Genetic co-segregation of renal haemodynamics and blood pressure in the spontaneously hypertensive rat

1988 ◽  
Vol 74 (1) ◽  
pp. 63-69 ◽  
Author(s):  
S. B. Harrap ◽  
A. E. Doyle
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Filtration Rate ◽  
Spontaneously Hypertensive Rat ◽  
Plasma Renin ◽  
Spontaneously Hypertensive

1. To determine the relevance of renal circulatory abnormalities found in the immature spontaneously hypertensive rat (SHR) to the genetic hypertensive process, glomerular filtration rate and renal blood flow were measured in conscious F2 rats, derived from crossbreeding SHR and normotensive Wistar–Kyoto rats (WKY), at 4, 11 and 16 weeks of age by determining the renal clearances of 51Cr-ethylenediaminetetra-acetate and 125I-hippuran respectively. Plasma renin activity was measured at 11 and 16 weeks of age. 2. Mean arterial pressure, glomerular filtration rate and renal blood flow increased between 4 and 11 weeks of age. Between 11 and 16 weeks the mean glomerular filtration rate and renal blood flow did not alter, although the mean arterial pressure rose significantly. At 11 weeks of age, during the developmental phase of hypertension, a significant negative correlation between mean arterial pressure and both glomerular filtration rate and renal blood flow was noted. However, by 16 weeks when the manifestations of genetic hypertension were more fully expressed, no correlation between mean arterial pressure and renal blood flow or glomerular filtration rate was observed. Plasma renin activity was negatively correlated with both glomerular filtration rate and renal blood flow, but the relationship was stronger at 11 than at 16 weeks of age. 3. These results suggest that the reduction in renal blood flow and glomerular filtration rate, found in immature SHR, is genetically linked to the hypertension and may be of primary pathogenetic importance. It is proposed that the increased renal vascular resistance in these young animals stimulates the rise of systemic arterial pressure which returns renal blood flow and glomerular filtration rate to normal.

Effects of the enantiomers of a new dihydropyridine derivative, S12968 and S12967, on renal functions in rats

1993 ◽  
Vol 71 (10-11) ◽  
pp. 848-853
Author(s):  
José M. López-Novoa ◽  
Inmaculada Montañés
Keyword(s):  
Blood Flow ◽  
Renal Function ◽  
Glomerular Filtration Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Hypotensive Effect

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.

Renal actions of atrial natriuretic peptide on the postischemic kidney

1988 ◽  
Vol 66 (5) ◽  
pp. 601-607 ◽  
Author(s):  
Satoshi Akabane ◽  
Masahito Imanishi ◽  
Yohkazu Matsushima ◽  
Minoru Kawamura ◽  
Morio Kuramochi ◽  
...  
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Arterial Pressure ◽  
Atrial Natriuretic Peptide ◽  
Renal Artery ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Natriuretic Peptide ◽  
Filtration Rate ◽  
Systemic Arterial Pressure

The objective of this study was to evaluate the renal actions of atrial natriuretic peptide (ANP) in the unilateral postischemic kidney of anesthetized dogs with a severe reduction in glomerular filtration rate. The dose of atrial natriuretic peptide (50 ng∙kg−1∙min−1) we gave did not alter the mean systemic arterial pressure, renal blood flow, and glomerular filtration rate in the normal kidney, as determined in foregoing studies. ANP was infused into the intrarenal artery continuously for 60 min after the release from 45 min of complete renal artery occlusion. In the vehicle-infused group, the glomerular filtration rate fell dramatically (6% of control), the renal blood flow decreased (60% of control), and the mean systemic arterial pressure tended to increase (136% of control). The urine flow rate and urinary excretion of sodium decreased significantly (25 and 25%, respectively) at 30 min after reflow in the postischemic period. Continuous renal artery infusion of ANP resulted in a marked increase in urine flow rate (246% of control) and the urinary excretion of sodium (286% of control). The administration of ANP led to an improvement in renal blood flow (99% of control) and glomerular filtration rate (40% of control), and attenuated the rise in mean systemic arterial pressure (109% of control), compared with findings in the vehicle-infused group. Plasma renin activity and prostaglandin E2 concentration in the renal venous blood were elevated after the release from complete renal artery occlusion in both groups. These results indicate that the vascular effects of ANP on the postischemic kidney were enhanced and that the peptide maintained the natriuretic effect.

Changes in renal function resulting from norepinephrine infusion

1962 ◽  
Vol 202 (5) ◽  
pp. 893-896 ◽  
Author(s):  
Jimmy B. Langston ◽  
Arthur C. Guyton ◽  
James H. DePoyster ◽  
George G. Armstrong
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Arterial Pressure ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Direct Effect ◽  
Infusion Rate ◽  
Filtration Rate ◽  
Urinary Output ◽  
Infusion Of Norepinephrine

The experiments of this study show that intravenous infusion of norepinephrine has a direct effect on the kidneys of areflex dogs to cause a decrease in renal blood flow, glomerular filtration rate, and urinary output. However, when the infusion rate is below an average of 0.0006 mg/kg/min, the renal blood flow, glomerular filtration rate, and urinary output increase as a result of an increase in arterial pressure which accompanies the infusion of norepinephrine. Above this infusion rate, the direct effect of the norepinephrine on the kidneys is greater than the effect of the rising arterial pressure, thus causing the blood flow, glomerular filtration rate, and urinary output to decrease. The results from this study indicate that changes in renal arterial pressure result in very significant changes in renal blood flow, glomerular filtration rate, and urinary output in spite of the local autoregulation of renal blood flow.

Protective effect of renal denervation on normotensive endotoxemia-induced acute renal failure in mice

2002 ◽  
Vol 283 (3) ◽  
pp. F583-F587 ◽  
Author(s):  
Wei Wang ◽  
Sandor A. Falk ◽  
Suparoek Jittikanont ◽  
Patricia E. Gengaro ◽  
Charles L. Edelstein ◽  
...  
Keyword(s):  
Renal Failure ◽  
Blood Flow ◽  
Acute Renal Failure ◽  
Glomerular Filtration Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Filtration Rate ◽  
Renal Denervation ◽  
Plasma Renin

Acute renal failure (ARF) contributes substantially to the high morbidity and mortality observed during endotoxemia. We hypothesized that selective blockade of the renal nerves would be protective against ARF during the early (16 h) stage of endotoxemia [5 mg lipopolysaccharide (LPS)/kg ip in mice]. At 16 h after LPS, there was no change in mean arterial pressure, but plasma epinephrine (4,604 ± 719 vs. 490 ± 152 pg/ml, P < 0.001), norepinephrine (2,176 ± 306 vs. 1,224 ± 218 pg/ml, P < 0.05), and plasma renin activity (40 ± 5 vs. 27 ± 2 ng · ml−1 · h−1, P < 0.05) were higher in the LPS-treated vs. control mice. The high plasma renin activity level decreased to the control level with renal denervation in endotoxemic mice. After intravenous injection of phentolamine (200 μg/kg), the decrement in mean arterial pressure was significantly greater in LPS-treated vs. control mice (19.4 ± 3.5 vs. 8.1 ± 1.5 mmHg, P < 0.01). Sixteen hours after LPS administration, there were significant decreases in glomerular filtration rate (52 ± 18 vs. 212 ± 23 μl/min, P < 0.01) and renal blood flow (0.58 ± 0.08 vs. 0.85 ± 0.06 ml/min, P < 0.01) in sham-operated mice. The decrement in glomerular filtration rate during endotoxemia was significantly attenuated in mice with denervated kidneys (32 vs. 79%). Moreover, there was no change in renal blood flow during endotoxemia in mice with renal denervation. The present results therefore demonstrate a protective role of renal denervation during normotensive endotoxemia-related ARF in mice, an effect that may be, at least in part, due to a diminished activation of the renin-angiotensin system.

Transient response of glomerular filtration rate and renal blood flow to step changes in arterial pressure

1977 ◽  
Vol 233 (5) ◽  
pp. F396-F402 ◽  
Author(s):  
T. E. Jackson ◽  
A. C. Guyton ◽  
J. E. Hall
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Steady State ◽  
Arterial Pressure ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Filtration Rate ◽  
Hemodynamic Changes ◽  
Proximal Tubular ◽  
Anesthetized Dogs

Measurement of rapid renal hemodynamic changes were made for 90 s in pentobarbital-anesthetized dogs following step increases and decreases in renal arterial pressure between 80 and 120 mm Hg. Transient analysis was used to observe time characteristics of the autoregulatory relationships which are obscured in steadystate measurements. Temporal decoupling of blood flow and glomerular filtration rate (GFR) occurred with both step increases and decreases of arterial pressure. Steady-state autoregulation of blood flow was attained in about 30 s, whereas steady-state autoregulation of GFR was not demonstrably attained even 90 s after the arterial pressure maneuver. The temporal decoupling of renal blood flow and GRR supports the concept of transient involvement of proximal tubular dynamics and efferent resistance changes during acute autoregulation of GFR following step changes in arterial pressure.

Autoregulation of zonal glomerular filtration rate and renal blood flow in spontaneously hypertensive rats

1995 ◽  
Vol 269 (4) ◽  
pp. F515-F521 ◽  
Author(s):  
X. Wang ◽  
K. Aukland ◽  
J. Ofstad ◽  
B. M. Iversen
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Spontaneously Hypertensive Rats ◽  
Filtration Rate ◽  
Left Kidney ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Inner Cortex

Autoregulation of total and zonal glomerular filtration rate (GFR) in outer, middle and inner cortex was estimated in spontaneously hypertensive rats (SHR), from the tubular uptake of 125I-labeled aprotinin (125I-Ap), injected at control renal arterial pressure (RAP), and 131I-Ap, injected at reduced RAP in left kidney. Normotensive Wistar-Kyoto (WKY) rats were used as controls. Renal blood flow (RBF) autoregulation was reset to higher pressure levels in SHR. When RAP was lowered close to the lower pressure limit of RBF autoregulation, total GFR was reduced to 89.5 +/- 3.1 and 88.1 +/- 3.3% of control in 10- and 40-wk WKY and to 87.7 +/- 2.3 and 88.0 +/- 2.2% in 10- and 40-wk SHR. In WKY, the fall of GFR in the three cortical layers was not different during RAP reduction. In 10- and 40-wk-old SHR, however, GFR fell significantly less in inner than in middle and outer cortex (P < 0.05). We conclude that autoregulation of GFR is most efficient in the inner cortex of SHR. In all animals, GFR was less well autoregulated than RBF.

Acute effect of changes in renal arterial pressure and sympathetic blockade on kidney function

1959 ◽  
Vol 197 (3) ◽  
pp. 595-600 ◽  
Author(s):  
Jimmy B. Langston ◽  
Arthur C. Guyton ◽  
William J. Gillespie
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Arterial Pressure ◽  
Glomerular Filtration ◽  
Spinal Anesthesia ◽  
Renal Blood Flow ◽  
Kidney Function ◽  
Filtration Rate ◽  
Sympathetic Blockade ◽  
Urine Formation

The effect of varying the renal arterial pressure on kidney function has been studied before and after complete spinal anesthesia. It is concluded that an increase in renal arterial pressure between 60 and 300 mm Hg always results in an increase in renal blood flow, glomerular filtration rate and urine formation, and that filtration rate and urinary output are related to renal arterial pressure in a linear fashion at pressures above 120 mm Hg. Sympathetic blockade, accomplished by complete spinal anesthesia, resulted in a higher rate of urine formation and renal blood flow but not of glomerular filtration rate at each level of arterial pressure than before the spinal anesthesia was administered. Since the sympathetic blockade was not followed by an increase in glomerular filtration rate, it is concluded that the diuresis which followed this blockade resulted from a decrease in reabsorption of glomerular filtrate.

Influence of the renin–angiotensin system in the renal haemodynamic responses to modest renal nerve stimulation in the rat

1982 ◽  
Vol 93 (1) ◽  
pp. 65-70 ◽  
Author(s):  
Stephen Ball ◽  
E. J. Johns
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Plasma Renin Activity ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Nerve Stimulation ◽  
Filtration Rate ◽  
Plasma Renin ◽  
Renal Nerves ◽  
Filtration Fraction

The renal nerves of the left kidney of sodium-replete anaesthetized rats were stimulated for 30-min periods at 2–3 Hz (15 V, 0·2 ms). Renal blood flow was reduced by 22% and glomerular filtration rate by 14% which resulted in a rise in filtration fraction of 12%. Circulating plasma renin activity was increased by 30% during such nerve stimulation. In rats treated for 3–4 weeks with deoxycorticosterone acetate (DOCA) and saline (150 mm-NaCl) basal values of arterial blood pressure, renal blood flow, glomerular filtration rate and filtration fraction were not significantly different from those observed in sodium-replete rats. However, plasma renin activity was lower, being approximately one-third of that observed in sodium-replete animals. Stimulation of the renal nerves in rats treated with DOCA and saline resulted in a fall in renal blood flow of 32% and a much larger fall in glomerular filtration rate of 33% which resulted in no change in filtration fraction. Plasma renin activity was not changed by renal nerve stimulation in the animals treated with DOCA and saline. It is suggested that these renal responses provide evidence in the rat for a role of locally generated angiotensin II in regulating glomerular filtration rate during electrical activation of the renal nerves by causing preferential vasoconstriction of the efferent arteriole.

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