Blood pressure and tubuloglomerular feedback mechanism in chronically salt-loaded spontaneously hypertensive rats

Ushiogi, Yasuyuki; Takabatake, Toshikazu; Häberle, D. A.

doi:10.1038/ki.1991.150

Cited by 14 publications

(12 citation statements)

References 16 publications

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“…In contrast to Dahl SS, we found that SHR fed a normal salt diet have a much greater TGF response than WKY or Dahl SS and that TGF resetting induced by high salt intake was minimal or nonexistent, consistent with previous reports 26,27 . Furthermore, in SHR antagonism of CTGF to the TGF response and its contribution to TGF resetting were also minimal, indicating that a diminished CTGF may at least partially explain the enhancement in TGF and reduced TGF resetting.…”

Section: Discussionsupporting

confidence: 92%

Connecting Tubule Glomerular Feedback in Hypertension

Wang

D’Ambrosio²,

Garvin³

et al. 2013

Hypertension

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In Dahl salt-sensitive rats (Dahl SS), glomerular capillary pressure (PGC) increases in response to high salt intake and this is accompanied by significant glomerular injury compared to spontaneously hypertensive rats (SHR) with similar blood pressure. PGC is controlled mainly by afferent arteriolar (Af-Art) resistance, which is regulated by the vasoconstrictor tubuloglomerular feedback (TGF) and the vasodilator connecting tubule glomerular feedback (CTGF). We hypothesized that Dahl SS have a decreased TGF response and enhanced TGF resetting compared to SHR, and that these differences are due in part to an increase in CTGF. In vivo, using micropuncture we measured stop-flow pressure (PSF, a surrogate of PGC). TGF was calculated as the maximal decrease in PSF caused by increasing nephron perfusion, TGF resetting as the attenuation in TGF induced by high salt diet, and CTGF as the difference in TGF response before and during CTGF inhibition with benzamil. Compared to SHR, Dahl SS had 1) lower TGF responses in normal (6.6±0.1 vs. 11.0±0.2 mm Hg; P<0.001) and high-salt diets (3.3±0.1 vs. 10.1±0.3 mmHg; P<0.001), 2) greater TGF resetting (3.3±0.1 vs. 1.0±0.3 mmHg; P<0.001), and 3) greater CTGF (3.4±0.4 vs. 1.2±0.1 mmHg; P<0.001). We conclude that Dahl SS have lower TGF and greater CTGF than SHR, and that CTGF antagonizes TGF. Furthermore, CTGF is enhanced by a high-salt diet and contributes significantly to TGF resetting. Our findings may explain in part the increase in vasodilatation, PGC, and glomerular damage in salt-sensitive hypertension during high salt intake.

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Section: Discussionsupporting

confidence: 92%

Connecting Tubule Glomerular Feedback in Hypertension

Wang

D’Ambrosio²,

Garvin³

et al. 2013

Hypertension

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“…Ang II is the principal modulator known for strengthening the TGF response (13,14), and macula densa nitric oxide is the principal modulator known for weakening the TGF response (15)(16)(17)(18). Nonetheless, there is precedent for dietary salt to lack influence over the range of the TGF response evoked by perfusing Henle's loop with artificial tubular fluid (ATF) (11,19). Furthermore, the present data regarding the TGF response are in keeping with expectations inasmuch as angiotensin receptor blockade reduced the range of the TGF response by about half (Table 2 and Figure 1).…”

Section: Discussionsupporting

confidence: 77%

An unexpected role for angiotensin II in the link between dietary salt and proximal reabsorption

Thomson

Deng²,

Wead³

et al. 2006

Journal of Clinical Investigation

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We set out to confirm the long-held, but untested, assumption that dietary salt affects proximal reabsorption through reciprocal effects on the renin-angiotensin system in a way that facilitates salt homeostasis. Wistar rats were fed standard or high-salt diets for 7 days and then subjected to renal micropuncture for determination of single-nephron GFR (SNGFR) and proximal reabsorption. The tubuloglomerular feedback (TGF) system was used as a tool to manipulate SNGFR in order to distinguish primary changes in net proximal reabsorption (Jprox) from changes due to glomerulotubular balance. The influence of Ang II over Jprox was determined by the sensitivity of Jprox to the AT1 receptor antagonist, losartan. Plasma, whole kidneys, and fluid from midproximal tubules were assayed for Ang II content by radioimmunoassay. In rats on the standard diet, losartan reduced Jprox by 25% and reduced the maximum range of the TGF response by 50%. The highsalt diet suppressed plasma and whole-kidney Ang II levels. But the high-salt diet failed to reduce the impact of losartan on Jprox or the TGF response and actually caused tubular fluid Ang II content to increase. The persistent effect of Ang II on Jprox prevented a major rise in late proximal flow rate in response to the high-salt diet. These observations challenge the traditional model and indicate that the role of proximal tubular Ang II in salt-replete rats is to stabilize nephron function rather than to contribute to salt homeostasis.

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“…Supplemental dietary Cl Ϫ that induces chloruresis induces an increased delivery of Cl Ϫ to the macula densa of the thick ascending limb of the renal tubule, and that increased delivery can entrain constriction of the afferent arteriole as part of the normal tubuloglomerular feedback response (34). In the SHR an exaggeration of this response has been observed (35), even into adulthood (36,37), and proposed as a mechanism of hypertension (35,37,38). In the SHRSP, a Cl Ϫ -mediated constriction of the renal afferent arteriole that further narrows it might then exacerbate hypertension.…”

Section: Discussionmentioning

confidence: 99%

Genetically determined chloride-sensitive hypertension and stroke

Tanaka¹,

Schmidlin²,

Sl³

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

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The stroke-prone spontaneously hypertensive rat (SHRSP) is a genetically determined model of ''saltsensitive'' stroke and hypertension whose full phenotypic expression is said to require a diet high in Na ؉ and low in K ؉ . We tested the hypothesis that dietary Cl ؊ determines the phenotypic expression of the SHRSP. In the SHRSP fed a normal NaCl diet, supplementing dietary K ؉ with KCl exacerbated hypertension, whereas supplementing either KHCO 3 or potassium citrate (KB͞C) attenuated hypertension, when blood pressure (BP) was measured radiotelemetrically, directly and continually. Supplemental KCl, but not KB͞C, induced strokes, which occurred in all and only those rats in the highest quartiles of both BP and plasma renin activity (PRA). PRA was higher with KCl than with KB͞C. These observations demonstrate that with respect to both severity of hypertension and frequency of stroke the phenotypic expression of the SHRSP is (i) either increased or decreased, depending on whether the anionic component of the potassium salt supplemented is, or is not, Cl ؊ ; (ii) increased by supplementing Cl ؊ without supplementing Na ؉ , and despite supplementing K ؉ ; and hence (iii) both selectively Cl ؊ -sensitive and Cl ؊ -determined. The observations suggest that in the SHRSP selectively supplemented with Cl ؊ the likelihood of stroke depends on the extent to which both BP and PRA increase.

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Blood pressure and tubuloglomerular feedback mechanism in chronically salt-loaded spontaneously hypertensive rats

Cited by 14 publications

References 16 publications

Connecting Tubule Glomerular Feedback in Hypertension

Connecting Tubule Glomerular Feedback in Hypertension

An unexpected role for angiotensin II in the link between dietary salt and proximal reabsorption

Genetically determined chloride-sensitive hypertension and stroke

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