Acute arterial hypertension inhibits proximal tubular fluid reabsorption in normotensive rat but not in SHR

Abstract

Walstead, Christopher, and Kay-Pong Yip. Acute arterial hypertension inhibits proximal tubular fluid reabsorption in normotensive rat but not in SHR. Am J Physiol Regul Integr Comp Physiol 286: R726-R733, 2004. First published December 24, 2003 10.1152/ ajpregu.00352.2003.-The effect of acute arterial hypertension on proximal tubular fluid reabsorption was investigated in SpragueDawley rats and spontaneously hypertensive rats (SHR) by measuring proximal tubular flow with a nonobstructive optical method. Under control conditions, spontaneous tubular flow was oscillating at 0.02-0.03 Hz in Sprague-Dawley rats. Acute hypertension induced an immediate increase of mean tubular flow (50% increase after 20 min of hypertension) and augmentation of oscillatory amplitude. Acute hypertension did not alter single-nephron blood flow as measured by laser-Doppler velocimetry (n ϭ 12), suggesting that the increase of tubular flow was due to inhibition of reabsorption but not increase of filtration. By contrast, spontaneous tubular flow was fluctuating aperiodically in SHR. Acute hypertension did not induce a continuous increase of tubular flow or an increase in amplitude of fluctuations (n ϭ 15). When apical Na ϩ /H ϩ exchanger activity of proximal tubule was monitored, acute hypertension did not alter the activity in SHR (n ϭ 8), while similar procedures had been shown to inhibit apical Na ϩ /H ϩ exchanger activity of proximal tubules by more than 40% in Sprague-Dawley rats. These observations suggest that acute hypertension inhibits proximal tubular fluid reabsorption by inhibiting apical Na ϩ /H ϩ exchanger activity in Sprague-Dawley rats and that this mechanism is impaired in SHR.laser-Doppler velocimetry; sodium/hydrogen exchangers; oscillations; tubuloglomerular feedback ACUTE ARTERIAL HYPERTENSION induced by increasing total peripheral resistance with aortic clamps triggers a reversible inhibition of apical Na ϩ /H ϩ exchange activity in proximal tubules of Sprague-Dawley rats (32). Apical Na ϩ /H ϩ exchangers are responsible for 90% of NaCl transcellular reabsorption and 70% of NaHCO 3 reabsorption in the proximal tubule (1). Inhibition of apical Na ϩ /H ϩ exchange activity by acute hypertension is likely to increase proximal tubular flow because of the reduction in NaCl and NaHCO 3 reabsorption. However, the conventional methods of measuring tubular flow by collecting tubular fluid interrupts ambient tubular flow, which might increase glomerular filtration via tubuloglomerular feedback. To circumvent this complication, a nonobstructive optical method was used in the present study to monitor directly the changes of spontaneous proximal tubular flow during the induction of acute hypertension. Moreover, single-nephron blood flow on the efferent arteriole was monitored with a noninvasive laser-Doppler velocimetry device (23, 29) to delineate whether the increase of tubular flow induced by acute hypertension is due to the inhibition of tubular fluid reabsorption or the increase of glomerular filtration.Acute hypertension-...

Mechanisms of renal blood flow autoregulation: dynamics and contributions

“…An acute rise in renal arterial pressure not only increases single nephron GFR but also induces a progressive reduction of proximal tubular reabsorption (34,67,107,204). The increase of fluid remaining in the distal tubule will add to the tubular load entering the loop of Henle and thereby enhance the error signal reaching the macula densa.…”

“…Accordingly, a progressive reduction of reabsorption will slowly augment the regulatory strength of TGF (132). Although the pressuredependent modulation of proximal tubular reabsorption may stretch out over a course of 20 -30 min after the change in pressure, the majority of this adaptation seems to occur within the initial 5 min (34,204,222). Furthermore, the change in reabsorption has been found to be associated with a redistribution of Na ϩ -H ϩ -transporter (NHE3), Na ϩ -phosphate-cotransporter (NaPi2) in the proximal tubular epithelium from the tip of the apical brush border to the base of the villi and finally to intracellular vesicles, and accompanied by a reduction in Na ϩ -K ϩ -ATPase activity (124,127,222).…”

Acute pressure–natriuresis function shows early impairment in Lyon hypertensive rats

“…Thus renal factors are likely to be predominant in the altered pressure natriuresis in LH rats. The intra-renal alterations can be numerous such as an enhanced proximal tubular fluid reabsorption [18], a deficit in renal nitric oxide activity [19] and an alteration in renal medullary blood flow [20]. We previously observed that in LH rats, the reduced urinary sodium excretion was associated with a lack of medullary blood flow increase in response to arterial pressure elevations [8] and an altered medullary blood flow response to angiotensin II [21].…”

Flash photolysis of caged nitric oxide inhibits proximal tubular fluid reabsorption in free-flow nephron

“…5). The imaging system used for detecting DAF-FM emission from proximal tubule is similar to that used for detecting BCECF emission as described previously (20,22). Uncaging of NO in luminal perfusate was achieved by delivering the laser pulses to the kidney surface via an optical fiber.…”

“…This prediction has been verified using EIPA to inhibit apical Na ϩ /H ϩ exchanger in the proximal tubule of free-flow nephron. Intratubular perfusion of EIPA into the proximal tubule decreases proximal tubular flow when TGF is intact, and the same maneuver increases proximal tubular flow when TGF is inhibited by furosemide (20). cGMP is the mediator of NO to inhibit proximal tubular reabsorption (4).…”