Chloride anion concentration as a determinant of renal vascular responsiveness to vasoconstrictor agents

Quilley, C P; Lin, Yu-Shi R.; McGiff, John C.

doi:10.1111/j.1476-5381.1993.tb13447.x

Cited by 79 publications

(35 citation statements)

References 22 publications

(23 reference statements)

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“…33,34 In the SHR, pharmacological inhibition of the angiotensin converting enzyme dose-dependently attenuates hypertension and the narrowing of the renal afferent arteriole, 33,34 the extent of narrowing varying directly with the severity of pharmacologically attenuated hypertension. 33 Even in the normal rat, Cl Ϫ selectively loaded either in the diet 13,14 or in the isolated perfused kidney 35 induces renal vasoconstriction and amplifies that induced by angiotensin II, 14,36 likely by constricting the renal afferent arteriole 37 such that glomerular filtration rate is reduced. 35 An increased delivery of Cl Ϫ to the macula densa of the thick ascending limb of the renal tubule, as presumably occurred with the chlorureses currently induced in the SHRSP, elicits dose-dependent constriction of the renal afferent arteriole as part of the normal tubuloglomerular feedback (TGF) response.…”

Section: Discussionmentioning

confidence: 99%

Chloride-Dominant Salt Sensitivity in the Stroke-Prone Spontaneously Hypertensive Rat

et al. 2005

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Abstract-We tested the hypothesis that in the stroke-prone spontaneously hypertensive rat (SHRSP), the Cl Ϫ component of dietary NaCl dominantly determines its pressor effect (salt-sensitivity). We telemetrically measured systolic aortic blood pressure (SBP) in SHRSP loaded with: nothing (CTL); NaCl alone (NaCl) (44 mmol/100 grams chow); KCl (KCl) alone (44 mmol); NaCl (44 mmol) combined with KHCO 3 (77 mmol) (NaCl/KBC) or with KCl (77 mmol) (NaCl/KCl). Across all groups, from age 10 to 15 or 16 weeks, SBP increased linearly (mm Hg/week) (dp/dt, change in SBP as a function of time): CTL, 5.6; NaCl, 9.5; KCl, 8.8; NaCl/KBC, 9.1; and NaCl/KCl, 14.6. Thus, the value of dp/dt in KCl matched that in NaCl. The value of dp/dt in NaCl/KCl exceeded that in NaCl in direct proportion to the greater Cl Ϫ load. Across all groups, only Cl Ϫ load bore a direct, highly linear relationship with dp/dt. Strokes occurred only, but always with SBP Ͼ250 mm Hg, a value observed almost exclusively in NaCl/KCl. Thus, Cl Ϫ dominantly determined the pressor effect induced with dietary NaCl, both with NaCl loaded alone and combined with either KCl or KHCO 3 , and thereby likely determined the occurrence of stroke with NaCl loading. Over the initial 3-day period of NaCl loading and exacerbating hypertension, external balance of Na ϩ increased similarly among all groups. However, within 24 hours of initiating NaCl loading, urinary creatinine excretion decreased in direct proportion to dp/dt and urinary Cl Ϫ excretion. We conclude that in the SHRSP, the Cl Ϫ component of a dietary NaCl dominantly determines salt sensitivity and thereby phenotypic expression. We suggest that Cl

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Section: Discussionmentioning

confidence: 99%

Chloride-Dominant Salt Sensitivity in the Stroke-Prone Spontaneously Hypertensive Rat

et al. 2005

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“…Renal retention of Na ϩ and water that expands plasma volume is widely believed to initiate the pathogenesis of human ''essential hypertension'' (43,44), and the genetically determined hypertension of the Dahl ''salt-sensitive'' rat (20,45). However, the fact of selective Cl Ϫ sensitivity in the salt-sensitive SHRSP suggests the possibility that a genetically determined mechanism of saltsensitive hypertension might primarily affect the renal tubular transport of Cl Ϫ , or the capacity of Cl Ϫ to stimulate renal vasoconstriction (16,17), which might take the form of an exaggerated tubuloglomerular feedback response (35,38) that reduces medullary blood flow and the capacity of the kidney to excrete salt (46). Whatever the precise mechanism of selective Cl Ϫ sensitivity in the SHRSP, the phenomenon and its demonstration with KCl, a salt well known to have natriuretic and diuretic effects, raise the possibility that an increased renal retention of Na ϩ and water need not be the initial physiological consequence of all genetically determined mechanisms of salt-sensitive hypertension either in rats or humans.…”

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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“…Several reports have observed that Cl -mediates vascular smooth muscle cell Ca 2+ -dependent contraction [31], may modify vascular responses to vasoconstrictor agents in the kidney [32] and may affect plasma renin activity and systemic blood pressure [33]. Moreover, a very well-known physiologic mechanism underlying the regulation of Na + and water balance in the renal system, i.e.…”

Section: The Importance Of Chloride Content and Its Pathophysiologic mentioning

confidence: 99%

Intravenous balanced solutions: from physiology to clinical evidence

Länger

Santini

Scotti

et al. 2015

Anaesthesiol Intensive Ther

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Abstract"Balanced" solutions are commonly defined as intravenous fluids having an electrolyte composition close to that of plasma. As such, they should minimally affect acid-base equilibrium, as compared to the commonly reported 0.9% NaCl-related hyperchloremic metabolic acidosis. Recently, the term "balanced" solution has been also employed to indicate intravenous fluids with low chloride content, being the concentration of this electrolyte the most altered in 0.9% NaCl as compared to plasma, and based upon a suggested detrimental alteration of renal function associated with hyperchloremia. Despite efforts made towards its identification, the ideal balanced solution, with minimal effects on acid-base status, low chloride content, and adequate tonicity, is not yet available. After the accumulation of pre-clinical and clinical physiologic data, in the last three years, several clinical trials, mostly observational and retrospective, have addressed the question of whether the use of balanced solutions has beneficial effects as compared to the standard of care, sometimes even suggesting an improvement in survival. Nonetheless, the first large randomized controlled trial comparing the effects of a balanced vs. unbalanced solutions on renal function in critically-ill patients (SPLIT trial, the 0.9% saline vs. Plasma-Lyte 148 for Intensive Care Unit Fluid Therapy), just recently published, showed identical equipoise between the two treatments. In the present review, we offer a comprehensive and updated summary on this issue, firstly, by providing a full physiological background of balanced solutions; secondly, by summarizing their potential pathophysiologic effects; and lastly, by presenting the clinical evidence available to support their use at the present time.

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Chloride anion concentration as a determinant of renal vascular responsiveness to vasoconstrictor agents

Cited by 79 publications

References 22 publications

Chloride-Dominant Salt Sensitivity in the Stroke-Prone Spontaneously Hypertensive Rat

Chloride-Dominant Salt Sensitivity in the Stroke-Prone Spontaneously Hypertensive Rat

Genetically determined chloride-sensitive hypertension and stroke

Intravenous balanced solutions: from physiology to clinical evidence

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