Renal vascular responses and eicosanoid release in diabetic rats

1989 ◽  
Vol 257 (5) ◽  
pp. F762-F768
Author(s):  
D. Sarubbi ◽  
J. C. McGiff ◽  
J. Quilley
Keyword(s):  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Ang Ii ◽  
Glucose Levels ◽  
Renal Perfusion Pressure ◽  
Male Wistar Rats ◽  
Eicosanoid Release ◽  
Renal Vascular

Changes in renal perfusion pressure and eicosanoid release in response to arginine vasopressin (AVP; 1-10 ng) and angiotensin II (ANG II; 1-10 ng) were determined 5 days, 2 wk, and 8-12 wk after the induction of diabetes with streptozotocin (STZ) in male Wistar rats. Renal perfusion pressure responses to AVP and ANG II were reduced at 2 and 8-12 wk, but not at 5 days, after the induction of diabetes. However, AVP- and ANG II-stimulated release of prostaglandins into the renal venous effluent was depressed at all times tested. Inhibition of cyclooxygenase with indomethacin did not significantly influence the perfusion pressure responses to ANG II and AVP. Likewise, raising perfusate glucose levels to 400 mg/dl or adding insulin (180 microU/ml) to the perfusate failed to modify responses to ANG II. In contrast, administration of 0.3 microgram arachidonic acid (AA), a dose approaching threshold in control rat kidneys, to the kidney of the diabetic rat resulted in a marked increase in perfusion pressure. Associated with the increase in renal perfusion pressure to AA in the diabetic rat were significant increases in renal venous efflux of prostaglandin E2 and prostacyclin compared with control. These data suggest a defect in renal deacylation-reacylation of AA associated with an increase in cyclooxygenase activity in the diabetic rat.

Membrane potential measurements in renal afferent and efferent arterioles: actions of angiotensin II

1997 ◽  
Vol 273 (2) ◽  
pp. F307-F314 ◽  
Author(s):  
R. Loutzenhiser ◽  
L. Chilton ◽  
G. Trottier
Keyword(s):  
Angiotensin Ii ◽  
Perfusion Pressure ◽  
Rat Kidney ◽  
Renal Perfusion ◽  
Membrane Potentials ◽  
Ang Ii ◽  
Ca Channels ◽  
Renal Perfusion Pressure

An adaptation of the in vitro perfused hydronephrotic rat kidney model allowing in situ measurement of arteriolar membrane potentials is described. At a renal perfusion pressure of 80 mmHg, resting membrane potentials of interlobular arteries (22 +/- 2 microns) and afferent (14 +/- 1 microns) and efferent arterioles (12 +/- 1 microns) were -40 +/- 2 (n = 8), -40 +/- 1 (n = 45), and -38 +/- 2 mV (n = 22), respectively (P = 0.75). Using a dual-pipette system to stabilize the impalement site, we measured afferent and efferent arteriolar membrane potentials during angiotensin II (ANG II)-induced vasoconstriction. ANG II (0.1 nM) reduced afferent arteriolar diameters from 13 +/- 1 to 8 +/- 1 microns (n = 8, P = 0.005) and membrane potentials from -40 +/- 2 to -29 +/- mV (P = 0.012). ANG II elicited a similar vasoconstriction in efferent arterioles, decreasing diameters from 13 +/- 1 to 8 +/- 1 microns (n = 8, P = 0.004), but failed to elicit a significant depolarization (-39 +/- 2 for control; -36 +/- 3 mV for ANG II; P = 0.27). Our findings thus indicate that resting membrane potentials of pre- and postglomerular arterioles are similar and lie near the threshold activation potential for L-type Ca channels. ANG II-induced vasoconstriction appears to be closely coupled to membrane depolarization in the afferent arteriole, whereas mechanical and electrical responses appear to be dissociated in the efferent arteriole.

Effects of renal perfusion pressure on the natriuresis induced by atrial natriuretic factor

1987 ◽  
Vol 253 (2) ◽  
pp. F234-F238
Author(s):  
A. A. Seymour ◽  
S. G. Smith ◽  
E. K. Mazack
Keyword(s):  
Vascular Resistance ◽  
Atrial Natriuretic Factor ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Renal Vascular Resistance ◽  
Base Line ◽  
Renal Perfusion Pressure ◽  
Natriuretic Factor ◽  
Renal Vascular ◽  
Atrial Natriuretic

Synthetic atrial natriuretic factor (ANF 101-126) was infused at 1, 5, 25, and 125 pmol X kg-1 X min-1 into the renal artery of anesthetized, one-kidney dogs. During administration of 25 and 125 pmol X kg-1 X min-1 of ANF 101-126, fractional sodium excretion (FENa) rose from 1.4 +/- 0.3 to 6.6 +/- 1.1 and 5.6 +/- 1.3% when renal perfusion pressure (RPP) was at its basal level (112 +/- 5 mmHg). When base-line RPP was lowered to 101 +/- 5 mmHg by tightening a suprarenal aortic constriction, the same doses raised FENa to only 5.6 +/- 1.6 and 5.1 +/- 1.6%. A larger reduction of beginning RPP to 82 +/- 4 mmHg suppressed the natriuretic responses to 25 and 125 pmol X kg-1 X min-1 of ANF 101-126 to only 1.4 +/- 0.8 and 0.8 +/- 0.3%, respectively.During the peak natriuretic dose of 25 pmol X kg-1 X min-1, renal vascular resistance (RVR) fell from 0.88 +/- 0.10 to 0.68 +/- 0.07, from 0.78 +/- 0.10 to 0.68 +/- 0.12, and from 0.60 +/- 0.06 to 0.61 +/- 0.06 mmHg X ml-1 X min-1 at RPP = RPP = 112, 101, and 82 mmHg, respectively. ANF 101-126 did not affect glomerular filtration rate (GFR) at any level of RPP tested. In conclusion, the natriuretic responses to ANF 101-126 occurred without changes in GFR and were modulated by the prevailing levels of renal perfusion pressure and renal vascular resistance.

Renal Vascular and Biochemical Responses to Systemic Renin Inhibition in Dogs at Low Renal Perfusion Pressure

1999 ◽  
Vol 34 (5) ◽  
pp. 674-682 ◽  
Author(s):  
Jean-Paul Clozel ◽  
Murielle M. Véniant ◽  
Changbin Qiu ◽  
Urs Sprecher ◽  
Robert Wolfgang ◽  
...  
Keyword(s):  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Renal Perfusion Pressure ◽  
Biochemical Responses ◽  
Renin Inhibition ◽  
Renal Vascular

scholarly journals Purinergic P2X1 receptor, purinergic P2X7 receptor, and angiotensin II type 1 receptor interactions in the regulation of renal afferent arterioles in angiotensin II-dependent hypertension

2020 ◽  
Vol 318 (6) ◽  
pp. F1400-F1408 ◽  
Author(s):  
Supaporn Kulthinee ◽  
Weijian Shao ◽  
Martha Franco ◽  
L. Gabriel Navar
Keyword(s):  
Angiotensin Ii ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Ang Ii ◽  
Renal Perfusion Pressure ◽  
Arteriolar Resistance ◽  
Purinergic P2x7 Receptor ◽  
Afferent Arterioles ◽  
Purinergic P2x Receptors

In ANG II-dependent hypertension, ANG II activates ANG II type 1 receptors (AT1Rs), elevating blood pressure and increasing renal afferent arteriolar resistance (AAR). The increased arterial pressure augments interstitial ATP concentrations activating purinergic P2X receptors (P2XRs) also increasing AAR. Interestingly, P2X1R and P2X7R inhibition reduces AAR to the normal range, raising the conundrum regarding the apparent disappearance of AT1R influence. To evaluate the interactions between P2XRs and AT1Rs in mediating the increased AAR elicited by chronic ANG II infusions, experiments using the isolated blood perfused juxtamedullary nephron preparation allowed visualization of afferent arteriolar diameters (AAD). Normotensive and ANG II-infused hypertensive rats showed AAD responses to increases in renal perfusion pressure from 100 to 140 mmHg by decreasing AAD by 26 ± 10% and 19 ± 4%. Superfusion with the inhibitor P2X1Ri (NF4490; 1 μM) increased AAD. In normotensive kidneys, superfusion with ANG II (1 nM) decreased AAD by 16 ± 4% and decreased further by 19 ± 5% with an increase in renal perfusion pressure. Treatment with P2X1Ri increased AAD by 30 ± 6% to values higher than those at 100 mmHg plus ANG II. In hypertensive kidneys, the inhibitor AT1Ri (SML1394; 1 μM) increased AAD by 10 ± 7%. In contrast, treatment with P2X1Ri increased AAD by 21 ± 14%; combination with P2X1Ri plus P2X7Ri (A438079; 1 μM) increased AAD further by 25 ± 8%. The results indicate that P2X1R, P2X7R, and AT1R actions converge at receptor or postreceptor signaling pathways, but P2XR exerts a dominant influence abrogating the actions of AT1Rs on AAR in ANG II-dependent hypertension.

NO mediates downregulation of RBF after a prolonged reduction of renal perfusion pressure in SHR

2003 ◽  
Vol 285 (2) ◽  
pp. R329-R338 ◽  
Author(s):  
Charlotte Mehlin Sorensen ◽  
Paul Peter Leyssac ◽  
Ole Skott ◽  
Niels-Henrik Holstein-Rathlou
Keyword(s):  
Lower Limit ◽  
Perfusion Pressure ◽  
Renin Angiotensin System ◽  
Renal Perfusion ◽  
Control Group ◽  
Ang Ii ◽  
Spontaneously Hypertensive ◽  
Renal Perfusion Pressure ◽  
System A ◽  
Cox 2

The aim of the study was to investigate mechanisms underlying the downregulation of renal blood flow (RBF) after a prolonged reduction in renal perfusion pressure (RPP) in adult spontaneously hypertensive rats (SHR). We tested the effect on the RBF response of clamping plasma ANG II in sevoflurane-anesthetized SHR. We also tested the effect of general cyclooxygenase (COX) inhibition and inhibition of the inducible COX-2. Furthermore, we assessed the effect of clamping the nitric oxide (NO) system. A prolonged period (15 min) of reduced RPP induced a downregulation of RBF. This was unchanged after clamping of plasma ANG II concentrations, general COX inhibition, and specific inhibition of COX-2. In contrast, clamping the NO system diminished the ability of SHR to downregulate RBF to a lower level. The downregulation of RBF was not associated with a resetting of the lower limit of autoregulation in the control group, in the ANG II-clamped group, or the NO clamped group. However, general COX inhibition and specific COX-2 inhibition enabled downward resetting of the lower limit of autoregulation. In conclusion, in SHR the renin-angiotensin system does not appear to play a major role in the downregulation of RBF after prolonged reduction of RPP. This response appears to be mediated partly by the NO system. We hypothesize that, in SHR, lack of downward resetting of the lower limit of autoregulation in response to a prolonged lowering of RPP could be the result of increased COX-2-mediated production of vasoconstrictory prostaglandins.

Inhibition of renal vascular 20-HETE production impairs autoregulation of renal blood flow

1994 ◽  
Vol 266 (2) ◽  
pp. F275-F282 ◽  
Author(s):  
A. P. Zou ◽  
J. D. Imig ◽  
M. Kaldunski ◽  
P. R. Ortiz de Montellano ◽  
Z. Sui ◽  
...  
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Epoxyeicosatrienoic Acids ◽  
Blood Flows ◽  
Renal Perfusion Pressure ◽  
Renal Vascular

The present study evaluated the role of endogenous P-450 metabolites of arachidonic acid (AA) on autoregulation of renal blood flow in rats. Whole kidney and cortical blood flows were well autoregulated when renal perfusion pressure was varied from 150 to 100 mmHg. Infusion of 17-octadecynoic acid (17-ODYA) into the renal artery (33 nmol/min) increased cortical and papillary blood flows by 12.6 +/- 2.5 and 26.5 +/- 4.6%, respectively. After 17-ODYA, autoregulation of whole kidney and cortical blood flows was impaired. Intrarenal infusion of miconazole (8 nmol/min) had no effect on autoregulation of whole kidney, cortical, or papillary blood flows. 17-ODYA (1 microM) inhibited the formation of 20-hydroxyeicosatetraenoic acid (20-HETE) and 11,12- and 14,15-epoxyeicosatrienoic acids (EETs) by renal preglomerular microvessels in vitro by 83.7 +/- 7.4% and 89.0 +/- 4.9%, respectively. Miconazole (1 microM) reduced the formation of EETs by 86.4 +/- 5.7%, but it had no effect on the production of 20-HETE. These results suggest that endogenous P-450 metabolites of AA, particularly 20-HETE, may participate in the autoregulation of renal blood flow.

scholarly journals Impaired autoregulation of renal blood flow in the fawn-hooded rat

1999 ◽  
Vol 276 (1) ◽  
pp. R189-R196 ◽  
Author(s):  
Richard P. E. Van Dokkum ◽  
Magdalena Alonso-Galicia ◽  
Abraham P. Provoost ◽  
Howard J. Jacob ◽  
Richard J. Roman
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Filtration Rate ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Urinary Protein Excretion ◽  
Renal Perfusion Pressure ◽  
Protein Excretion ◽  
Low Blood Pressure ◽  
Renal Vascular

The responses to changes in renal perfusion pressure (RPP) were compared in 12-wk-old fawn-hooded hypertensive (FHH), fawn-hooded low blood pressure (FHL), and August Copenhagen Irish (ACI) rats to determine whether autoregulation of renal blood flow (RBF) is altered in the FHH rat. Mean arterial pressure was significantly higher in conscious, chronically instrumented FHH rats than in FHL rats (121 ± 4 vs. 109 ± 6 mmHg). Baseline arterial pressures measured in ketamine-Inactin-anesthetized rats averaged 147 ± 2 mmHg ( n = 9) in FHH, 132 ± 2 mmHg ( n = 10) in FHL, and 123 ± 4 mmHg ( n = 9) in ACI rats. Baseline RBF was significantly higher in FHH than in FHL and ACI rats and averaged 9.6 ± 0.7, 7.4 ± 0.5, and 7.8 ± 0.9 ml ⋅ min−1 ⋅ g kidney wt−1, respectively. RBF was autoregulated in ACI and FHL but not in FHH rats. Autoregulatory indexes in the range of RPPs from 100 to 150 mmHg averaged 0.96 ± 0.12 in FHH vs. 0.42 ± 0.04 in FHL and 0.30 ± 0.02 in ACI rats. Glomerular filtration rate was 20–30% higher in FHH than in FHL and ACI rats. Elevations in RPP from 100 to 150 mmHg increased urinary protein excretion in FHH rats from 27 ± 2 to 87 ± 3 μg/min, whereas it was not significantly altered in FHL or ACI rats. The percentage of glomeruli exhibiting histological evidence of injury was not significantly different in the three strains of rats. These results indicate that autoregulation of RBF is impaired in FHH rats before the development of glomerulosclerosis and suggest that an abnormality in the control of renal vascular resistance may contribute to the development of proteinuria and renal failure in this strain of rats.

ANG II-induced downregulation of RBF after a prolonged reduction of renal perfusion pressure is due to pre- and postglomerular constriction

2004 ◽  
Vol 286 (5) ◽  
pp. R865-R873 ◽  
Author(s):  
Charlotte Mehlin Sorensen ◽  
Paul Peter Leyssac ◽  
Max Salomonsson ◽  
Ole Skott ◽  
Niels-Henrik Holstein-Rathlou
Keyword(s):  
Perfusion Pressure ◽  
Plasma Renin ◽  
Renal Perfusion ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Renal Perfusion Pressure ◽  
Sprague Dawley Rats ◽  
Proximal Tubular ◽  
Tubular Flow ◽  
Over Time

Previous experiments from our laboratory showed that longer-lasting reductions in renal perfusion pressure (RPP) are associated with a gradual decrease in renal blood flow (RBF) that can be abolished by clamping plasma ANG II concentration ([ANG II]). The aim of the present study was to investigate the mechanisms behind the RBF downregulation in halothane-anesthetized Sprague-Dawley rats during a 30-min reduction in RPP to 88 mmHg. During the 30 min of reduced RPP we also measured glomerular filtration rate (GFR), proximal tubular pressure (Pprox), and proximal tubular flow rate (QLP). Early distal tubular fluid conductivity was measured as an estimate of early distal [NaCl] ([NaCl]ED), and changes in plasma renin concentration (PRC) over time were measured. During 30 min of reduced RPP, RBF decreased gradually from 6.5 ± 0.3 to 6.0 ± 0.3 ml/min after 5 min (NS) to 5.2 ± 0.2 ml/min after 30 min ( P < 0.05). This decrease occurred in parallel with a gradual increase in PRC from 38.2 ± 11.0 × 10-5 to 87.1 ± 25.1 × 10-5 Goldblatt units (GU)/ml after 5 min ( P < 0.05) to 158.5 ± 42.9 × 10-5 GU/ml after 30 min ( P < 0.01). GFR, Pprox, and [NaCl]ED all decreased significantly after 5 min and remained low. Estimates of pre- and postglomerular resistances showed that the autoregulatory mechanisms initially dilated preglomerular vessels to maintain RBF and GFR. However, after 30 min of reduced RPP, both pre- and postglomerular resistance had increased. We conclude that the decrease in RBF over time is caused by increases in both pre- and postglomerular resistance due to rising plasma renin and ANG II concentrations.

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