Systemic hemodynamics and renal function during long-term pathophysiological increases in circulating endothelin

1995 ◽  
Vol 268 (2) ◽  
pp. R375-R381 ◽  
Author(s):  
F. C. Wilkins ◽  
A. Alberola ◽  
H. L. Mizelle ◽  
T. J. Opgenorth ◽  
J. P. Granger
Keyword(s):  
Renal Function ◽  
Renal Plasma Flow ◽  
Peripheral Resistance ◽  
Plasma Renin ◽  
Chronic Hypertension ◽  
Systemic Hemodynamic ◽  
Endothelin 1 ◽  
Control Value ◽  
Renal Vascular

Although recent studies have reported endogenous plasma endothelin levels to be elevated two- to fivefold in chronic pathophysiological states, whether such an increase in circulating endothelin levels alone can lead to significant long-term alterations in cardiovascular and renal function is not known. The purpose of this study was to examine the long-term systemic hemodynamic and renal effects of a pathophysiological increase in plasma endothelin concentration in chronically instrumented, conscious dogs (n = 7). Infusion of endothelin-1 (2.5 ng.kg-1.min-1) for 8 days increased plasma concentration of immunoreactive endothelin approximately two- to threefold from 6.7 +/- 0.4 to 16.0 +/- 2.2 pg/ml. Mean arterial pressure increased 21% from a control value of 86.7 +/- 2.1 to 105.0 +/- 2.5 mmHg during the endothelin infusion period. Cardiac output averaged 2,200 +/- 205 ml/min during control and fell by 33% on day 4 of endothelin infusion (1,484 +/- 146 ml/min) and was still 14% below control after day 8 of endothelin infusion (1,885 +/- 154 ml/min). Endothelin increased total peripheral resistance from 42.0 +/- 3.1 to 80.3 +/- 9.1 mmHg.l-1.min. Increasing plasma endothelin two- to threefold was associated with an increase in renal vascular resistance and decreases in glomerular filtration rate and renal plasma flow. Endothelin-1 had no long-term effect on plasma renin activity or aldosterone concentration. These data indicate the importance of pathophysiological levels of endothelin in controlling renal and cardiovascular function in chronic conditions. Furthermore, the results indicate that endothelin may play a role as a mediator of chronic hypertension in pathophysiological states associated with endothelial dysfunction.

Acute and chronic actions of bradykinin on renal function and arterial pressure

1985 ◽  
Vol 248 (1) ◽  
pp. F87-F92 ◽  
Author(s):  
J. P. Granger ◽  
J. E. Hall
Keyword(s):  
Arterial Pressure ◽  
Renal Plasma Flow ◽  
Urine Volume ◽  
Plasma Renin ◽  
Urinary Sodium Excretion ◽  
Renal Perfusion ◽  
Acute Effects ◽  
Plasma Aldosterone Concentration ◽  
Control Value ◽  
Renal Vascular

The present study was designed to examine the acute and chronic effects of increased levels of circulating bradykinin (BK) on control of renal hemodynamics, electrolyte excretion, and arterial pressure. Intrarenal infusion of BK (50 ng X kg-1 X min-1) for 60 min in five anesthetized dogs with renal perfusion pressure maintained at a constant level of 108 +/- 1 mmHg had no significant effect on glomerular filtration rate (GFR), whereas it increased renal blood flow (RBF) from a control value of 230 +/- 14 to 282 +/- 18, 266 +/- 15, and 253 +/- 17 ml/min after 15, 30, and 60 min of infusion, respectively. Acute intrarenal infusion of BK also increased urine volume (UV) from 0.255 +/- 0.044 to 0.523 +/- 0.103 ml/min and urinary sodium excretion (UNaV) from 5.72 +/- 1.5 to 13.7 +/- 3.4 mueq/min. To determine whether the potent acute effects of BK on RBF, UV, and UNaV lead to a chronic reduction in arterial pressure, BK (50 ng X kg-1 X min-1) was infused intrarenally for 7 days in conscious dogs. Intrarenal infusion of BK for 7 days had no significant effect on GFR, UNaV, UV, or arterial pressure. However, BK elevated renal plasma flow and decreased renal vascular resistance throughout the 7 days of infusion. Chronic intrarenal BK infusion caused no significant changes in plasma renin activity or plasma aldosterone concentration. Results from these studies indicate that although increased levels of bradykinin in the renal circulation can have potent acute effects on RBF, UV, and UNaV, these effects on UV and UNaV are not sustained and therefore do not result in long-term changes in arterial pressure.

Evidence that dopamine-2 mechanisms control renal function

1990 ◽  
Vol 259 (5) ◽  
pp. F793-F800 ◽  
Author(s):  
H. M. Siragy ◽  
R. A. Felder ◽  
N. L. Howell ◽  
R. L. Chevalier ◽  
M. J. Peach ◽  
...  
Keyword(s):  
Renal Function ◽  
Renal Plasma Flow ◽  
Plasma Renin ◽  
Urinary Flow ◽  
Plasma Aldosterone Concentration ◽  
Arterial Blood ◽  
Ly 171555 ◽  
Renal Vascular ◽  
Dose Dependent

Dopamine is synthesized by the kidney, and dopamine-2 (DA2) receptors are present in the renal glomerulus. However, no role for DA2 receptors in the kidney has been defined. We investigated the possible role of DA2 receptors in control of renal function by intrarenal infusion of a highly specific DA2 antagonist YM-09151 (YM), in conscious uninephrectomized dogs (n = 5) in metabolic balance at Na intake 40 meq/day. YM infused at 0.01 pmol.kg-1.min-1 did not cause any changes in urinary flow rate or Na excretion. Administration of YM (infusions from 0.1 to 10.0 pmol.kg-1.min-1) caused a significant dose-dependent diuresis (F = 20.3; P less than 0.001) and natriuresis (F = 35.2; P less than 0.0001) and an increase in glomerular filtration rate (F = 45.4; P less than 0.0001), renal plasma flow (F = 209.3; P less than 0.0001), and filtration fraction (F = 11.2; P less than 0.0001). No significant changes in plasma renin activity, plasma aldosterone concentration, or mean arterial blood pressure occurred with any of the doses of YM infused into the renal artery. Coinfusion of LY-171555, a specific DA2 agonist, at a dose that itself did not affect renal function, completely abrogated the renal hemodynamic and excretory changes induced by YM. The data suggest that dopamine produced intrarenally may act at renal vascular and/or glomerular DA2 receptors to control renal function.

Cardiac output and renal function during insulin hypertension in Sprague-Dawley rats

1996 ◽  
Vol 271 (1) ◽  
pp. R276-R281 ◽  
Author(s):  
M. W. Brands ◽  
W. F. Lee ◽  
H. L. Keen ◽  
M. Alonso-Galicia ◽  
D. H. Zappe ◽  
...  
Keyword(s):  
Heart Rate ◽  
Renal Function ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Insulin Infusion ◽  
Renal Plasma Flow ◽  
Control Period ◽  
Peripheral Resistance ◽  
Sodium Balance ◽  
Control Value

Hyperinsulinemia has been reported to cause hypertension in rats; however, the renal and hemodynamic mechanisms are not known. In this study, changes in renal function, cardiac output (CO), and total peripheral resistance (TPR) were measured during chronic insulin infusion in eight rats (approximately 350 g). After a 4-day control period, a 7-day insulin infusion was begun (1.5 mU.kg-1.min-1 iv), together with glucose (22 mg.kg-1.min-1 iv) to prevent hypoglycemia. Mean arterial pressure (MAP), CO, TPR, and heart rate were measured 24 h/day. MAP increased from 92 +/- 1 to 100 +/- 2 mmHg on day 1 and was 108 +/- 4 mmHg by day 7 of insulin. CO tended to decrease during insulin infusion, although not significantly, averaging 94 +/- 4% of the control value of 121 +/- 7 ml/min. Heart rate did not change significantly from the control value of 384 +/- 8 beats/min. TPR increased significantly to 122 +/- 11% of control by day 7. In five rats, glomerular filtration rate and effective renal plasma flow decreased to 73 +/- 4 and 66 +/- 5% of control, respectively, during insulin. Urinary sodium excretion averaged 2.6 +/- 0.1 and 2.7 +/- 0.1 meq/day during the control and insulin-infusion periods, respectively. These results indicate that insulin hypertension in rats is initiated by an increase in TPR rather than by increased CO. Also, the fact that sodium balance was maintained at elevated arterial pressure suggests that the ability of the kidneys to excrete sodium was impaired chronically during insulin infusion.

scholarly journals The Long-Term Effect of Preterm Birth on Renal Function: A Meta-Analysis

2021 ◽  
Vol 18 (6) ◽  
pp. 2951
Author(s):  
Ju Sun Heo ◽  
Jiwon M. Lee
Keyword(s):  
Renal Function ◽  
Preterm Birth ◽  
Glomerular Filtration ◽  
Renal Plasma Flow ◽  
Meta Analysis ◽  
Full Term ◽  
Significant Difference ◽  
Preterm Group ◽  
Preterm Born

The preterm-born adult population is ever increasing following improved survival rates of premature births. We conducted a meta-analysis to investigate long-term effects of preterm birth on renal function in preterm-born survivors. We searched PubMed and EMBASE to identify studies that compared renal function in preterm-born survivors and full-term-born controls, published until 2 February 2019. A random effects model with standardized mean difference (SMD) was used for meta-analyses. Heterogeneity of the studies was evaluated using Higgin’s I2 statistics. Risk of bias was assessed using the Newcastle–Ottawa quality assessment scale. Of a total of 24,388 articles screened, 27 articles were finally included. Compared to full-term-born controls, glomerular filtration rate and effective renal plasma flow were significantly decreased in preterm survivors (SMD −0.54, 95% confidence interval (CI), −0.85 to −0.22, p = 0.0008; SMD −0.39, 95% CI, −0.74 to −0.04, p = 0.03, respectively). Length and volume of the kidneys were significantly decreased in the preterm group compared to the full-term controls (SMD −0.73, 95% CI, −1.04 to −0.41, p < 0.001; SMD −0.82, 95% CI, −1.05 to −0.60, p < 0.001, respectively). However, serum levels of blood urea nitrogen, creatinine, and cystatin C showed no significant difference. The urine microalbumin to creatinine ratio was significantly increased in the preterm group. Both systolic and diastolic blood pressures were also significantly elevated in the preterm group, although the plasma renin level did not differ. This meta-analysis demonstrates that preterm-born survivors may be subject to decreased glomerular filtration, increased albuminuria, decreased kidney size and volume, and hypertension even though their laboratory results may not yet deteriorate.

Treatment of Renal-Vascular Injury by Transcatheter Embolization: Immediate and Long-Term Effects on Renal Function

2006 ◽  
Vol 20 (6) ◽  
pp. 405-409 ◽  
Author(s):  
Vassilis Poulakis ◽  
Nikolaos Ferakis ◽  
Eduard Becht ◽  
Charalabos Deliveliotis ◽  
Markus Duex
Keyword(s):  
Renal Function ◽  
Vascular Injury ◽  
Transcatheter Embolization ◽  
Long Term Effects ◽  
Renal Vascular

Intrarenal renin inhibition increases renal function by an angiotensin II-dependent mechanism

1988 ◽  
Vol 255 (4) ◽  
pp. F749-F754 ◽  
Author(s):  
H. M. Siragy ◽  
N. E. Lamb ◽  
C. E. Rose ◽  
M. J. Peach ◽  
R. M. Carey
Keyword(s):  
Renal Function ◽  
Angiotensin Ii ◽  
Sodium Intake ◽  
Renal Plasma Flow ◽  
Plasma Renin ◽  
Competitive Inhibitor ◽  
Urinary Flow ◽  
Renin Substrate ◽  
Plasma Aldosterone Concentration ◽  
Renin Inhibition

ACRIP is a competitive inhibitor of renin in which an analogue of statine, (3R,4S)-4-amino-3-hydroxy-6-methylheptanoic acid, is incorporated into analogues of porcine renin substrate. ACRIP inhibits the enzymatic activity of renin, thus blocking the initiation of the angiotensin cascade. We studied the intrarenal action of ACRIP in small quantities without measurable systemic effects on renal function. In the first experiment, ACRIP was administered intrarenally at 0.02, 0.2, and 2 micrograms.kg-1.min-1 to uninephrectomized conscious dogs (n = 6) in metabolic balance at sodium intake of 10 meq/day. ACRIP, in doses of 0.02 and 0.2 micrograms.kg-1.min-1, markedly increased urine sodium excretion (UNaV) from 5.8 +/- 1.4 to 15.1 +/- 5.1 and 19.9 +/- 3.2 mu eq/min, respectively. Urinary flow rate (UV) underwent a similar increase and glomerular filtration rate (GFR) increased from 25.7 +/- 2.5 to 35.6 +/- 2.5 at 0.02 micrograms.kg-1.min-1 of ACRIP. Renal plasma flow (RPF), plasma renin activity (PRA), and plasma aldosterone concentration (PAC) were not affected. At 2 micrograms.kg-1.min-1, ACRIP traversed the kidney in quantities large enough to produce a reduction in systemic PRA and mean arterial pressure and caused natriuresis, diuresis, and increased GFR. In a second experiment, ACRIP was administered intrarenally at 0.2 micrograms.kg-1.min-1 in a separate group (n = 4) under identical conditions. ACRIP-induced increases in UV and UNaV were completely blocked by concurrent intrarenal administration of angiotensin II. The results indicate that intrarenal angiotensin II acts as a physiological regulator of renal sodium and fluid homeostasis.

Effects of sulindac on renal function and prostaglandin synthesis in patients with moderate chronic renal insufficiency

1986 ◽  
Vol 70 (5) ◽  
pp. 501-505 ◽  
Author(s):  
C. D. Mistry ◽  
C. J. Lote ◽  
R. Gokal ◽  
W. J. C. Currie ◽  
M. Vandenburg ◽  
...  
Keyword(s):  
Renal Function ◽  
Renal Insufficiency ◽  
Creatinine Clearance ◽  
Chronic Renal Disease ◽  
Renal Plasma Flow ◽  
Plasma Renin ◽  
Breakdown Product ◽  
Predisposing Factor ◽  
A Minor ◽  
Therapeutic Doses

1. The renal effects of therapeutic doses of sulindac were studied in nine patients with stable renal insufficiency, mean creatinine clearance 37.0 ± 2.2 ml min−1 1.73 m−2 (range 24.7–54.6 ml min−1 1.73 m−2). 2. Nine days' treatment with sulindac produced a small, but significant, reduction in the mean creatinine clearance (37.0 ± 2.2 to 34.7 ± 2.2 ml min−1 1.73 m−2; P < 0.02) and 99mTc diethylenetriaminepenta-acetate (DTPA) clearance (35.5 ± 3.4 to 31.4 ± 3.6 ml min−1 1.73 m−2; P < 0.02) without altering body weight, effective renal plasma flow [131I]hippuran clearance), plasma renin activity (PRA), 24 h urinary volume or electrolyte excretion. 3. After discontinuation of sulindac, creatinine clearance returned to pretreatment values. 4. In five female patients, pretreatment urinary excretion of the 6-ketoprostaglandin F1α (6-keto-PGF1α), a stable breakdown product of prostacyclin (PGI2), was significantly reduced (P < 0.02) when compared with four healthy controls, whereas prostaglandin E2 (PGE2) was unchanged. Administration of sulindac did not significantly alter the excretion rate of PGE2 or 6-ketoPGF1α in this group of patients. 5. In chronic renal disease with moderate renal impairment, reduced renal prostacyclin synthesis may be an important predisposing factor to the renal toxicity associated with the use of nonsteroidal anti-inflammatory drugs (NSAID). Short term use of sulindac in therapeutic doses does not appear to influence the excretion of prostaglandins and produces only a minor reversible change in renal function; used cautiously it may have advantages over other NSAID in these patients.-

Hemodynamic changes induced by reversal of early and late renovascular hypertension

1983 ◽  
Vol 245 (5) ◽  
pp. H734-H740
Author(s):  
G. I. Russell ◽  
R. F. Bing ◽  
J. D. Swales ◽  
H. Thurston
Keyword(s):  
Blood Pressure ◽  
Renovascular Hypertension ◽  
Early Phase ◽  
Peripheral Resistance ◽  
Chronic Phase ◽  
Plasma Renin ◽  
Chronic Hypertension ◽  
Radioactive Microspheres ◽  
Hemodynamic Changes ◽  
Rapid Reduction

The hemodynamic changes associated with reversal of Goldblatt two-kidney, one-clip hypertension in conscious rats were studied using radioactive microspheres. In both the early phase (less than 6 wk from clipping) when plasma renin was elevated and the chronic phase (greater than 4 mo) when plasma renin was normal, hypertension was maintained by elevated peripheral resistance. Unclipping or removal of the ischemic kidney normalized blood pressure within 24 h by reduction in peripheral resistance. In early-phase hypertension blood pressure remained normal at 60 days after nephrectomy or unclipping, but in chronic-phase hypertension blood pressure was significantly elevated at 60 days after nephrectomy despite a similar fall in peripheral resistance. Plasma renin fell to normal or subnormal values after reversal in both early and chronic hypertension. Thus reversal of hypertension is associated with a rapid reduction in peripheral resistance even in longstanding hypertension. Since removal of the ischemic kidney and unclipping were equally effective, reversal must depend on either inhibition of a pressor system derived from the ischemic kidney or activation of a peripheral vasodepressor system not dependent on a revascularized kidney.

Age-related changes in renal hemodynamics in female rats: role of multiple pregnancy and NO

1997 ◽  
Vol 272 (6) ◽  
pp. R1985-R1989 ◽  
Author(s):  
J. F. Reckelhoff
Keyword(s):  
Renal Function ◽  
Renal Plasma Flow ◽  
Multiple Pregnancy ◽  
Renal Hemodynamics ◽  
Female Rats ◽  
No Production ◽  
Renal Vasculature ◽  
Pregnant Rats ◽  
Age Related ◽  
Renal Vascular

The objective of the present study was to evaluate 1) the effect of multiple pregnancy and aging on renal function and 2) the effect of NO inhibition on renal function in aged virgin and multiply pregnant rats. Renal hemodynamics were measured in the presence or absence of chronic (2 wk) NO synthase inhibition (nitro-L-arginine methyl ester, L-NAME) in young virgins (YV, 3-4 mo), old virgins (OV, 17-18 mo), and old retired breeders (ORB, 17-18 mo) that had sustained eight to nine pregnancies and lactations. Blood pressure was not different between control YV and OV. Glomerular filtration rate (GFR), renal plasma flow (RPF), and renal vascular resistance (RVR) were similar in OV and control YV. In contrast, the renal vasculature of ORB was more vasoconstricted in ORB than in YV or OV:GFR was decreased by 35% and RVR was higher than in YV or OV. With L-NAME there were similar increases in arterial pressure in all rats. In control YV, L-NAME had no effect on GFR, decreased RPF by 20%, and increased RVR by twofold. In OV, L-NAME decreased GFR by 30% and RPF by 60% and increased RVR by 3.3-fold. In ORB, L-NAME had no effect on GFR, decreased RPF by 30%, and increased RVR by 1.8-fold. These data suggest that the renal vasculature of ORB is vasoconstricted and that the mechanism may be due to a decrease in NO production.

Effects of a new dihydropyridine derivative, S12968 (pranedipine), and its stereoisomer, S12967, on renal effects of endothelin-1

1994 ◽  
Vol 72 (11) ◽  
pp. 1294-1298 ◽  
Author(s):  
Immaculada Montañés ◽  
Olga Flores ◽  
Nélida Eleno ◽  
José M. López-Novoa
Keyword(s):  
Renal Function ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Fold Increase ◽  
Urine Flow ◽  
Renal Vascular Resistance ◽  
Potassium Excretion ◽  
Endothelin 1 ◽  
Dihydropyridine Derivative ◽  
Renal Vascular

The purpose of the present study was to assess in rats the prevention by two enantiomers of a new dihydropyridine derivative (pranedipine) (called S12967 for the dextrogyre(+) and S12968 for the levogyre (−) molecules) of the renal and cardiovascular effects induced by endothelin-1. The injection of endothelin-1 (1 nmol/kg body weight) induced a sharp and transient decrease in urine flow, sodium and potassium excretion, glomerular filtration rate, renal plasma flow, and renal blood flow, a significant increase in renal vascular resistance, and a small but significant increase in arterial pressure. Treatment with S12968 alone (0.3 mg/kg) induced a 2.5-fold increase in urine flow and potassium excretion and a 4.5-fold increase in sodium excretion. Pretreatment with S12968 completely blocked the endothelin-1 induced increase in arterial pressure, did not affect the acute effect of endothelin-1 on urine flow, sodium and potassium excretion, filtration rate, and renal blood flow, but blunted the effect on renal vascular resistance. Administration of S12967 alone (1 mg/kg) did not induce changes in either renal function or arterial pressure. In S12967-treated animals, endothelin-1 also induced a transient increase in arterial pressure and renal vascular resistance but failed to change renal function in a significant manner. In summary, the above reported experiments show that at the higher, nonhypotensive doses, the levogyre enantiomer (S12968) of a new dihydropyridine derivative (pranedipine) completely prevented the hypertensive effect of endothelin 1, and partially prevented the effect of endothelin-1 on renal vascular resistance. The dextrogyre enantiomer (S12967) had almost no effect on either mean arterial pressure or renal vascular resistance but completely blocked the endothelin-1-induced decrease in urine flow and urinary sodium excretion.Key words: calcium antagonists, endothelin, dihydropyridines, kidney, renal function (rat).

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