Effects of High or Low Sodium Intake in Spontaneously Hypertensive Rats

Aoki, Kyuzo; Yamori, Yukio; Ooshima, Akira; Okamoto, Kozo

doi:10.1253/jcj.36.539

Cited by 131 publications

(45 citation statements)

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“…12 Neonatal sympathectomy by 6-OH dopamine results in a further slight increase in sodium retention in SHRSP and may be responsible for the expansion of the intravascular volume after chemical sympathectomy; the rise in blood pressure, however, is not accelerated, but abolished for the first 10 weeks after systemic denervation. 13 Since these observations are difficult to reconcile with the hypothesis that sodium affects blood pressure only insofar as it changes body fluid volumes, the effects of dietary sodium-loading in SHRSP on blood pressure and plasma volume have been investigated.…”

Section: Discussionmentioning

confidence: 99%

“…13 The aim of the present study was to evaluate possible interrelationships among sodium-loading, changes in intravascular volume, sympathetically mediated vasoconstriction, and changes in blood pressure in SHRSP. Information about the activity of the sympathetic nervous system in this study is based on: plasma norepinephrine and epinephrine concentrations under basal conditions and after stimulation; norepinephrine uptake and metabolism by peripheral sympathetic nerve endings; and the responsiveness of resistance vessels to the neurotransmitter norepinephrine.…”

Section: *"mentioning

confidence: 99%

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Contribution of the sympathetic nervous system to the hypertensive effect of a high sodium diet in stroke-prone spontaneously hypertensive rats.

Dietz¹,

Schömig²,

Rascher³

et al. 1982

Hypertension

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SUMMARY In stroke-prone spontaneously hypertensive rats (SHRSP) plasma norepinephrine levels and vascular reactivity to norepinephrine are increased and intravascular volume is reduced during the developmental phase of hypertension. Since the accelerated rise in blood pressure following sodium-loading in SHRSP cannot be attributed to the volume-retaining properties of sodium, the effects of an increased dietary intake of sodium on biochemical parameters of sympathetic vascular tone were investigated. The following results were obtained. First, the increased reactivity of vascular smooth muscle was further augmented in sodium-treated SHRSP; the degree of supersensitivity was positively correlated to the plasma sodium concentration. After blockade of the neuronal uptake by 30 fiM cocaine, no difference in vascular reactivity to norepinephrine was detected between SHRSP on a normal and SHRSP on a high-sodium diet. Second, the inactivation of norepinephrine by the neuronal uptake was impaired in rats on a high-sodium diet, the impairment being more pronounced in SHRSP than in Wistar-Kyoto (WKY) rats. This decreased inactivation could be expected to cause higher concentrations of the neurotransmitter at the receptor site if the transmitter release from the nerve ending remains constant. Third, the release of norepinephrine and epinephrine into the plasma was increased in sodium-loaded SHRSP but not in sodium-loaded WKY. Cold exposure exaggerates these differences between normotensive and hypertensive rats. These findings suggest that a high-sodium intake modifies the transmission of sympathetic impulses at the level of the nerve terminal in both WKY and SHRSP. In the normotensive rats, moderate impairment of norepinephrine inactivation, however, was balanced by an appropriate reduction in central sympathetic discharge following sodium-loading. In the hypertensive rats, the peripheral disturbance in norepinephrine inactivation due to sodium-loading was obviously not balanced by an adequate withdrawal of central sympathetic discharge. The resultant hemodynamic change was a further increase in the sympathetically mediated vasoconstriction, which is regarded as at least one of the main mechanisms of the sodium-dependent acceleration of hypertension in SHRSP. (Hypertension 4: 773-781, 1982) KEY WORDS • sodium • stroke-prone spontaneously hypertensive rats sympathetic activity • vascular reactivity • norepinephrine metabolism T HE reciprocal relationship between intravascular volume and the degree of vasoconstriction is mediated by changes in the activity of vasopressor systems in response to changes in volume.' Thus, salt-loading, which is accompanied by fluid volFrom the Department of Cardiology, and the Department of Pharmacology, University of Heidelberg, West Germany.Supported by a grant from the Deutsche Forschungsgemeinschaft, Bonn, within the SFB90, Heidelburg.Address for Wolfgang Rascher and Ursula Ganten: Department of Pharmacology, University of Heidelberg, D6900 Heidelberg, West Germany.Address for reprints:...

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Section: Discussionmentioning

confidence: 99%

Section: *"mentioning

confidence: 99%

Contribution of the sympathetic nervous system to the hypertensive effect of a high sodium diet in stroke-prone spontaneously hypertensive rats.

Dietz¹,

Schömig²,

Rascher³

et al. 1982

Hypertension

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“…The spontaneously hypertensive rat (SHR)' is one of the most widely studied genetic models of human hypertension, having been characterized as closely paralleling the human disorder in its hemodynamic, endocrine, and end-organ manifestations (3). The development of the SHR's hypertension is not sodium dependent, though modifying Na' intake may produce modest blood pressure changes (4). Reports have noted, though, a sensitivity of the adult SHR's pressure to manipulations of Ca2+ intake (5).…”

Section: Introductionmentioning

confidence: 99%

Blood pressure development of the spontaneously hypertensive rat after concurrent manipulations of dietary Ca2+ and Na+. Relation to intestinal Ca2+ fluxes.

McCarron¹,

Lucas²,

Shneidman³

et al. 1985

J. Clin. Invest.

120

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The blood pressure of the spontaneously hypertensive rat (SHR) is influenced by the Ca2" content of its diet. As the SHR's greater dependence on dietary calcium may reflect a defect in intestinal calcium absorption, we measured in vitro unidirectional Ca2" flux (J) in the duodenum-jejunum (four segments each) of the SHR (n = 6) and the normotensive Wistar-Kyoto rat (WKY; n = 6) by a modified Ussing apparatus. Because of the known and postulated interactions between Ca2' and Na+ in both intestinal and vascular tissue, we assessed in vivo the influence of a concurrent manipulation of Na+ intake (three levels: 0.25%, 0.45%, and 1.0%) on the blood pressure development of SHRs (n = 35) and WKYs (n = 35), between 6 and 20 wk of age, exposed to three levels of dietary calcium (0.1, 1.0, and 2%).Net calcium flux (J4t) (mean±SEM) was significantly (P < 0.01) lower in the SHR (-2.8±6.3 nmol/cm2 * h) than in the WKY (34.6±8.8 nmol/cm2 * h). The SHR's decreased J.t resulted from a significantly (P < 0.03) lower mucosa-to-serosa flux (Jm.) in the SHR (41.0±5.6 nmol/cm2-h) compared with the J.,, of the WKY (70.1±9.1 nmol/cm2 -h). Serosa-to-mucosa flux for calcium did not differ between the SHR (43.8±6.6 nmol/ cm * h) and the WKY (35.5±8.0 nmol/cm2 * h). The SHR's decreased (P < 0.002) J., was confirmed by additional measurements in SHRs and WKYs. Jm. was 36.2±3.7 nmol/cm2 h in the SHRs (n = 11) and 64.4±6.7 nmol/cm2 * h in the WKYs (n = 9).The provision of an increased dietary Ca2+ (2% by weight) and increased Na+ (1%) to the SHR prevented the emergence of hypertension (P < 0.001) (mean±SEM systolic blood pressure at 20 wk of age; 135±5 mmHg for the 2% Ca2 , 1% Na+ SHR vs. 164±2 mmHg for the control diet SHR). Ca2+ (0.1%) and Na+ (0.25%) restriction accelerated the SHR's hypertension (192±2 mmHg) (P < 0.001) and was associated with higher pressures in the WKY (146±4 mmHg in the restricted WKY vs. 134±4 mmHg in the control WKY). In a parallel group of 24 SHRs and 24 WKYs fed one of three diets (2% Ca2+/1% Na+; 1% Ca2+/0.45% Na+; or 0.1% Ca2+/0.25% Na+), the heart (P < 0.05) and kidney (P = 0.08) weight of the SHRs varied depending on the diet at 20 wk of age. Low Ca2' and Na+ intake was associated with increased heart weight (1.6±0.9 g) compared

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“…[1][2][3][4][5] In fact, in humans and animals with salt-sensitive hypertension, selective dietary loading of Na ϩ and of Cl Ϫ has repeatedly failed to induce a pressor effect. 3,6 -14 Yet, in the spontaneously hypertensive rat (SHR), 15 selective Cl Ϫ loading with glycine and choline chloride combined induced an exacerbation of hypertension but also an apparent systemic toxicity that complicated its interpretation. 16 In the more salt-sensitive genetic substrain of the SHR, the stroke-prone SHR (SHRSP), 17 selective Cl Ϫ loading with KCl exacerbated hypertension and microangiopathic nephropathy and induced numerous strokes, 18,19 much as does NaCl loading, 20 but not NaHCO 3 loading.…”

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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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Effects of High or Low Sodium Intake in Spontaneously Hypertensive Rats

Cited by 131 publications

References 24 publications

Contribution of the sympathetic nervous system to the hypertensive effect of a high sodium diet in stroke-prone spontaneously hypertensive rats.

Contribution of the sympathetic nervous system to the hypertensive effect of a high sodium diet in stroke-prone spontaneously hypertensive rats.

Blood pressure development of the spontaneously hypertensive rat after concurrent manipulations of dietary Ca2+ and Na+. Relation to intestinal Ca2+ fluxes.

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

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