Autoregulation of renal blood flow in two-kidney, one-clip hypertensive rats

1986 ◽  
Vol 251 (2) ◽  
pp. F245-F250 ◽  
Author(s):  
B. M. Iversen ◽  
K. J. Heyeraas ◽  
I. Sekse ◽  
K. J. Andersen ◽  
J. Ofstad
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Renal Blood Flow ◽  
Perfusion Pressure ◽  
Complete Loss ◽  
Hypertensive Rats ◽  
Functional Changes ◽  
Pressure Limit ◽  
Renal Vascular

Renal blood flow (RBF) autoregulation was examined in the clipped and nonclipped kidneys in two groups of two-kidney, one-clip (2K-1C) hypertensive rats 10 wk after clipping. The arterial pressure distal to the clip and the renin secretion rate (RSR) were also examined. The blood pressure (BP) was 149 +/- 4 and 162 +/- 6 mmHg in the two hypertensive groups vs. 114 +/- 3 mmHg in the controls (P less than 0.02). The RBF (in ml X min-1 X kidney-1) was 4.27 +/- 0.41 in the nonclipped and 2.18 +/- 0.23 in the clipped kidneys (P less than 0.001). The pressure distal to the clip was 104 +/- 7 mmHg. The renal vascular resistance (RVR) (in mmHg X ml-1 X min-1 X g-1) was 25.0 +/- 1.4 in the control kidneys vs. 58.4 +/- 4.5 in the nonclipped (P less than 0.001) and 39.9 +/- 6.6 in the clipped kidneys (P less than 0.01). The RBF autoregulation was well preserved in the nonclipped kidneys but reset to a higher lower pressure limit of autoregulation of 106 +/- 4 mmHg, which was significantly higher than in the normotensive controls (84 +/- 6 mmHg) (P less than 0.01). In the clipped kidneys there was complete loss of RBF autoregulation. RSR decreased with reduction of the perfusion pressure in the clipped kidneys. The increased RVR might have been due to a combination of structural and functional changes in both kidneys.

Resetting of renal blood flow autoregulation in spontaneously hypertensive rats

1987 ◽  
Vol 252 (3) ◽  
pp. F480-F486 ◽  
Author(s):  
B. M. Iversen ◽  
I. Sekse ◽  
J. Ofstad
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Spontaneously Hypertensive Rats ◽  
Lower Pressure ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Pressure Limit ◽  
Wistar Kyoto ◽  
Renal Vascular ◽  
Renal Blood Flow Autoregulation

Renal blood flow (RBF) autoregulation was examined in untreated 10- and 40-wk-old spontaneously hypertensive rats (SHR) [mean arterial pressure (MAP) 125 +/- 4 and 167 +/- 7 mmHg] and in captopril-treated (7 days) 10- and 40-wk-old SHR (88 +/- 7 and 112 +/- 5 mmHg). Age-matched Wistar-Kyoto rats (WKY) were used as controls (MAP 91 +/- 3 and 104 +/- 2 mmHg). The study was carried out in rats with and without acute uninephrectomy. In 10-wk-old acutely uninephrectomized animals, the lower pressure limit of autoregulation was 78 +/- 4 mmHg in WKY, 102 +/- 5 mmHg in SHR (P less than 0.02), and 78 +/- 7 mmHg in captopril-treated SHR (P greater than 0.10). The renal vascular resistance (RVR) was significantly elevated at the lower pressure limit of RBF autoregulation in untreated SHR (P less than 0.02) but became normal after treatment (P greater than 0.10). Neither uninephrectomy nor variation of RBF between different batches seemed to influence the lower pressure limit of RBF autoregulation. In 40-wk-old acutely nephrectomized animals, the lower pressure limit of RBF autoregulation in WKY was 85 +/- 4 mmHg, 128 +/- 3 mmHg in SHR (P less than 0.001), and 101 +/- 5 mmHg in captopril-treated SHR (P less than 0.01). RVR at the lower pressure limit was increased in untreated SHR (P less than 0.01), but fell to normal values during captopril treatment. Neither the uninephrectomy nor variation of RBF between different batches of rats seemed to influence the lower pressure limit of RBF autoregulation.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Effects of Saralasin Infusion on Bilateral Renal Function in Two-Kidney, One-Clip Goldblatt Hypertensive Rats

1982 ◽  
Vol 62 (6) ◽  
pp. 573-579 ◽  
Author(s):  
Wann-Chu Huang ◽  
D. W. Ploth ◽  
L. G. Navar
Keyword(s):  
Blood Flow ◽  
Renal Function ◽  
Glomerular Filtration Rate ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Renal Blood Flow ◽  
Filtration Rate ◽  
Hypertensive Rats ◽  
Excretory Function ◽  
Renal Vascular

1. Previous studies have shown that administration of converting enzyme inhibitor (CEI, SQ 20 881) to two-kidney, one-clip Goldblatt hypertensive (GH) rats clipped for 3–4 weeks resulted in marked increases in glomerular filtration rate (GFR), water and sodium excretion by the non-clipped kidneys. The clipped kidneys exhibited reduced function that was due, in part, to the reductions in arterial pressure. To evaluate further the hypothesis that the renal responses to CEI were due primarily to the inhibition of angiotensin II rather than other factors, we infused the angiotensin II competitive blocker, saralasin, into GH rats under sodium pentobarbital anaesthesia and examined renal haemodynamics and excretory function of each kidney before and during saralasin infusion and after cessation of saralasin infusion. 2. Saralasin reduced mean arterial blood pressure from 164 ± 4 to 124 ± 4 mmHg. Despite the profound fall of arterial pressure, significant increases in renal blood flow from 5.82 ± 0.22 to 9.15 ± 0.76 ml/min and glomerular filtration rate from 1.46 ± 0.10 to 2.18 ± 0.14 ml/min were observed in the non-clipped kidneys. Renal vascular resistance decreased from 2.34 (± 0.14) × 105 to 1.17 (± 0.19) × 105 kPa l−1 s [2.34 (± 0.14) × 106 to 1.17 (± 0.19) × 106 dyn s cm−5]. Also, concomitant diuresis and kaliuresis and a delayed natriuresis occurred. Correspondence: Dr L. G. Navar, University of Alabama in Birmingham Medical Center, University Station, 727 CDLD Bldg, Birmingham, Alabama 35294, U.S.A. 3. The clipped kidneys exhibited reductions in renal blood flow, GFR and excretory function during saralasin infusion. 4. Normal rats receiving the identical dose of saralasin responded with a slight but significant decrease in arterial pressure. The increases in renal blood flow and GFR were less than those observed in the non-clipped kidneys of hypertensive rats. 5. These data provide further support to the hypothesis that an angiotensin II-mediated elevation in renal vascular resistance and impairment of renal function exist in the non-clipped kidneys of GH rats.

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.

Effect of prostaglandin synthetase inhibitors on renal blood flow in the rat

1976 ◽  
Vol 231 (5) ◽  
pp. 1541-1545 ◽  
Author(s):  
WF Finn ◽  
WJ Arendshorst
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Perfusion Pressure ◽  
Small Diameter ◽  
Base Line ◽  
Sodium Pentobarbital ◽  
Prostaglandin Synthetase ◽  
Flow Transducer ◽  
Renal Vascular

Using a small-diameter electromagnetic flow transducer, the effect on the autoregulation of renal blood flow (RBF) of two structurally different prostaglandin synthetase inhibitors, indomethacin, 4 mg/kg BW, and meclofenamate, 5 mg/kg BW, was studied in nondiuretic rats anesthetized with either the oxybarbiturate, sodium pentobarbital, or the thiobarbiturate, Inactin. Regardless of the anesthetic agent, RBF remained relatively constant above a perfusion pressure of 105 mmHg. Treatment with either indomethacin or meclofenamate had no measurable effect on the autoregulatory response. Each agent, however, resulted in an increase in the renal vascular response to exogenous angiotensin II, an effect consistent with prostaglandin synthetase inhibition. Base-line RBF was significantly reduced by indomethacin or meclofenamate only in those animals that had previously received angiotensin. These results support the hypothesis that, in th rat, autoregulation of RBF occurs independently of prostaglandin activity, but that a relationship does exist between the renal vascular actions of angiotensin II and prostaglandins.

Effects of various sympathicomimetic drugs on renal hemodynamics in normotensive and hypotensive dogs

1960 ◽  
Vol 198 (6) ◽  
pp. 1279-1283 ◽  
Author(s):  
Lewis C. Mills ◽  
John H. Moyer ◽  
Carrol A. Handley
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Adrenergic Receptors ◽  
Filtration Rate ◽  
Renal Hemodynamics ◽  
Marked Activity ◽  
Renal Vascular

The effects of l-epinephrine, l-norepinephrine, phenylephrine, methoxamine, metaraminol and mephentermine on renal hemodynamics were studied in six groups of dogs. Although comparable rises in blood pressure were obtained, there were marked differences in the effects on renal hemodynamics. While infusion of mephentermine led to only slight reductions in glomerular filtration rate and renal blood flow, and only a slight increase in renal vascular resistance, methoxamine produced a marked fall in flow and a marked increase in resistance. The other agents tested had effects which were intermediate between these two. The effects of these same drugs on renal hemodynamics were also compared in dogs made hypotensive by bleeding. While blood pressure increased significantly in all groups, glomerular filtration rate and renal blood flow increased significantly only during infusion of mephentermine, metaraminol and phenylephrine. Since assays relative to the inherent vasodilator properties of these agents revealed epinephrine to be the only agent with marked activity, it seems unlikely that the observed effects were due to this factor. It is concluded that the observed changes were due to a greater reactivity of renal vascular vasoconstrictor adrenergic receptors with certain sympathicomimetic drugs than those of the vasculature in general.

scholarly journals Losartan does not decrease renal oxygenation and norepinephrine effects in rats after resuscitated hemorrhage

2018 ◽  
Vol 315 (2) ◽  
pp. F241-F246
Author(s):  
Sofia Jönsson ◽  
Jacqueline M. Melville ◽  
Mediha Becirovic-Agic ◽  
Michael Hultström
Keyword(s):  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Renal Blood Flow ◽  
Oxygen Tension ◽  
Vascular Resistance ◽  
Renal Vascular Resistance ◽  
Renal Oxygen Consumption ◽  
Significant Difference ◽  
Renal Vascular

Renin-angiotensin-system blockers are thought to increase the risk of acute kidney injury after surgery and hemorrhage. We found that losartan does not cause renal cortical hypoxia after hemorrhage in rats because of decreased renal vascular resistance, but we did not evaluate resuscitation. We aimed to study losartan’s effect on renal cortical and medullary oxygenation, as well as norepinephrine’s vasopressor effect in a model of resuscitated hemorrhage. After 7 days of losartan (60 mg·kg−1·day−1) or control treatment, male Wistar rats were hemorrhaged 20% of their blood volume and resuscitated with Ringerʼs acetate. Mean arterial pressure, renal blood flow, and kidney tissue oxygenation were measured at baseline and after resuscitation. Finally, the effect of norepinephrine on mean arterial pressure and renal blood flow was investigated. As expected, losartan lowered mean arterial pressure but not renal blood flow. Losartan did not affect renal oxygen consumption and oxygen tension. Mean arterial pressure and renal blood flow were lower after resuscitated hemorrhage. A smaller increase of renal vascular resistance in the losartan group translated to a smaller decrease in cortical oxygen tension, but no significant difference was seen in medullary oxygen tension, either between groups or after hemorrhage. The effect of norepinephrine on mean arterial pressure and renal blood flow was similar in control- and losartan-treated rats. Losartan does not decrease renal oxygenation after resuscitated hemorrhage because of a smaller increase in renal vascular resistance. Further, losartan does not decrease the efficiency of norepinephrine as a vasopressor, indicating that blood pressure may be managed effectively during losartan treatment.

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.

scholarly journals Altered renal hemodynamics and impaired myogenic responses in the fawn-hooded rat

1999 ◽  
Vol 276 (3) ◽  
pp. R855-R863 ◽  
Author(s):  
Richard P. E. van Dokkum ◽  
Cheng-Wen Sun ◽  
Abraham P. Provoost ◽  
Howard J. Jacob ◽  
Richard J. Roman
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Renal Damage ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Myogenic Response ◽  
Renal Perfusion Pressure ◽  
Medullary Blood Flow ◽  
Low Blood Pressure

The present study examined whether an abnormality in the myogenic response of renal arterioles that impairs autoregulation of renal blood flow (RBF) and glomerular capillary pressure (PGC) contributes to the development of renal damage in fawn-hooded hypertensive (FHH) rats. Autoregulation of whole kidney, cortical, and medullary blood flow and PGC were compared in young (12 wk old) FHH and fawn-hooded low blood pressure (FHL) rats in volume-replete and volume-expanded conditions. Baseline RBF, cortical and medullary blood flow, and PGCwere significantly greater in FHH than in FHL rats. Autoregulation of renal and cortical blood flow was significantly impaired in FHH rats compared with results obtained in FHL rats. Myogenically mediated autoregulation of PGC was significantly greater in FHL than in FHH rats. PGC rose from 46 ± 1 to 71 ± 2 mmHg in response to an increase in renal perfusion pressure from 100 to 150 mmHg in FHH rats, whereas it only increased from 39 ± 2 to 53 ± 1 mmHg in FHL rats. Isolated perfused renal interlobular arteries from FHL rats constricted by 10% in response to elevations in transmural pressure from 70 to 120 mmHg. In contrast, the diameter of vessels from FHH rats increased by 15%. These results indicate that the myogenic response of small renal arteries is altered in FHH rats, and this contributes to an impaired autoregulation of renal blood flow and elevations in PGC in this strain.

Atriopeptins: correlation between renal vasodilation and natriuresis

1985 ◽  
Vol 249 (1) ◽  
pp. F49-F53 ◽  
Author(s):  
K. Wakitani ◽  
B. R. Cole ◽  
D. M. Geller ◽  
M. G. Currie ◽  
S. P. Adams ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Rank Order ◽  
Urine Volume ◽  
Systemic Blood Pressure ◽  
Functional Changes ◽  
Positive Linear Correlation ◽  
Diuretic Agents

The effect of atrial peptides on renal function was studied in intact anesthetized dogs. A quantitative comparison of bolus intra-arterial injections demonstrated a rank order potency as renal vasodilators and natriuretic/diuretic agents as follows: ser-leu-arg-arg-atriopeptiin III (SLRR-APIII) greater than high molecular weight artrial peptide greater than or equal to atriopeptin (AP)III = APII much greater than API (essentially inactive). A sustained infusion of APIII was employed in order to study the temporal and quantitative correlation of the renal functional changes induced by the atrial peptide. Both intra-arterial and intravenous administration of the peptide produced concentration-dependent increases in renal blood flow, urine volume, sodium excretion, and osmotic clearance. Infusion of APIII into the renal artery did not alter systemic blood pressure or heart rate. Intravenous infusions of APIII required 10 times higher doses to induce the changes in renal vascular resistance and electrolyte excretion, and a fall in blood pressure and tachycardia resulted. The natriuretic-diuretic effect of the atriopeptins appears to be closely associated with renal vasodilation, exhibiting a positive linear correlation between the peptide-induced changes in sodium excretion and changes in renal blood flow.

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