium also enhanced the constriction observed with norepinephrine (-12.5 +/- 2.0%) and phenylephrine (-11.4 +/- 1.6%), but not with B-HT 920 (-1.8 +/- 0.5%). The changes in arterial pressure, iliac blood flow, iliac vascular resistance, and heart rate induced by any of the agonists did not differ before and after removal of the endothelium. These results indicate that the endothelium mediates the dilation in response to epinephrine and also serves an important role in protecting against alpha 1-adrenergic vasoconstriction of large iliac arteries.

Effect of Pentoxifylline on Cerebral Blood Flow in Patients with Chronic Cerebrovascular Disease

1981 ◽  
Vol 9 (3) ◽  
pp. 211-214 ◽  
Author(s):  
Stefano Passero ◽  
Marcello Nardini ◽  
Noé Battistini
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebrovascular Disease ◽  
Pharmacological Treatment ◽  
Intravenous Infusion ◽  
Chronic Administration ◽  
Before And After ◽  
Clearance Technique

The effect of pentoxifylline on cerebral blood flow (CBF) was studied with the intravenous 133Xe clearance technique in eleven patients with chronic cerebrovascular disease. Pentoxifylline was administered orally at a dose of 1200 mg/day over a period of 30 days (eight patients) or by intravenous infusion of 100 ml saline containing 400 mg of the drug in 1 hour (three patients). CBF was measured before and after pharmacological treatment. CBF was found to be significantly increased by both acute and chronic administration of pentoxifylline.

Endothelin resets renal blood flow autoregulatory efficiency during acute blockade of NO in the rat

2001 ◽  
Vol 281 (6) ◽  
pp. F1132-F1140 ◽  
Author(s):  
R. Kramp ◽  
P. Fourmanoir ◽  
N. Caron
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Receptor Subtypes ◽  
Receptor Blockade ◽  
Flow Probe ◽  
Relative Contribution ◽  
No Inhibition ◽  
Electromagnetic Flow Probe ◽  
Bq 610

First published August 15, 2001; 10.1152/ajprenal.00078.2001.—Renal blood flow (RBF) autoregulatory efficiency may be enhanced during NO inhibition in the rat, as recently reported. Under these conditions, endothelin (ET) synthesis and release may be increased. Our purpose was therefore to determine the role of ET in RBF autoregulatory changes induced by NO inhibition. To address this point, ETA/B receptors were blocked in anesthetized rats with bosentan, or selectively with BQ-610 or BQ-788. NO synthesis was inhibited with N G-nitro-l-arginine methyl ester (l-NAME). Mean arterial pressure (MAP) was decreased after bosentan (−10 mmHg; P < 0.01) or increased after l-NAME (25 mmHg; P < 0.001). RBF measured with an electromagnetic flow probe was reduced byl-NAME (−50%) and by BQ-788 (−24%). The pressure limits of the autoregulatory plateau (PA ∼100 mmHg) and of no RBF autoregulation (Po ∼80 mmHg) were significantly lowered by 15 mmHg after l-NAME but were unchanged after bosentan, BQ-610, or BQ-788. During NO inhibition, autoregulatory resetting was completely hindered by bosentan (PA ∼100 mmHg) and by ETB receptor blockade with BQ-788 (PA ∼106 mmHg), but not by ETA receptor blockade with BQ-610 (PA ∼85 mmHg). These results suggest that the involvement of ET in the RBF autoregulatory resetting occurs during NO inhibition, possibly by preferential activation of the ETB receptor. However, the relative contribution of ET receptor subtypes remains to be further specified.

Intrarenal angiotensin I conversion at normal and reduced renal blood flow in the dog

1983 ◽  
Vol 245 (3) ◽  
pp. F408-F415 ◽  
Author(s):  
L. Rosivall ◽  
D. F. Rinder ◽  
J. Champion ◽  
M. C. Khosla ◽  
L. G. Navar ◽  
...  
Keyword(s):  
Blood Flow ◽  
Renal Artery ◽  
Renal Blood Flow ◽  
Formation Rate ◽  
Secretion Rate ◽  
Renin Secretion ◽  
Generation Rate ◽  
Ang Ii ◽  
Angiotensin I ◽  
Single Passage

Intrarenal conversion of angiotensin I (ANG I) to angiotensin II (ANG II) under conditions of normal and reduced renal blood flow (RBF) elicited by constriction of the renal artery was examined in pentobarbital-anesthetized dogs. In eight animals, tracer doses of 125I-ANG I (5-12 pmol) were injected into the renal artery and 125I-ANG I, 125I-ANG II, and 125I-labeled metabolites were measured in renal venous effluent by high-voltage paper electrophoresis. The mean conversion of ANG I to ANG II during a single passage through the kidney was 21.8 +/- 2.1% at control RBF. When RBF was decreased by 25 and 53%, percent ANG I conversion was not altered significantly. In six dogs percent conversion of 125I-[Sar1, Ile5]ANG I, an ANG I analogue refractory to hydrolysis by aminopeptidases, was 18.1 +/- 1.7% at control RBF and did not change significantly when the RBF was reduced by 55%. Although there were severalfold increases in renal renin secretion rate and net ANG I generation rate during reduced RBF, net renal ANG II formation rate did not change significantly. These data indicate that there is substantial conversion of ANG I in a single passage through the dog kidney and that intrarenal ANG I conversion is independent of RBF even under conditions in which renin secretion rate and ANG I generation rate are increased severalfold.

Sign in / Sign up

Export Citation Format

Share Document