Effect of nitrendipine on renal function and on hormonal parameters after intravascular iopromide

1998 ◽  
Vol 39 (4) ◽  
pp. 375-380 ◽  
Author(s):  
J. K. Madsen ◽  
L. Winther Jensen ◽  
J. Sandermann ◽  
N. Johannesen ◽  
W. P. Paaske ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Renal Plasma Flow ◽  
Randomized Study ◽  
Atherosclerotic Disease ◽  
Constant Infusion ◽  
Double Blind ◽  
Blood Pressure Treatment ◽  
Renal Tubular ◽  
Infusion Technique

Purpose: To evaluate the effect of the low-molecular nonionic radiographic contrast agent iopromide (Ultravist) on renal function, vasoactive peptides (angiotensin II, aldosterone, arginine vasopressin, and atrial natriuretic factor (ANF)), and blood pressure, and to evaluate the influence of the calcium antagonist nitrendipine on these parameters. The findings were evaluated in a prospective, double-blind and placebo-controlled randomized study. Material and Methods: Twenty-six patients undergoing routine aortofemoral arteriography for peripheral atherosclerotic disease were treated with nitrendipine tablets (10 mg) or placebo twice daily for a week. Angiography was performed on the fifth day of medication. Efficacy variables were determined on the day before and 2 days after arteriography. The glomerular filtration rate and renal plasma flow were measured by the constant infusion technique. Renal tubular function was estimated from the clearance of lithium. Hormones were measured by radioimmunoassays. Results: Arteriography with iopromide did not change renal function. No differences between the nitrendipine and placebo groups were found in renal hemodynamics, tubular sodium handling, or blood pressure. Nitrendipine changed ANF (26.1%) compared to placebo (1.5%), whereas the other hormones were not affected. Conclusion: The use of iopromide for angiography did not affect renal function in normotensive patients with peripheral atherosclerotic disease. Shortterm treatment with nitrendipine may lower the plasma levels of ANF but it had no effect on renal function or blood pressure. Treatment with calcium antagonists prior to arteriography with iopromide is not indicated in these patients.

Effects of NG-nitro-L-arginine methyl ester on renal function and blood pressure

1991 ◽  
Vol 261 (6) ◽  
pp. F1033-F1037 ◽  
Author(s):  
V. Lahera ◽  
M. G. Salom ◽  
F. Miranda-Guardiola ◽  
S. Moncada ◽  
J. C. Romero
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Renal Function ◽  
Methyl Ester ◽  
Renal Plasma Flow ◽  
Urinary Sodium Excretion ◽  
Systemic Blood Pressure ◽  
Synthesis Inhibitor ◽  
Renal Changes ◽  
Dose Dependent

The dose-dependent effects of intravenous infusions of nitric oxide (NO) synthesis inhibitor, NG-nitro-L-arginine methyl ester (L-NAME; 0.1, 1, 10, and 50 micrograms.kg-1.min-1), were studied in anesthetized rats to determine whether the inhibitory actions of L-NAME are manifested primarily in alterations of renal function or whether they are the consequences of the increase in systemic blood pressure. Mean arterial pressure (MAP) was not altered by the intravenous L-NAME infusions of 0.1 and 1.0 microgram.kg-1.min-1. However, 0.1 microgram.kg-1.min-1 L-NAME induced a 30% decrease in urine flow rate (UV). The administration of 1.0 microgram.kg-1.min-1 L-NAME, in addition to decreasing UV, also decreased urinary sodium excretion (UNaV) and renal plasma flow (RPF). The intravenous L-NAME infusions of 10.0 and 50.0 microgram.kg-1.min-1 intravenous L-NAME infusions of 10.0 and 50.0 microgram.kg-1.min-1 produced significant increases in MAP that reversed the initial fall in UV and UNaV, despite decreasing RPF and glomerular filtration rate (GFR). The administration of L-arginine alone (10 micrograms.kg-1.min-1) did not modify any of the parameters measured, but it effectively prevented all the hemodynamic and renal changes induced by the infusion of 50 micrograms.kg-1.min-1 L-NAME. These results suggest that the decrease in nitric oxide production induced by the intravenous infusion of L-NAME affects renal excretion of sodium and water in the absence of any significant change in blood pressure. At larger doses, L-NAME also produces hypertension that overrides the initial antinatriuretic effect.

Is l-arginine infusion an adequate tool to assess endothelium-dependent vasodilation of the human renal vasculature?

2000 ◽  
Vol 99 (4) ◽  
pp. 293-302 ◽  
Author(s):  
Markus P. SCHLAICH ◽  
Johannes JACOBI ◽  
Stefan JOHN ◽  
Christian DELLES ◽  
Ingrid FLEISCHMANN ◽  
...  
Keyword(s):  
Renal Plasma Flow ◽  
Urinary Sodium Excretion ◽  
Renal Haemodynamics ◽  
Constant Infusion ◽  
Renal Vasculature ◽  
Double Blind ◽  
Arginine Infusion ◽  
Haemodynamic Changes ◽  
Induced Changes ◽  
Renal Vascular

Systemic administration of L-arginine alters renal haemodynamics in humans. We examined whether L-arginine-induced vasodilation of the renal vasculature is related to an increased production and release of NO by comparing the effects of L- and D-arginine on renal endothelium-dependent vasodilation. In a double-blind randomized cross-over study including 20 young, healthy male white subjects (age 26±2 years), we determined the effects of intravenous administration of L-arginine or its enantiomer D-arginine, at doses of 100 mg/kg body weight for 30 min or 500 mg/kg for 30 min, on renal haemodynamics. Renal plasma flow (RPF) and glomerular filtration rate (GFR) were assessed by a constant-infusion input-clearance technique (using p-aminohippuric acid and inulin respectively). In addition, changes in blood pressure, heart rate, urinary sodium excretion (UNa) and urinary cGMP were measured. HPLC was used to determine L- and D-arginine concentrations. Intravenous infusion of L-arginine at 100 mg/kg for 30 min increased RPF from 641±87 to 677±98 ml/min (P = 0.019), whereas infusion of D-arginine did not (from 642±74 to 657±86 ml/min; not significant). The change in RPF was more marked during the infusion of L-arginine than during the infusion of D-arginine (+36±61 versus +16±57 ml/min; P = 0.037). Infusion of both L- and D-arginine at doses of 500 mg/kg for 30 min increased RPF from baseline [from 641±87 to 762±133 ml/min (P < 0.001) and from 642±74 to 713±120 ml/min (P = 0.004) respectively], but the change in RPF again was greater in response to L-arginine infusion than to infusion with D-arginine (+121±97 versus +71±94 ml/min; P = 0.018). In accordance, changes in renal vascular resistance (RVR) were higher in response to L-arginine compared with D-arginine for both doses (P < 0.05 and P< 0.001 respectively). UNa increased only with L-arginine (change in UNa, +0.33±0.26 mmol/min; P< 0.01) but not with D-arginine (change in UNa, +0.11±0.17 mmol/min; not significant). The change in UNa was more pronounced during infusion of L-arginine compared with infusion of D-arginine (P = 0.023). In parallel, urinary excretion of cGMP only increased in response to L-arginine (+676±272 pmol/l; P = 0.038) and not during D-arginine infusion (+185±153 pmol/l; not significant). L-Arginine-induced changes in RPF, RVR, UNa and cGMP excretion differed significantly from those induced by D-arginine. Thus although no direct measurements of NO synthesis were performed, putative markers of NO synthesis suggest that the renal vasodilatory response to L-arginine, at least in part, was due to increased production and release of NO. The dose of L-arginine at 100 mg/kg for 30 min emerged as the most suitable, because of the absence of systemic haemodynamic changes. The effects of infusion of L-arginine at 500 mg/kg for 30 min on renal endothelium-dependent vasodilation need to be corrected for the effects of D-arginine before conclusions can be drawn.

scholarly journals THE EFFECT OF DESOXYCORTICOSTERONE ACETATE ON BLOOD PRESSURE, RENAL FUNCTION, AND ELECTROLYTE PATTERN IN THE INTACT RAT

1948 ◽  
Vol 87 (4) ◽  
pp. 329-338 ◽  
Author(s):  
Sydney M. Friedman ◽  
John R. Polley ◽  
Constance L. Friedman
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
No Reduction ◽  
Renal Plasma Flow ◽  
Excretory Function ◽  
Small Doses ◽  
Cent Saline ◽  
Electrolyte Change ◽  
Desoxycorticosterone Acetate ◽  
Pellet Form

Small doses of DCA administered at intervals in pellet form are capable of raising the blood pressure, altering renal function, and changing the electrolyte pattern in the intact rat. The concomitant feeding of 1 per cent saline intensifies the process. The elevation in blood pressure occurs prior to demonstrable changes in renal excretory function. The alteration in renal function consists first of a reduction in CPAH with the maintenance of a normal filtration rate. Filtration fraction is elevated while there is no reduction in renal plasma flow per unit of tubular excretory tissue. Later, filtration is interfered with and renal ischemia occurs. The electrolyte change is characterized by a sustained fall in plasma K and Cl, a rise in plasma Na, an increase in the Na/Cl ratio, and finally an elevation of Na plus K. Plasma Ca is unaffected. These observations suggest the possible etiological significance of the adrenal cortex in some types of hypertension.

ASPIRIN AND THE KIDNEY IN PATIENTS WITH CEREBRAL ISCHEMIA

1987 ◽  
Author(s):  
M Monreal ◽  
E Lafoz ◽  
M Foz ◽  
J Monasterio
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Body Weight ◽  
Cerebral Ischemia ◽  
Adverse Effects ◽  
Diastolic Blood Pressure ◽  
Water Retention ◽  
Aspirin Therapy ◽  
Double Blind ◽  
History Of

The acceptance of aspirin therapy for prevention of cerebral ischemia is based onpositive results of several large clinicaltrials, and the usual dose is 1000-1500 mg/day. Several recent reports emphasize the adverse effects of aspirin and other nonsteroidal anti-inflamatory agents on renal function. We examined wether two extreme doses of aspirin (60 mg vs 1200 mg/day) could alter renal function in patients recently admitted to hospital with cerebral ischemia. We studied 33 patients with cerebralischemia and no history of ingestion of aspirin nor other drugs two weeks prior to admission. During the first 5 days all patients received a 50 mEq sodium diet and no drugs, while during the second 5 days (trial) the patients were randomly assigned (double blind) to placebo, aspirin 20 mg or aspirin 400 mg, 3 times daily, with meals.Overall, body weight increased by 650 gin patients taking 1400 mg/day of aspirin (p≺0,01), but not in patients taking 60 mg/day. Also increases in systolic and diastolic blood pressure did not reach significant differences. While waiting morereports, aspirin at doses near 1000 mg should be administered cautiously in sodium restricted patients with cerebral ischemia.Acute water retention may be specially troublesome.

GSK2256294 Decreases sEH (Soluble Epoxide Hydrolase) Activity in Plasma, Muscle, and Adipose and Reduces F2-Isoprostanes but Does Not Alter Insulin Sensitivity in Humans

Hypertension ◽  
2021 ◽  
Author(s):  
James M. Luther ◽  
Justina Ray ◽  
Dawei Wei ◽  
John R. Koethe ◽  
Latoya Hannah ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Epoxide Hydrolase ◽  
Renal Plasma Flow ◽  
Soluble Epoxide Hydrolase ◽  
Improve Insulin Sensitivity ◽  
Double Blind ◽  
Phosphorylated Akt

Epoxyeicosatrienoic acids (EETs) reduce blood pressure by acting in the vasculature and kidney, and interventions to increase circulating EETs improve insulin sensitivity and prevent diabetes in animal models. Inhibition of EET hydrolysis with a sEH (soluble epoxide hydrolase) inhibitor is an attractive approach for hypertension and diabetes. We tested the hypothesis that sEH inhibition increases circulating EETs, reduces blood pressure, and improves insulin sensitivity, blood flow, and inflammation in a randomized, double-blind, placebo-controlled crossover study. Sixteen participants with obesity and prediabetes were randomized to GSK2256294 10 mg QD or placebo for 7 days, insulin sensitivity was assessed by hyperinsulinemic-euglycemic clamp, and adipose and muscle tissues biopsies were performed to assess insulin-stimulated Akt phosphorylation. We assessed tissue and plasma EETs and their respective diol concentrations and sEH activity within plasma, muscle, and adipose tissues. GSK2256294 reduced circulating and adipose tissue sEH activity, but blood pressure, circulating EET, and tissue EETs were unchanged. Plasma sEH activity correlated with muscle and adipose tissue sEH activity. Insulin sensitivity assessed during hyperinsulinemic clamps, as well as adipose and muscle phosphorylated-Akt/Akt expression were similar during GSK2256294 and placebo. sEH inhibition with GSK2256294 reduced plasma F2-isoprostanes (50.7±15.8 versus 37.2±17.3 pg/mL; P =0.03) but not IL (interleukin)-6. Resting blood pressure, forearm blood flow, and renal plasma flow were similar during GSK2256294 and placebo. We demonstrate that GSK2256294 administration for 7 days effectively inhibits sEH activity in plasma, muscle, and adipose tissue and reduces F2-isoprostanes—a marker of oxidative stress—but does not improve insulin sensitivity or blood pressure.

Renal Effects of Angiotensin I-Receptor Blockade and Angiotensin Convertase Inhibition in Man

1996 ◽  
Vol 90 (3) ◽  
pp. 205-213 ◽  
Author(s):  
Francois Schmitt ◽  
Svetlozar Natov ◽  
Frank Martinez ◽  
Bernard Lacour ◽  
Thierry P. Hannedouche
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Plasma Renin Activity ◽  
Plasma Flow ◽  
Renal Plasma Flow ◽  
Plasma Renin ◽  
Renin Activity ◽  
Angiotensin Converting Enzyme Inhibition ◽  
Converting Enzyme ◽  
Converting Enzyme Inhibition

1. The objective was to compare two means of inhibition of the renin—angiotensin system [angiotensin-converting enzyme inhibition and selective antagonism of angiotensin II subtype 1 (AT1) receptor] on renal function in 10 healthy normotensive volunteers on a normal sodium diet. Since mechanisms of action may differ between both drugs, a synergistic action was further studied by combining the two drugs. 2. The design was a double-blind randomized acute administration of either placebo or a single oral dose of enalapril, 20 mg, followed in each case by administration of the AT1 selective antagonist losartan potassium, 50 mg orally. 3. The methods included measurements of hormones (plasma renin activity, plasma aldosterone), blood pressure and renal function from 45 to 135 min after administration of placebo or enalapril, and from 45 to 135 min after losartan and placebo or losartan and enalapril. Renal function was studied using clearance of sodium, lithium, uric acid, inulin and para-aminohippuric acid. To examine further the determinants of glomerular filtration at the microcirculation level, fractional clearance of neutral dextran was determined and sieving curves were applied on a hydrodynamic model of ultrafiltration. 4. Losartan did not change plasma renin activity, blood pressure or glomerular filtration rate, but increased significantly renal plasma flow and urinary excretion of sodium and uric acid. Enalapril increased plasma renin activity and renal plasma flow, and decreased blood pressure without natriuretic, lithiuretic or uricosuric effects. The renal vasodilatation was potentiated when losartan and enalapril were combined, despite a further rise in plasma renin. In contrast to enalapril, losartan either alone or in combination with enalapril significantly depressed fractional clearances of dextran of small radii (34–42 Å). These changes in fractional clearances of dextran were presumably related to the rise in glomerular plasma flow since the other major determinants of filtration, i.e. transcapillary glomerular pressure gradient, ultrafiltration coefficient and membrane property, were computed as unchanged by either losartan, enalapril or a combination of both. 5. In conclusion, these findings suggest that in normal sodium-repleted man the renal, hormonal and blood pressure effects of AT1 antagonism and angiotensin-converting enzyme inhibition are not strictly similar and could be synergistic.

Drawbacks of the constant-infusion technique for measurement of renal function

1995 ◽  
Vol 268 (4) ◽  
pp. F543-F552 ◽  
Author(s):  
B. A. Van Acker ◽  
G. C. Koomen ◽  
L. Arisz
Keyword(s):  
Renal Function ◽  
Steady State ◽  
Plasma Concentrations ◽  
Constant Infusion ◽  
Urinary Recovery ◽  
Infusion Method ◽  
Pah Clearance ◽  
The Difference ◽  
Infusion Technique ◽  
Extrarenal Clearance

We investigated the validity of the steady-state constant infusion method (CIM), in which quantitative urinary recovery and constant plasma concentrations of the solute infused are required. Successive 3-h clearances of inulin and p-aminohippuric acid (PAH) were determined for 27 h in 25 patients with renal disease. Results were compared with the standard method of bladder clearance (StM) and with a modified CIM (ModCIM). The 24-h urinary recovery was incomplete for both inulin and PAH. Mean 24-h ModCIM inulin clearance overestimated StM by 4.5 ml.min-1 x 1.73 m-2 (range 0–9, P < 0.001) independent of the extent of renal impairment and pointed to slow distribution and/or extrarenal clearance of inulin. For PAH, the difference between ModCIM and StM clearance was related to the average PAH clearance by ModCIM and StM (r = 0.78). Furthermore, neither plasma inulin nor PAH became completely constant, because of the circadian rhythm in renal function. In conclusion, the conditions of the steady-state CIM technique are not fulfilled, and the method is not suitable for accurate measurement of inulin and PAH clearance, especially when the clearance is low.

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