Effects of Ca<sup>2+</sup>channel activity on renal hemodynamics during acute attenuation of NO synthesis in the rat

Kramp, R.; Fourmanoir, P; Ladrière, Laurence; Joly, Emma; Gerbaux, Cécile; Hassani, Amir Hajjam El; Caron, Nathalie

doi:10.1152/ajprenal.2000.278.4.f561

Cited by 15 publications

(21 citation statements)

References 32 publications

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“…Accordingly, the myogenic response becomes more pronounced following inhibition of NO synthesis, and the relative contribution of the myogenic mechanism to the overall reaction increases. This is in line with several recent reports on the effect of NO on the myogenic mechanism (10,13,16,17,25,27,28).…”

Section: Discussionsupporting

confidence: 93%

The step response: a method to characterize mechanisms of renal blood flow autoregulation

Wronski

Seeliger

Persson

et al. 2003

American Journal of Physiology-Renal Physiology

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The step response: a method to characterize mechanisms of renal blood flow autoregulation. Am J Physiol Renal Physiol 285: F758-F764, 2003. First published July 8, 2003 10.1152/ ajprenal.00420.2002Response of renal vasculature to changes in renal perfusion pressure (RPP) involves mechanisms with different frequency characteristics. Autoregulation of renal blood flow (RBF) is mediated by the rapid myogenic response, by the slower tubuloglomerular feedback (TGF) mechanism, and, possibly, by an even slower third mechanism. To evaluate the individual contribution of these mechanisms to RBF autoregulation, we analyzed the response of RBF to a step increase in RPP. In anesthetized rats, the suprarenal aorta was occluded for 30 s, and then the occlusion was released to induce a step increase in RPP. Three dampened oscillations were observed; their oscillation periods ranged from 9.5 to 13 s, from 34.2 to 38.6 s, and from 100.5 to 132.2 s, respectively. The two faster oscillations correspond with previously reported data on the myogenic mechanism and the TGF. In accordance, after furosemide, the amplitude of the intermediate oscillation was significantly reduced. Inhibition of nitric oxide synthesis by N -nitro-L-arginine methyl ester significantly increased the amplitude of the 10-s oscillation. It is concluded that the parameters of the dampened oscillations induced by the step increase in RPP reflect properties of autoregulatory mechanisms. The oscillation period characterizes the individual mechanism, the dampening is a measure for the stability of the regulation, and the square of the amplitudes characterizes the power of the respective mechanism. In addition to the myogenic response and the TGF, a third rather slow mechanism of RBF autoregulation exists. myogenic reaction; tubuloglomerular feedback; furosemide; N -nitro-L-arginine methyl ester VARIOUS STUDIES ARE AIMED at determining the pressure range and the efficiency of renal blood flow (RBF) autoregulation under various conditions (3,7,25). Typically, in these studies, renal perfusion pressure (RPP) is changed according to a staircase-shaped or a rampshaped function to obtain pressure-flow relationships (7,8,22). Although this experimental approach allows us to determine the autoregulatory pressure range and to compare the autoregulatory efficiency under different conditions, it does not allow us to determine the individual contribution of the underlying mechanisms to the overall response. Our understanding of the relative importance of the myogenic response and the tubuloglomerular feedback (TGF) mechanism stems mainly from studies in which vascular diameters of isolated vessels, isolated nephrons, or hydronephrotic kidneys were measured (1, 26). In these studies, step changes in perfusion pressure were used as a stimulus, and the time constant of the vascular response was used to assess the contribution of the mechanisms. This was also done in preparations, which lack the TGF [hydronephrotic kidney, isolated nephron without distal tubule (4)].Other experim...

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Section: Discussionsupporting

confidence: 93%

The step response: a method to characterize mechanisms of renal blood flow autoregulation

Wronski

Seeliger

Persson

et al. 2003

American Journal of Physiology-Renal Physiology

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“…This conclusion, although reasonable at the time it was drawn, is difficult to reconcile with current understanding of the role of nitric oxide in renal autoregulation. First, nonselective inhibition of NOSs causes a pronounced left shift of the lower limit of autoregulation (31,43,44,64,79). Second, inhibition of NOSs enhances autoregulation within the normal autoregulatory range of renal perfusion pressure (44,64,79).…”

Section: Discussionmentioning

confidence: 99%

“…First, nonselective inhibition of NOSs causes a pronounced left shift of the lower limit of autoregulation (31,43,44,64,79). Second, inhibition of NOSs enhances autoregulation within the normal autoregulatory range of renal perfusion pressure (44,64,79). Third, both the left shift and hyperfiltration were seen (DM-N) and abrogated by high salt intake (DM-H) in rats in which we were unable to detect modulation of RBF dynamics by nitric oxide.…”

Section: Discussionmentioning

confidence: 99%

Salt-resistant blood pressure and salt-sensitive renal autoregulation in chronic streptozotocin diabetes

Lau¹,

Sudbury²,

Thomson³

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Hyperfiltration occurs in early type 1 diabetes mellitus in both rats and humans. It results from afferent vasodilation and thus may impair stabilization of glomerular capillary pressure by autoregulation. It is inversely related to dietary salt intake, the "salt paradox." Restoration of normal glomerular filtration rate (GFR) involves increased preglomerular resistance, probably mediated by tubuloglomerular feedback (TGF). To begin to test whether the salt paradox has pathogenic significance, we compared intact vs. diabetic (streptozotocin) Long-Evans rats with normal and increased salt intake, 1 and approximately 3% by weight of food eaten, respectively. Weekly 24-h blood pressure records were acquired by telemetry before and during diabetes. Blood glucose was maintained at approximately 20 mmol/l by insulin implants. GFR was significantly elevated only in diabetic rats on normal salt intake, confirming diabetic hyperfiltration and the salt paradox. Renal blood flow dynamics show strong contributions to autoregulation by both TGF and the myogenic mechanism and were not impaired by diabetes or by increased salt intake. Separately, systolic pressure was not elevated in diabetic rats at any time during 12 wk with normal or high salt intake. Autoregulation was effective in all groups, and the diabetic-normal salt group showed significantly improved autoregulation at low perfusion pressures. Histological examination revealed very minor glomerulosclerosis and modest mesangial expansion, although neither was diagnostic of diabetes. Periodic acid-Schiff-positive droplets found in distal tubules and collecting duct segments were diagnostic of diabetic kidneys. Biologically significant effects attributable to increased salt intake were abrogation of hyperfiltration and of the left shift in autoregulation in diabetic rats.

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“…From RBF autoregulatory curves, several methods have been proposed for the determination of P LL . It is frequently calculated as the intersection of the two straight lines corresponding to the autoregulatory plateau and to the subautoregulatory zone after the data points were fitted either by eye (21) or by progressive linear regression (17,18). Recently, a new method of determination has been proposed (22).…”

Section: Discussionmentioning

confidence: 99%

“…AUTOREGULATION OF TOTAL RENAL blood flow (RBF) is usually explored by measuring RBF responses to externally induced stepwise reductions of arterial pressure (AP) in both anesthetized (6,8,11,13,17,21,22) and conscious (2,4,16,18,(24)(25)(26) animals. Steady-state levels of RBF are plotted as a function of AP, which allows the drawing of autoregulation curves from which the plateau and lower pressure limit of RBF autoregulation (P LL ) are estimated.…”

mentioning

confidence: 99%

Spontaneous renal blood flow autoregulation curves in conscious sinoaortic baroreceptor-denervated rats

Pires

Julien

Chapuis

et al. 2002

American Journal of Physiology-Renal Physiology

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Pires, Silene L. S., Claude Julien, Bruno Chapuis, Jean Sassard, and Christian Barrè s. Spontaneous renal blood flow autoregulation curves in conscious sinoaortic baroreceptor-denervated rats. Am J Physiol Renal Physiol 282: F51-F58, 2002. First published August 8, 2001 10.1152/ajprenal.00186.2001.-These experiments examined whether the conscious sinoaortic baroreceptor-denervated (SAD) rat, owing to its high spontaneous arterial pressure (AP) variability, might represent a model for renal blood flow (RBF) autoregulation studies. In eight SAD and six baroreceptor-intact rats, AP and RBF were recorded (1-h periods) before and after furosemide (10 mg/kg followed by 10 mg ⅐ kg Ϫ1 ⅐ h Ϫ1 iv) administration. In control conditions, AP variability was markedly enhanced in SAD rats (coefficient of variation: 16.0 Ϯ 1.2 vs. 5.4 Ϯ 0.5% in intact rats), whereas RBF variability was only slightly increased (8.7 Ϯ 0.6 vs. 6.1 Ϯ 0.5% in intact rats), suggesting buffering by autoregulatory mechanisms. In SAD rats, but not in intact rats, the AP-RBF relationships could be modeled with a four-parameter sigmoid Weibull equation (r 2 ϭ 0.24 Ϯ 0.07, 3,600 data pairs/rat), allowing for estimation of an autoregulatory plateau (10.1 Ϯ 0.7 ml/min) and a lower limit of RBF autoregulation (PLL ϭ 93 Ϯ 6 mmHg, defined as AP at RBF 5% below the plateau). After furosemide treatment, autoregulation curves (r 2 ϭ 0.49 Ϯ 0.07) in SAD rats were shifted downward (plateau ϭ 8.6 Ϯ 0.8 ml/min) and rightward (PLL ϭ 102 Ϯ 5 mmHg). In five of six intact rats, PLL became measurable (104 Ϯ 1 mmHg), albeit with limited accuracy (r 2 ϭ 0.09 Ϯ 0.03). In conclusion, the conscious SAD rat offers the possibility of describing RBF autoregulation curves under dynamic, unforced conditions. The tubuloglomerular feedback and myogenic mechanisms cooperate in setting PLL and thus in stabilizing RBF during spontaneous depressor episodes.arterial pressure variability; furosemide; modeling AUTOREGULATION OF TOTAL RENAL blood flow (RBF) is usually explored by measuring RBF responses to externally induced stepwise reductions of arterial pressure (AP) in both anesthetized (6,8,11,13,17,21,22) and conscious (2,4,16,18,(24)(25)(26) animals. Steady-state levels of RBF are plotted as a function of AP, which allows the drawing of autoregulation curves from which the plateau and lower pressure limit of RBF autoregulation (P LL ) are estimated. It is not known whether such information can be gained under spontaneous unforced conditions, i.e., using RBF responses to naturally occurring AP fluctuations.The conscious sinoaortic baroreceptor-denervated (SAD) rat is a well-recognized model of exaggerated AP variability, which is characterized by the spontaneous occurrence of pressor and depressor episodes of occasionally large amplitude (3,28). Recently, we have investigated in conscious SAD rats the relationships between AP variability and RBF variability (20). Although AP variability was markedly increased, RBF variability was only slightly increased, suggesting a powerful participa...

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Effects of Ca²⁺channel activity on renal hemodynamics during acute attenuation of NO synthesis in the rat

Cited by 15 publications

References 32 publications

The step response: a method to characterize mechanisms of renal blood flow autoregulation

The step response: a method to characterize mechanisms of renal blood flow autoregulation

Salt-resistant blood pressure and salt-sensitive renal autoregulation in chronic streptozotocin diabetes

Spontaneous renal blood flow autoregulation curves in conscious sinoaortic baroreceptor-denervated rats

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Effects of Ca2+channel activity on renal hemodynamics during acute attenuation of NO synthesis in the rat

Cited by 15 publications

References 32 publications

The step response: a method to characterize mechanisms of renal blood flow autoregulation

The step response: a method to characterize mechanisms of renal blood flow autoregulation

Salt-resistant blood pressure and salt-sensitive renal autoregulation in chronic streptozotocin diabetes

Spontaneous renal blood flow autoregulation curves in conscious sinoaortic baroreceptor-denervated rats

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Effects of Ca²⁺channel activity on renal hemodynamics during acute attenuation of NO synthesis in the rat