Renal Blood Flow and Noradrenaline Secretion during Treatment with Propranolol

1980 ◽  
Vol 59 (s6) ◽  
pp. 477s-478s ◽  
Author(s):  
P. W. De Leeuw ◽  
R. Punt ◽  
W. H. Birkenhager

1. Fifty-five patients with uncomplicated essential hypertension were admitted to hospital, where 25 of them were treated with propranolol (average daily dose 240 mg) and 30 were left untreated. 2. In all of them renal arteriography was carried out, after which procedure renal plasma flow ([123I]hippuran clearance), cortical blood flow (xenon washout) and renal noradrenaline release were measured. 3. Compared with the untreated hypertensive patients, responders to propranolol (mean blood pressure ≤ 110 mmHg) during treatment showed enhanced cortical blood flow and reduced noradrenaline secretion. Non-responders had reduced cortical flow rates, but increased noradrenaline secretion. 4. Both in the untreated group and in the propranolol-treated group an inverse relationship between arterial noradrenaline concentration and cortical blood flow was found. 5. The results indicate that sympathetic activity may be an important determinant of renal blood flow in hypertension. The effectiveness of propranolol seems to depend upon a reduction in α-adrenergic tone.

1986 ◽  
Vol 250 (4) ◽  
pp. F613-F618 ◽  
Author(s):  
T. H. Hostetter

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)


1978 ◽  
Vol 55 (s4) ◽  
pp. 85s-87s ◽  
Author(s):  
P. W. De Leeuw ◽  
H. E. Falke ◽  
R. Punt ◽  
W. H. Birkenhäger

1. In 20 subjects with uncomplicated essential hypertension, 10 of whom were on propranolol treatment, several blood samples were drawn simultaneously from the renal artery and vein after angiographic studies. In these samples we determined concentrations of noradrenaline, active renin, aldosterone and cortisol. 2. Renal blood flow was measured in all patients by Hippuran-clearance and xenon-washout. 3. Despite marked variations in the arteriovenous difference of noradrenaline, it was apparent in both groups that the kidney is able to release noradrenaline. 4. In the propranolol-treated group noradrenaline secretion by the kidney was enhanced when compared with untreated hypertensive patients.


1985 ◽  
Vol 249 (4) ◽  
pp. F490-F496 ◽  
Author(s):  
J. A. Winston ◽  
R. Safirstein

Studies were designed to determine the cause of the reduced glomerular filtration rate (GFR) in early cisplatin-induced acute renal failure. Rats were studied 72 h following a single intraperitoneal injection of cisplatin (5 mg/kg) or vehicle (0.9% NaCl). Whole kidney GFR and blood flow were lower in cisplatin-treated animals than in controls (0.30 +/- 0.06 vs. 1.17 +/- 0.06 ml X min-1 X g kidney wt-1 and 5.30 +/- 0.62 vs. 8.25 +/- 0.43 ml X min-1 X g kidney wt-1, respectively; P less than 0.001), as were superficial nephron GFR and stop-flow pressure (20.2 +/- 2.1 vs. 34.5 +/- 2.0 nl X min-1 X g kidney wt-1 and 29.0 +/- 1.9 vs. 39.8 +/- 1.3 mmHg, respectively; P less than 0.001). After volume expansion, renal plasma flow increased in control rats, whereas whole kidney and single nephron GFR did not change. In experimental animals, whole kidney filtration rate rose to 0.58 +/- 0.07 ml X min-1 X g kidney wt-1, single nephron filtration rate increased to 29.9 +/- 3.5 nl X min-1 X g kidney wt-1 (P less than 0.005), and renal plasma flow increased to 5.62 +/- 0.60 ml X min-1 X g kidney wt-1 (P less than 0.05). Intratubular hydrostatic pressure was not different in the two groups before or after volume expansion. The results of these studies show that the reduced GFR in early cisplatin-induced renal failure is due, in part, to reversible changes in renal blood flow and renal vascular resistance.


1977 ◽  
Vol 233 (2) ◽  
pp. F89-F93
Author(s):  
C. Aizawa ◽  
N. Honda

The effect of indomethacin (10 mg/kg) on the distribution of cortical blood flow during postocclusive reactive hyperemia was evaluated in denervated kidneys of anesthetized rabbits by the radioactive microsphere technique. Renal denervation caused a slight but not significant increase in renal blood flow with no remarkable alteration in the distribution of cortical blood flow. After release of 1-min occlusion of the renal artery, hyperemic responses developed with a fractional flow redistribution toward the inner cortex. The absolute perfusion rate increased in the inner cortex but did not significantly change in the outer cortex. Indomethacin produced a decrease in renal blood flow despite elevated blood pressure. Even in the indomethacin-treated animals, postocclusive reactive hyperemia appeared concomitantly with the fractional flow redistribution to the inner cortex. The percentage repayment by reactive hyperemia of ischemia during the artery clamping was not significantly different before and after indomethacin administration. The findings indicate that indomethacin did not significantly affect the postocclusive vascular response in denervated kidneys of rabbits, thereby giving evidence against the role of prostaglandins as mediators of reactive hyperemia.


1976 ◽  
Vol 230 (2) ◽  
pp. 537-542 ◽  
Author(s):  
C Westenfelder ◽  
JA Arruda ◽  
R Lockwood ◽  
S Boonjarern ◽  
L Nascimento ◽  
...  

Studies were performed to determine whether the intrarenal distribution of cortical blood flow is altered in congestive heart failure. Utilizing the radioactive microsphere method, we studied eight dogs that developed congestive heart failure secondary to the construction of an aortocaval fistula. They had marked reduction in total renal blood flow not accompanied by intracortical redistribution of blood flow. All dogs had developed edema and/or ascites, and gained a mean of 3.4 kg; glomerular filtration rate, hematocrit, and urinary sodium excretion fell significantly. Renal vascular resistance increased; mean blood pressure and filtration fraction were unchanged. Furosemide was administered to a second group of nine fistula dogs. The drug produced a marked natriuresis associated with a decrease in outer cortical blood flow (zone 1) and an increase in midcortical zones 2 and 3; no change was observed in zone 4. We conclude: 1) chronic salt retention occurs in high-output heart failure in the absence of redistribution of renal cortical blood flow, and 2) the effect of furosemide on intrarenal hemodynamics of dogs with heart failure is similar to that seen in normal animals.


1993 ◽  
Vol 71 (10-11) ◽  
pp. 848-853
Author(s):  
José M. López-Novoa ◽  
Inmaculada Montañés

The aim of this study was to evaluate the effects of the two enantiomers of a new dihydropyridine, S12967 and S12968, on rat renal function. Male Wistar rats were injected intravenously with saline, S12967, or S12968 (0.1, 0.3, or 1 mg/kg body weight). Urinary flow, glomerular filtration rate, renal plasma flow, urinary sodium, potassium, and calcium excretions, mean arterial pressure, and renal vascular resistance were determined before and every 30 min up to 180 min after administration of the tested substance. The levogyre enantiomer S12968, at a dose of 0.3 mg/kg, induced a 4-fold increase in urinary sodium excretion, without significant or with minor changes in glomerular filtration rate, renal plasma flow, or renal blood flow. The hypotensive effect was small and nonsignificant. At 1 mg/kg, S12968 caused a profound hypotensive effect that impaired the renal function, induced marked oliguria, and decreased glomerular filtration rate and renal blood flow to almost negligible values. The dextrogyre enantiomer S12967 had much less effect on renal function. These data showing specific stereoselective renal effects are in agreement with pharmacological studies that have demonstrated that S12968 possesses a higher affinity for the dihydropyridine-binding site than its dextrogyre enantiomer, S12967.Key words: Ca channel antagonists, dihydropyridine, glomerular filtration rate, renal blood flow, natriuresis, mean arterial pressure.


1993 ◽  
Vol 264 (3) ◽  
pp. R578-R583 ◽  
Author(s):  
D. L. Mattson ◽  
S. Lu ◽  
R. J. Roman ◽  
A. W. Cowley

The present study examined the autoregulation of blood flow in different regions of the renal cortex and medulla in volume-expanded or hydropenic anesthetized rats. Blood flow was measured in the whole kidney by electromagnetic flowmetry, in the superficial cortex with implanted fibers and external probes for laser-Doppler flowmetry, and in the deep cortex and inner and outer medulla with implanted fibers for laser-Doppler flowmetry. At renal perfusion pressure > 100 mmHg, renal blood flow, superficial cortical blood flow, and deep cortical blood flow were all very well autoregulated in both volume-expanded and hydropenic rats. Inner and outer medullary blood flow were also well autoregulated in hydropenia, but blood flow in these regions was very poorly autoregulated in volume-expanded animals. As renal perfusion pressure was decreased below 100 mmHg in volume-expanded and hydropenic animals, renal blood flow, superficial and deep cortical blood flow, and inner and outer medullary blood flow all decreased. The results of these experiments demonstrate that blood flow in both the inner and outer portions of the renal medulla of the kidney is poorly autoregulated in volume-expanded rats but well autoregulated in hydropenic animals. In contrast, blood flow in all regions of the renal cortex is well autoregulated in both volume-expanded and hydropenic animals. These results suggest that changes in resistance in the postglomerular circulation of deep nephrons are responsible for the poor autoregulation of medullary blood flow in volume expansion despite well autoregulated cortical blood flow.


1963 ◽  
Vol 205 (1) ◽  
pp. 153-161 ◽  
Author(s):  
Mary Jo Elpers ◽  
Ewald E. Selkurt

Serum albumin (25%) was infused into anesthetized dogs undergoing a saline diuresis. No significant effect was seen on arterial pressure, but renal venous pressure was elevated slightly. GFR remained unchanged, while Cpah, renal plasma flow, total renal blood flow, and flow to medullary tissue increased significantly. Accompanying these changes were marked declines in PAH and creatinine extraction ratios. Urine volume, Cna, and Cosm declined appreciably during albumin infusion; TcHH2O tended to decrease. The ratio of Na and osmolar constituents in renal venous blood to that in arterial blood increased above unity, and calculations indicated that at this time Na was washed from the kidney. Tmpah remained unchanged during albumin infusion. It is concluded that during albumin infusion, there is an increase in plasma volume and renal blood flow accompanied by a diversion of part of this blood through aglomerular regions, possibly through A-V anastomoses, as evidenced by the accompanying decrease in Ecr and Epah. This could involve increased perfusion of the medullary papillary zone, including the vasa recta vessels, supported by the observations that during albumin infusion there is a washout of osmotic constituents, primarily Na, presumably from a zone of high Na concentration.


1999 ◽  
Vol 277 (2) ◽  
pp. F312-F318 ◽  
Author(s):  
Geraldine Corrigan ◽  
Deepa Ramaswamy ◽  
Osun Kwon ◽  
F. Graham Sommer ◽  
Edward J. Alfrey ◽  
...  

We determined the effect of postischemic injury to the human renal allograft on p-aminohippurate (PAH) extraction (EPAH) and renal blood flow. We evaluated renal function in 44 allograft recipients on two occasions: 1–3 h after reperfusion ( day 0) and again on postoperative day 7. On day 0 subsets underwent intraoperative determination of renal blood flow ( n = 35) by Doppler flow meter and EPAH( n = 25) by renal venous assay. Blood flow was also determined in another subset of 16 recipients on postoperative day 7 by phase contrast-cine-magnetic resonance imaging, and EPAH was computed from the simultaneous PAH clearance. Glomerular filtration rate (GFR) on day 7 was used to divide subjects into recovering ( n = 23) and sustained ( n = 21) acute renal failure (ARF) groups, respectively. Despite profound depression of GFR in the sustained ARF group, renal plasma flow was only slightly depressed, averaging 296 ± 162 ml ⋅ min−1 ⋅ 1.73 m−2 on day 0 and 202 ± 72 ml ⋅ min−1 ⋅ 1.73 m−2 on day 7, respectively. These values did not differ from corresponding values in the recovering ARF group: 252 ± 133 and 280 ± 109 ml ⋅ min−1 ⋅ 1.73 m−2, respectively. EPAH was profoundly depressed on day 0, averaging 18 ± 14 and 10 ± 7% in recovering and sustained ARF groups, respectively, vs. 86 ± 6% in normal controls ( P < 0.001). Corresponding values on day 7remained significantly depressed at 65 ± 20 and 11 ± 22%, respectively. We conclude that postischemic injury to the renal allograft results in profound impairment of EPAH that persists for at least 7 days, even after the onset of recovery. An ensuing reduction in urinary PAH clearance results in a gross underestimate of renal plasma flow, which is close to the normal range in the initiation, maintenance, and recovery stages of this injury.


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