scholarly journals The Link Between Chronic Renal Blood Flow and Arterial Pressure Control by Angiotensin II in Mice.

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Hicham Labazi ◽  
Amy K.L. Banes‐Berceli ◽  
Michael W. Brands
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Renal Blood Flow ◽  
Pressure Control

Exaggerated renal vascular reactivity to angiotensin and thromboxane in young genetically hypertensive rats

1990 ◽  
Vol 259 (2) ◽  
pp. F372-F382 ◽  
Author(s):  
C. Chatziantoniou ◽  
F. H. Daniels ◽  
W. J. Arendshorst
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Renal Blood Flow ◽  
Receptor Agonist ◽  
Vascular Reactivity ◽  
Prostaglandin Synthesis ◽  
Genetic Hypertension ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Renal Vascular

The objective of this study was to test the hypothesis that angiotensin II and thromboxane A2 (TxA2) contribute to the elevated renal vascular resistance observed during the development of genetic hypertension. In 6-wk-old anesthetized spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats, renal blood flow (electromagnetic flowmetry) and carotid arterial pressure were measured during bolus injections of different doses of angiotensin II and U46619 (stable receptor agonist of TxA2) into the renal artery before and during inhibition of prostaglandin synthesis by indomethacin. In all cases, arterial pressure remained unchanged at the pre-injection levels. Under control conditions, angiotensin II reduced renal blood flow in SHR almost twice as much as in WKY. This strain difference was abolished by inhibition of prostaglandin synthesis, suggesting that a deficiency in the action of endogenous vasodilator prostaglandins is responsible for the enhanced response to angiotensin II in SHR. Under control conditions, the TxA2-receptor agonist produced similar reductions of renal blood flow in SHR and WKY. However, after indomethacin, the agonist-induced vasoconstriction was twice as large in SHR as in WKY, suggesting that SHR kidneys have an increased vascular reactivity to TxA2, which is unmasked when indomethacin reduces elevated levels of endogenous TxA2. These findings indicate important strain differences between young SHR and WKY in the renal vascular response to angiotensin II and TxA2 that may contribute to the renal vasoconstriction observed during the development of genetic hypertension.

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.

Angiotensin II induces insulin resistance independent of changes in interstitial insulin

1999 ◽  
Vol 277 (5) ◽  
pp. E920-E926 ◽  
Author(s):  
Joyce M. Richey ◽  
Marilyn Ader ◽  
Donna Moore ◽  
Richard N. Bergman
Keyword(s):  
Insulin Resistance ◽  
Heart Rate ◽  
Blood Flow ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Glucose Uptake ◽  
Peripheral Resistance ◽  
Glucose Turnover ◽  
Ang Ii

We set out to examine whether angiotensin-driven hypertension can alter insulin action and whether these changes are reflected as changes in interstitial insulin (the signal to which insulin-sensitive cells respond to increase glucose uptake). To this end, we measured hemodynamic parameters, glucose turnover, and insulin dynamics in both plasma and interstitial fluid (lymph) during hyperinsulinemic euglycemic clamps in anesthetized dogs, with or without simultaneous infusions of angiotensin II (ANG II). Hyperinsulinemia per se failed to alter mean arterial pressure, heart rate, or femoral blood flow. ANG II infusion resulted in increased mean arterial pressure (68 ± 16 to 94 ± 14 mmHg, P < 0.001) with a compensatory decrease in heart rate (110 ± 7 vs. 86 ± 4 mmHg, P < 0.05). Peripheral resistance was significantly increased by ANG II from 0.434 to 0.507 mmHg ⋅ ml−1⋅ min ( P < 0.05). ANG II infusion increased femoral artery blood flow (176 ± 4 to 187 ± 5 ml/min, P < 0.05) and resulted in additional increases in both plasma and lymph insulin (93 ± 20 to 122 ± 13 μU/ml and 30 ± 4 to 45 ± 8 μU/ml, P < 0.05). However, glucose uptake was not significantly altered and actually had a tendency to be lower (5.9 ± 1.2 vs. 5.4 ± 0.7 mg ⋅ kg−1⋅ min−1, P > 0.10). Mimicking of the ANG II-induced hyperinsulinemia resulted in an additional increase in glucose uptake. These data imply that ANG II induces insulin resistance by an effect independent of a reduction in interstitial insulin.

Characterization of the postocclusive response of renal blood flow in the cat

1978 ◽  
Vol 235 (4) ◽  
pp. F286-F290 ◽  
Author(s):  
W. S. Spielman ◽  
H. Osswald
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Artery ◽  
Renal Blood Flow ◽  
Artery Occlusion ◽  
Renal Nerves ◽  
Vasoconstrictor Response ◽  
Renal Artery Occlusion ◽  
Chronic Denervation

In contrast to the postocclusive hyperemia of brain, heart, and skeletal muscle, the hemodynamic response of the kidney following renal artery occlusion is highly variable in that both hyperemia and ischemia have been reported. The present study evaluates the factors influencing the renal response to complete renal artery occlusion (5-60 s) in the anesthetized cat. Marked postocclusive vasoconstriction could only be domonstrated in meclofenamate-treated (10 mg/kg) cats. The delta% renal blood flow (RBF) (30-s occlusion) was 16 +/- 4 in controls and 54 +/- 4 after meclofenamate (n= 10; P less than 0.001). Chronic denervation of the kidney, alpha-adrenergic receptor blockade, or infusion of [Sar1, Ile8]angiotensin II(2 microgram/min per kg) did not affect the postocclusive reduction of RBF, indicating that the vasoconstriction was independent of renal nerves, catecholamines, and circulating angiotesin II. Adenosine injected into the renal artery of five cats caused a dose-dependent transient fall of RBF. A dose of 100 nmol adenosine reduced RBF by 44 +/- 6% whereas after meclofenamate only 1 nmol produced the same degree of vasoconstriction. In summary, this study demonstrates a marked potentiation of the postocclusive vasoconstrictor response and the vasoconstrictive action of adenosine by meclofenamate in the anesthetized animal. No evidence was obtained to support a role for the sympathetic nervous system or circulating angiotensin II in mediating the postocclusive vasoconstriction.

L-arginine analogues inhibit aldosterone secretion in rats

1995 ◽  
Vol 268 (5) ◽  
pp. R1137-R1142 ◽  
Author(s):  
J. C. Simmons ◽  
R. H. Freeman
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Methyl Ester ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Bilateral Nephrectomy ◽  
Aldosterone Secretion ◽  
Series Of Experiments

L-Arginine analogues, e.g., NG-nitro-L-arginine methyl ester (L-NAME), increase arterial pressure and suppress renin release in the rat. On the basis of these observations, it was hypothesized that L-arginine analogues also would attenuate aldosterone secretion. This hypothesis was tested in anesthetized rats treated with L-NAME or NG-nitro-L-arginine (L-NNA, 185 mumol/kg ip). The aldosterone secretion rate, plasma renin activity, and adrenal blood flow were attenuated in rats treated with L-NAME and L-NNA compared with control animals. Similar experiments were performed in anephric rats to examine the effects of L-NAME on aldosterone secretion independent of the circulating reninangiotensin system. The administration of L-NAME reduced adrenal blood flow but failed to reduce aldosterone secretion in these anephric rats. Bilateral nephrectomy reduced plasma renin activity essentially to undetectable levels in these animals. In a third series of experiments, two groups of anephric rats were infused with angiotensin II (3 micrograms/kg body wt iv) to provide a stimulus for aldosterone secretion. Aldosterone secretion and adrenal blood flow were markedly reduced in angiotensin II-infused rats pretreated with L-NAME compared with the control anephric animals infused with angiotensin II. Overall these results suggest that L-arginine analogues attenuate aldosterone secretion by inhibiting the adrenal steroidogenic effects of endogenous or exogenous angiotensin II and/or by reducing plasma levels of renin/angiotensin.

Effect of chloride on renal blood flow in angiotensin II induced hypertension

1991 ◽  
Vol 69 (4) ◽  
pp. 507-511 ◽  
Author(s):  
John C. Passmore ◽  
Agnes E. Jimenez
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Sodium Chloride ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Dietary Sodium ◽  
Maximum Increase ◽  
High Sodium ◽  
Low Sodium ◽  
Chloride Effect

The effect of selective dietary sodium and (or) chloride loading on blood pressure and renal blood flow (RBF) in the rat angiotensin II (AII) model of hypertension was determined. AII (200 ng/min) or saline was infused intraperitoneally. Diets were provided with either high or low concentrations of sodium, chloride or both ions for 22 days. The blood pressure of saline-treated animals was not increased by the high sodium chloride diet. Animals on a high sodium, high chloride diet had a significantly greater increase of blood pressure at 8, 15, 18, and 22 days of AII infusion compared with AII-treated animals on a low sodium, low chloride diet (p < 0.05). Selective dietary loading of either high sodium or chloride in AII-treated rats produced no greater elevation of blood pressure than AII with the low sodium, low chloride diet. Selective high dietary chloride was associated with a lower RBF in AII- and vehicle-treated rats compared with low dietary chloride. The chloride effect on RBF was greater in AII-treated animals. In conclusion, both sodium and chloride are necessary to produce the maximum increase of blood pressure in AII animals. AII enhances the decreased RBF induced by dietary chloride.Key words: angiotensin II, sodium chloride, blood pressure.

scholarly journals Vascular Type 1A Angiotensin II Receptors Control BP by Regulating Renal Blood Flow and Urinary Sodium Excretion

2015 ◽  
Vol 26 (12) ◽  
pp. 2953-2962 ◽  
Author(s):  
Matthew A. Sparks ◽  
Johannes Stegbauer ◽  
Daian Chen ◽  
Jose A. Gomez ◽  
Robert C. Griffiths ◽  
...  
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Angiotensin Ii Receptors ◽  
Vascular Type

Contribution of renal nerves to renal blood flow variability during hemorrhage

1998 ◽  
Vol 274 (5) ◽  
pp. R1283-R1294 ◽  
Author(s):  
Simon C. Malpas ◽  
Roger G. Evans ◽  
Geoff A. Head ◽  
Elena V. Lukoshkova
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Renal Blood Flow ◽  
Spectral Power ◽  
Sympathetic Nerves ◽  
Renal Nerves ◽  
Similar Frequency ◽  
Blood Withdrawal ◽  
Conscious Rabbits ◽  
Renal Sympathetic

We have examined the role of the renal sympathetic nerves in the renal blood flow (RBF) response to hemorrhage in seven conscious rabbits. Hemorrhage was produced by blood withdrawal at 1.35 ml ⋅ min−1 ⋅ kg−1for 20 min while RBF and renal sympathetic nerve activity (RSNA) were simultaneously measured. Hemorrhage was associated with a gradual increase in RSNA and decrease in RBF from the 4th min. In seven denervated animals, the resting RBF before hemorrhage was significantly greater (48 ± 1 vs. 31 ± 1 ml/min intact), and the decrease in RBF did not occur until arterial pressure also began to fall (8th min); however, the overall percentage change in RBF by 20 min of blood withdrawal was similar. Spectral analysis was used to identify the nature of the oscillations in each variable. Before hemorrhage, a rhythm at ∼0.3 Hz was observed in RSNA, although not in RBF, whose spectrogram was composed mostly of lower-frequency (<0.25 Hz) components. The denervated group of rabbits had similar frequency spectrums for RBF before hemorrhage. RSNA played a role in dampening the effect of oscillations in arterial pressure on RBF as the transfer gain between mean arterial pressure (MAP) and RBF for frequencies >0.25 Hz was significantly less in intact than denervated rabbits (0.83 ± 0.12 vs. 1.19 ± 0.10 ml ⋅ min−1 ⋅ mmHg−1). Furthermore, the coherence between MAP and RBF was also significantly higher in denervated rabbits, suggesting tighter coupling between the two variables in the absence of RSNA. Before the onset of significant decreases in arterial pressure (up to 10 min), there was an increase in the strength of oscillations centered around 0.3 Hz in RSNA. These were accompanied by increases in the spectral power of RBF at the same frequency. As arterial pressure fell in both groups of animals, the dominant rhythm to emerge in RBF was centered between 0.15 and 0.20 Hz and was present in intact and denervated rabbits. It is speculated that this is myogenic in origin. We conclude that RSNA can induce oscillations in RBF at 0.3 Hz, plays a significant role in altering the effect of oscillations in arterial pressure on RBF, and mediates a proportion of renal vasoconstriction during hemorrhage in conscious rabbits.

Tubuloglomerular feedback dynamics and renal blood flow autoregulation in rats

1991 ◽  
Vol 260 (1) ◽  
pp. F53-F68 ◽  
Author(s):  
N. H. Holstein-Rathlou ◽  
A. J. Wagner ◽  
D. J. Marsh
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Renal Blood Flow ◽  
Slow Component ◽  
Broad Band ◽  
Experimental Results ◽  
Tubuloglomerular Feedback ◽  
Single Frequency ◽  
Vascular Control ◽  
Arterial Blood

To decide whether tubuloglomerular feedback (TGF) can account for renal autoregulation, we tested predictions of a TGF simulation. Broad-band and single-frequency perturbations were applied to arterial pressure; arterial blood pressure, renal blood flow and proximal tubule pressure were measured. Data were analyzed by linear systems analysis. Broad-band forcings of arterial pressure were also applied to the model to compare experimental results with simulations. With arterial pressure as the input and tubular pressure, renal blood flow, or renal vascular resistance as outputs, the model correctly predicted gain and phase only in the low-frequency range. Experimental results revealed a second component of vascular control active at 100-150 mHz that was not predicted by the simulation. Forcings at single frequencies showed that the system behaves linearly except in the band of 33-50 mHz in which, in addition, there are autonomous oscillations in TGF. Higher amplitude forcings in this band were attenuated by autoregulatory mechanisms, but low-amplitude forcings entrained the autonomous oscillations and provoked amplified oscillations in blood flow, showing an effect of TGF on whole kidney blood flow. We conclude that two components can be detected in the dynamic regulation of renal blood flow, i.e., a slow component that represents TGF and a faster component that most likely represents an intrinsic vascular myogenic mechanism.

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