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

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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 · kg−1· h−1iv)administration. In control conditions, AP variability was markedly enhanced in SAD rats (coefficient of variation: 16.0 ± 1.2 vs. 5.4 ± 0.5% in intact rats), whereas RBF variability was only slightly increased (8.7 ± 0.6 vs. 6.1 ± 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 ( r2= 0.24 ± 0.07, 3,600 data pairs/rat), allowing for estimation of an autoregulatory plateau (10.1 ± 0.7 ml/min) and a lower limit of RBF autoregulation (PLL= 93 ± 6 mmHg, defined as AP at RBF 5% below the plateau). After furosemide treatment, autoregulation curves ( r2= 0.49 ± 0.07) in SAD rats were shifted downward (plateau = 8.6 ± 0.8 ml/min) and rightward (PLL= 102 ± 5 mmHg). In five of six intact rats, PLLbecame measurable (104 ± 1 mmHg), albeit with limited accuracy ( r2= 0.09 ± 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 PLLand thus in stabilizing RBF during spontaneous depressor episodes.
Title: Spontaneous renal blood flow autoregulation curves in conscious sinoaortic baroreceptor-denervated rats
Description:
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 · kg−1· h−1iv)administration.
In control conditions, AP variability was markedly enhanced in SAD rats (coefficient of variation: 16.
0 ± 1.
2 vs.
5.
4 ± 0.
5% in intact rats), whereas RBF variability was only slightly increased (8.
7 ± 0.
6 vs.
6.
1 ± 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 ( r2= 0.
24 ± 0.
07, 3,600 data pairs/rat), allowing for estimation of an autoregulatory plateau (10.
1 ± 0.
7 ml/min) and a lower limit of RBF autoregulation (PLL= 93 ± 6 mmHg, defined as AP at RBF 5% below the plateau).
After furosemide treatment, autoregulation curves ( r2= 0.
49 ± 0.
07) in SAD rats were shifted downward (plateau = 8.
6 ± 0.
8 ml/min) and rightward (PLL= 102 ± 5 mmHg).
In five of six intact rats, PLLbecame measurable (104 ± 1 mmHg), albeit with limited accuracy ( r2= 0.
09 ± 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 PLLand thus in stabilizing RBF during spontaneous depressor episodes.

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