Renal effect of meclofenamate in presence and absence of superfusion bioassay

1976 ◽  
Vol 230 (3) ◽  
pp. 711-714 ◽  
Author(s):  
S Satoh ◽  
BG Zimmerman
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Renal Artery ◽  
Renal Blood Flow ◽  
Vascular Resistance ◽  
Systemic Blood Pressure ◽  
Prostaglandin E ◽  
Renal Effect ◽  
Systemic Blood ◽  
Renal Vascular

Systemic blood pressure (SBP), renal blood flow (RBF), renal vascular resistance (RVR), and arterial and renal venous prostaglandin E (PGE) concentrations were determined in pentobarbital-anesthetized dogs.The effect of sodium meclofenamate infused into the renal artery was compared under two sets of conditions. In experiments carried out under control conditions, SBP, RBF, and RVR were stable and meclofenamate caused only a slight decrease in RBF (5.4%) and increase in RVR.

Excessive Zinc Intake Increases Systemic Blood Pressure and Reduces Renal Blood Flow via Kidney Angiotensin II in Rats

2012 ◽  
Vol 150 (1-3) ◽  
pp. 285-290 ◽  
Author(s):  
Miyoko Kasai ◽  
Takashi Miyazaki ◽  
Tsuneo Takenaka ◽  
Hiroyuki Yanagisawa ◽  
Hiromichi Suzuki
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Systemic Blood Pressure ◽  
Systemic Blood ◽  
Zinc Intake

Renal vasodilatation after inhibition of renin or converting enzyme in marmoset

1986 ◽  
Vol 251 (5) ◽  
pp. H897-H902
Author(s):  
D. Neisius ◽  
J. M. Wood ◽  
K. G. Hofbauer
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Vascular Resistance ◽  
Enzyme Inhibitor ◽  
Renal Vascular Resistance ◽  
Converting Enzyme ◽  
Renin Inhibition ◽  
Renal Vascular

The relative importance of angiotensin II for the renal vasodilatory response after converting-enzyme inhibition was evaluated by a comparison of the effects of converting-enzyme and renin inhibition on renal vascular resistance. Renal, mesenteric, and hindquarter blood flows were measured with chronically implanted ultrasonic-pulsed Doppler flow probes in conscious, mildly volume-depleted marmosets after administration of a converting-enzyme inhibitor (enalaprilat, 2 mg/kg iv), a synthetic renin inhibitor (CGP 29,287, 1 mg/kg iv), or a renin-inhibitory monoclonal antibody (R-3-36-16, 0.1 mg/kg iv). Enalaprilat reduced blood pressure (-16 +/- 4 mmHg, n = 6) and induced a selective increase in renal blood flow (27 +/- 8%, n = 6). CGP 29,287 and R-3-36-16 induced comparable reductions in blood pressure (-16 +/- 4 mmHg, n = 6 and -20 +/- 4 mmHg, n = 5, respectively) and selective increases in renal blood flow (36 +/- 12%, n = 6 and 34 +/- 16%, n = 4, respectively). The decrease in renal vascular resistance was of similar magnitude for all of the inhibitors (enalaprilat -28 +/- 3%, CGP 29,287 -32 +/- 6%; and R-3-36-16 -33 +/- 7%). These results indicate that the renal vasodilatation induced after converting-enzyme or renin inhibition is mainly due to decreased formation of angiotensin II.

scholarly journals Impact of the NO-Sensitive Guanylyl Cyclase 1 and 2 on Renal Blood Flow and Systemic Blood Pressure in Mice

2018 ◽  
Vol 19 (4) ◽  
pp. 967 ◽  
Author(s):  
Evanthia Mergia ◽  
Manuel Thieme ◽  
Henning Hoch ◽  
Georgios Daniil ◽  
Lydia Hering ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Guanylyl Cyclase ◽  
Systemic Blood Pressure ◽  
Systemic Blood

Contralateral Natriuresis During Reduced Renal Artery Perfusion Pressure in "Renin-Depleted" Dogs

1972 ◽  
Vol 50 (3) ◽  
pp. 215-227
Author(s):  
L. J. Belleau ◽  
D. Mailhot
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Perfusion Pressure ◽  
Plasma Renin ◽  
Systemic Blood Pressure ◽  
Renal Perfusion ◽  
Systemic Blood ◽  
Renal Perfusion Pressure

The mechanism of contralateral natriuresis subsequent to reduction of renal perfusion pressure was studied. In control dogs a drop in the renal perfusion pressure caused a very significant increase in the arterial and renal venous plasma renin activity, as well as a significant contralateral natriuresis. Systemic blood pressure increased along with contralateral intrarenal resistance. Glomerular filtration rate and renal blood flow did not change in the opposite kidney.In "renin-depleted" dogs a comparable drop in the renal perfusion pressure failed to stimulate renal venous and arterial plasma renin activity. Contralateral natriuresis increased significantly as well as the systemic blood pressure. In the absence of renin, intrarenal resistance of the opposite kidney did not change. Contralateral glomerular filtration rate and renal blood flow remained unchanged.During reduction of renal perfusion pressure, the most significant findings were: (1) absence of renin release despite the stimulation in renin-depleted dogs, (2) increase in contralateral resistance explained by the renin–angiotensin system, (3) systemic blood pressure increment despite renin release inhibition, and (4) the renin–angiotensin system not directly responsible for the contralateral natriuresis following a reduction in the renal perfusion pressure.Contralateral natriuresis cannot be explained by changes in glomerular filtration, renal blood flow, or intrarenal resistance. It is suggested that the rise in blood pressure or another factor, possibly neural or humoral, could explain the contralateral natriuresis.

Renal vascular effects of epinephrine infusion in the halothane-anesthetized piglet

1994 ◽  
Vol 72 (4) ◽  
pp. 394-396 ◽  
Author(s):  
Keith J. Harrington ◽  
Robert G. Allen ◽  
Jay W. Dewald
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Mean Arterial Blood Pressure ◽  
Renal Vascular Resistance ◽  
Epinephrine Infusion ◽  
Arterial Blood ◽  
Renal Vascular

The objective of this study was to determine the dose–response effects of epinephrine, given by systemic intravenous infusion to the halothane-anesthetized newborn piglet, on renal blood flow, mean arterial blood pressure, and renal vascular resistance. Seven newborn piglets were acutely instrumented. A transit-time ultrasound flow probe was placed around the renal artery and a femoral arterial catheter was placed for blood pressure monitoring. Epinephrine was infused in doubling doses from 0.2 to 3.2 μg∙kg−1∙min−1. Mean arterial blood pressure increased from 54 mmHg (1 mmHg = 133.3 Pa) to an average of 96 mmHg at 3.2 μg∙kg−1∙min−1 of epinephrine. Renal blood flow increased from 165 mL∙min−1∙100 g−1 at baseline to 185 mL∙min−1∙100 g−1 at a dose of 0.2 μg∙kg−1∙min−1 and increased further at 0.4 and 0.8 μg∙kg−1∙min−1 to reach 261 mL∙min−1∙100 g−1. Renal blood flow began to fall at a dose of 3.2 μg∙kg−1∙min−1, remaining however, significantly above baseline (211 mL∙min−1∙100 g−1). Consequently, calculated renal vascular resistance fell as the dose was increased from 0.2 to 0.8 μg∙kg−1∙min−1 and then rose again at 1.6 and 3.2 μg∙kg−1∙min−1, being significantly above baseline at 3.2 μg∙kg−1∙min−1. These results demonstrate that epinephrine when given by systemic infusion to the halothane-anesthetized newborn pig is a renal vasodilator at low doses and causes renal vasoconstriction at moderate to high doses. Renal blood flow remained above baseline at all doses tested, and thus, within the dosage range tested, epinephrine infusion should not cause renal ischemia.Key words: epinephrine, kidney blood flow, piglet, renal vascular resistance.

Impaired Autoregulatory Responses in Contralateral Kidneys of Two-Kidney, One-Clip Hypertensive Rats

1980 ◽  
Vol 59 (s6) ◽  
pp. 381s-384s ◽  
Author(s):  
D. W. Ploth ◽  
R. N. Roy ◽  
Wann-Chu Huang ◽  
L. G. Navar
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Vascular Resistance ◽  
Urine Flow ◽  
Renal Vascular Resistance ◽  
Hypertensive Rats ◽  
Contralateral Kidney ◽  
Arterial Blood ◽  
Renal Vascular

1. Micropuncture and clearance experiments in two-kidney, one-clip renal vascular hypertensive rats examined the ability of the kidney contralateral to renal vascular stenosis to maintain renal function during conditions of reduced renal arterial blood pressure. 2. At their respective spontaneous blood pressures, renal vascular resistance was higher and glomerular filtration rate (GFR) and renal blood flow were not different in the contralateral kidneys of the hypertensive rats (170 ± 5 mmHg) compared with normal animals (129 ± 1 mmHg). Urine flow and absolute and fractional excretion of electrolyte were greater from the kidneys of the hypertensive animals. However, pressures in cortical structures were similar in the two groups. 3. As blood pressure was reduced acutely, the kidney contralateral to the renal artery stenosis achieved only small decreases in renal vascular resistance that failed to allow GFR, renal blood flow or pressures in cortical structures to be maintained. In contrast, normal rats efficiently autoregulated renal vascular resistance to allow GFR, renal blood flow and cortical pressures to be unchanged as blood pressure was altered between 130 and 115 mmHg. Urine flow and electrolyte excretion decreased to a greater extent in the hypertensive kidneys; at comparable blood pressure these indices of excretory function were not different in the two groups. 4. These observations indicate that the contralateral kidney can maintain normal haemodynamic and glomerular function only at elevated blood pressure and suggest the possibility that the impaired capacity to autoregulate renal resistances may contribute to the maintenance of hypertension observed in this model.

Inner medullary blood flow in postischemic acute renal failure in the rat

1989 ◽  
Vol 256 (3) ◽  
pp. F456-F461 ◽  
Author(s):  
Y. Yagil ◽  
M. Miyamoto ◽  
R. L. Jamison
Keyword(s):  
Blood Flow ◽  
Renal Artery ◽  
Renal Blood Flow ◽  
Vascular Resistance ◽  
Renal Ischemia ◽  
Renal Vascular Resistance ◽  
Left Renal Artery ◽  
Vasa Recta ◽  
Renal Vascular ◽  
Total Renal Blood Flow

To study the effect of renal ischemia on the circulation in the inner medulla, blood flow in descending and ascending vasa recta was determined by fluorescence videomicroscopy in the exposed papilla of the uninephrectomized rat after clamping of the renal artery for 45 min. Total renal blood flow was determined in parallel studies with an electromagnetic flowmeter. Animals were studied 90 min (group 1E) and 24 h (group 2E) after right nephrectomy and release of the left renal artery clamp. Control rats were studied 90 min (group 1C) and 24 h (group 2C) after right nephrectomy alone. In groups 1E and 2E, total renal blood flow was reduced to 70 and 80% of that in their respective controls; renal vascular resistance increased by 50 and 73%, respectively. In striking contrast, blood flow was markedly elevated in descending and ascending vasa recta in groups 1E and 2E compared with the values in their respective uninephrectomized controls. These results indicate that the circulation in the inner medulla is rapidly restored after 45 min of total renal ischemia and that vasa recta blood flow rises above normal after 90 min and 24 h, despite a reduction in total renal blood flow and an increase in renal vascular resistance.

Renal blood flow changes in contralateral kidney of Goldblatt hypertensive dog

1981 ◽  
Vol 241 (2) ◽  
pp. H145-H148
Author(s):  
B. G. Zimmerman ◽  
C. Mommsen
Keyword(s):  
Blood Flow ◽  
Renal Artery ◽  
Renal Blood Flow ◽  
Vascular Resistance ◽  
Control Level ◽  
Plasma Renin ◽  
Renal Vascular Resistance ◽  
Contralateral Kidney ◽  
Arterial Blood ◽  
Renal Vascular

Sequential changes in systemic arterial blood pressure (BP), renal blood flow (RBF) in the contralateral kidney, and plasma renin activity (PRA) were examined on conscious dogs with construction of a single renal artery (RAC). An increase of 24 mmHg in bP occurred within 2 days after RAC, and BP later plateaued at a lower level. RBF in the contralateral kidney transiently increased by 24% and then returned to the control level in 11-14 days. PRA also peaked early after RAC and then returned to control. The clamp was tightened and the renal artery was occluded (RAO) 3-20 days after RAC. BP, RBF, and PRA increased to an even greater degree than after RAC. BP peaked at 145 mmHg, and RBF increased 61.5% at 2-3 days after RAO. BP and RBF both decreased but remained above the control for the duration of the study, BP at 127 mmHg and RBF at 256 ml/min. RBF per gram for the hypertrophied contralateral kidney was calculated from the RBF before death and the weight at death. The final RBF per gram of the contralateral kidney (2.7 ml.min-1.g-1) decreased and renal vascular resistance increased compared with the estimated control RBF/g (3.7 ml.min-1.g-1) and renal vascular resistance. These results suggest that the final RBF of the contralateral kidney is not increased in proportion to its increase in weight and that it may be relatively hypoperfused in two-kidney one-clip Goldblatt hypertension.

Sign in / Sign up

Export Citation Format

Share Document