Glomerular Hemodynamics in Rats with Chronic Sodium Depletion

Steiner, Robert W.; Tucker, B. J.; Blantz, Roland C.

doi:10.1172/jci109488

Cited by 84 publications

(30 citation statements)

References 22 publications

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“…Losartan had no effect on SNGFR in the absence of a TGF stimulus. This is consistent with several prior micropuncture studies from our lab showing that glomerular hemodynamics, and hence the early peritubular capillary Starling forces, are unaffected by angiotensin blockade in salt-replete rats (7)(8)(9). This obviated concern over peritubular capillary physical factors originating from the glomerulus when analyzing the proximal diuretic effects of losartan.…”

Section: Resultssupporting

confidence: 90%

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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Section: Resultssupporting

confidence: 90%

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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“…min) in Ringer solution (0.84 ml/h) beginning at least 60 min before micropuncture. This dose has minimal effects on glomerular filtration rate (21,22), and inhibits early proximal bicarbonate reabsorption in hydropenic rats, owing to competitive inhibition ofendogenous angiotensin 11 (All) (22).…”

Section: Methodsmentioning

confidence: 99%

Effect of acute changes in glomerular filtration rate on Na+/H+ exchange in rat renal cortex.

Maddox

Fortin²,

Tartini³

et al. 1992

J. Clin. Invest.

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Studies were undertaken in Munich-Wistar rats to assess the influence of changes in filtered bicarbonate (FLHCo), induced by changes in GFR, on Na+/H' exchange activity in renal brush border membrane vesicles (BBMV). Whole-kidney and micropuncture measurements of GFR, FLHco3, and whole-kidney and proximal tubule HCO3 reabsorption (APRHCo) were coupled with BBMV measurements of H' gradient-driven 22Na' uptake in each animal studied. 22Na' uptake was measured at three Na' concentration gradients to allow calculation of V., and K. for Na+/H' exchange. GFR was varied by studying animals under conditions of hydropenia, plasma repletion, and acute plasma expansion. The increase in GFR, FLHco3, and APRHco3 induced by plasma administration correlated directly with an increase in the V.,, for Na+/H' exchange in BBMV.The K,. for sodium was unaffected. In the plasma-expanded rats, the V. for Na+/H' exchange was 22% greater than in the hydropenic rats (P < 0.025) whereas APRHco3 was 86% greater (P < 0.001). These results indicate that increases in FLHCo3, induced by acute increases in GFR, stimulate Na+/H' exchange activity in proximal tubular epithelium. This stimulation is a mechanism which can, in part, account for the delivery dependence of proximal bicarbonate reabsorption. (J. Clin. Invest. 1992Invest. . 89:1296Invest. -1303

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“…These neural influences on renal hemodynamics are reminiscent of actions of many other vasoactive substances. For example, suppression of endogenous angiotensin II actions in angiotensin levels are elevated, such as chronic extracellular fluid (ECF)' volume depletion induced by restriction of salt intake, administration of an angiotensin II inhibitor markedly alters renal hemodynamics and glomerular filtration (19). Therefore, it appeared warranted to examine whether the profound effects of renal nerves on renal vasculature demonstrated by experimental electrical stimulation do, in fact, participate in pathophysiologic settings.…”

Section: Introductionmentioning

confidence: 99%

Role of renal sympathetic nerves in mediating hypoperfusion of renal cortical microcirculation in experimental congestive heart failure and acute extracellular fluid volume depletion.

Kon¹,

Yared²,

Ichikawa³

1985

J. Clin. Invest.

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To evaluate the pathophysiologic importance of renal nerves in regulating the renal vasomotor tone, we measured several parameters of renal cortical microcirculation before and after acute renal denervation (DNx) in the following three groups of anesthetized Munich-Wistar rats: (group 1) congestive heart failure after surgically induced myocardial infarction (n = 10), (group 2) acute extracellular fluid volume depletion after deprivation of drinking water for 48 h (n = 8), and (group 3) sham or nontreated controls (n = 6). In the myocardial-infarcted rats, DNx led to a uniform increase in glomerular plasma flow rate of, on average, 36%. Single nephron glomerular filtration rate of myocardialinfarcted rats also increased despite a reduction in glomerular capillary hydraulic pressure. These changes were associated with a fall in arteriolar resistances, particularly in the efferent arteriole. The glomerular capillary ultrafiltration coefficient rose in all but one myocardial-infarcted animal. A similar hemodynamic pattern was seen after DNx in water-deprived animals. In every water-deprived animal, glomerular plasma flow rate and single nephron GFR increased on average by 28 and 14%, respectively. Again, afferent and efferent arteriolar resistances decreased significantly. Furthermore, the ultrafiltration coefficient increased uniformly and substantially with DNx.To ascertain the potential importance of the interaction between the renal nerves and angiotensin II in these circumstances, we compared the renal cortical hemodynamics in additional groups of water-deprived rats (group 4) after DNx (n = 15), (group 5) during inhibition of angiotensin II with saralasin (n = 15), and (group 6) during treatment with both saralasin and DNx (n = 15). No appreciable difference was detected between group 4 vs. 6. In contrast, substantial differences were noted between group 5 vs. 6: on average, the glomerular plasma flow rate was 26% higher and the afferent and efferent arteriolar resistances 25% and 27% lower, respectively, in group 6.Portions of these studies were presented at the annual meeting of the American Society of Nephrology, Washington, DC, 1984, and at the Annual Meeting of the Federations of American Societies for Experimental Biology, Washington, DC, 1985, and were published in abstract form (1984. Am. Soc. Nephrol. 17:134; and 1985. Clin. Res. 33:489A).Address correspondence to Dr. Kon, Laboratory of Renal Physiology.Receivedfor publication 8 January 1985 and in revisedform 12 July 1985.These observations provide direct evidence to indicate pathophysiologic importance of renal nerves in the profound intrarenal circulatory adjustments in prerenal circulatory impairment. The vasoconstrictive effects of renal nerves appear to be mediated in part by their stimulatory influence on angiotensin II release and their direct constrictor actions on pre-and postglomerular vessels as well.

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Glomerular Hemodynamics in Rats with Chronic Sodium Depletion

Cited by 84 publications

References 22 publications

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

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

Effect of acute changes in glomerular filtration rate on Na+/H+ exchange in rat renal cortex.

Role of renal sympathetic nerves in mediating hypoperfusion of renal cortical microcirculation in experimental congestive heart failure and acute extracellular fluid volume depletion.

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