Dietary sodium restriction and development of hypertension in spontaneously hypertensive rats

Toal, Corey B.; Leenen, F. H. H.

doi:10.1152/ajpheart.1983.245.6.h1081

Cited by 22 publications

(18 citation statements)

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“…However, as with blood pressure, the plasma volume of DS was higher than that of DR fed 1% NaCl; plasma volume was not affected by 5 days of 7% NaCl intake. Other investigators have also reported that net Na + balances do not differ in DR and prehypertensive DS, 28 and Roman and Osborn similar to those of Overbeck et al 5 , who reported that plasma volume, but not extracellular fluid volume, is expanded in hypertensive DS fed a high NaCl diet. Conceivably, an expanded plasma volume in the absence of a net increase of sodium balance may be related to a redistribution of fluid compartments resulting from alterations of vascular or interstitial compliance.…”

Section: Discussionsupporting

confidence: 65%

“…This blood pressure elevation may be attributed to the fact that animals were fed 1% NaCl chow from the time of weaning, and this is a relatively high NaCl intake for the rat. 28 Dahl et al 29 have previously reported that blood pressures are higher in DS fed 1% NaCl than in animals fed 0.4% NaCl. However, we have observed (unpublished observation) that DS and DR fed 0.4% NaCl gain weight at a slower rate than animals fed 1% NaCl.…”

Section: Discussionmentioning

confidence: 96%

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Failure of salt loading to inhibit tissue norepinephrine turnover in prehypertensive Dahl salt-sensitive rats.

et al. 1988

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SUMMARY To determine if alterations of electrolyte balance or sympathetic nervous system activity are present in Dahl salt-sensitive rats (DS) before the onset of hypertension, we compared electrolyte balances, extracellular fluid volume (inulin space), plasma volume (radiolabeled albumin), and norepinephrine turnover in peripheral tissues (heart and interscapular brown fat) in prehypertensive DS and Dahl salt-resistant rats (DR). Animals were maintained for 5 to 7 days on either a "normal" or high NaCl diet. Tissue norepinephrine turnover was evaluated by measuring the rate at whkh norepinephrine content decreased following tyrosine hydroxylase inhibition with a-methyl-p-tvrosine. Blood pressure was higher (p < 0.05) hi DS (135 ± 2 [SE] mm Hg) than hi DR (129 ± 2 mm Hg) and was not affected by the diets. Extracellular fluid volume and net Na + and Cl~ balances did not differ between DS and DR. However, plasma volume was greater hi DS than in DR (p < 0.05). In both fat and heart, norepinephrine turnover was decreased by dietary NaCl loading hi DR (p < 0.01), but not hi DS. Thus, the tendency of the DS to become hypertensive with high NaCl intake may be related to the combined effects of an increased plasma volume and the failure of high dietary NaCl to inhibit peripheral sympathetic nervous system activity. 1 -2 The blood pressure of the Dahl saltsensitive rat (DS) rises with increased NaCl intake, whereas that of the Dahl salt-resistant rat (DR) does not. DS excrete sodium less efficiently than do DR according to some 3 but not all 4 investigators, and evidence for an expansion of the extracellular fluid volume in the pathogenesis of hypertension in this salt-sensitive model is conflicting. 5 ' 6 Alternatively, there is increasing evidence for the participation of the nervous system in the pathogenesis of salt-sensitive hypertension. Lesions of the paraventricular nuclei or the anteroventral third ventricle region protect against the development of hypertension in the DS and other models of saltsensitive hypertension 7 -8 ; chemical sympathectomy with guanethidine or 6-hydroxydopamine also prevents hypertension in DS fed a high NaCl diet.9 -10

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Section: Discussionsupporting

confidence: 65%

Section: Discussionmentioning

confidence: 96%

Failure of salt loading to inhibit tissue norepinephrine turnover in prehypertensive Dahl salt-sensitive rats.

et al. 1988

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“…Using this strain with high blood pressure, numerous studies concerning essential hypertension, including pathophysiology and the effects of food, have been carried out (29,30). Descendants of SHRs, SHRSPs (11) were created through continuous brother-sister mating in a closed colony of SHRs after approximately one decade of mating.…”

Section: Discussionmentioning

confidence: 99%

“…An inbred strain of M-SHRSP shows SBPs of 250 mmHg or higher before 14 weeks of age, and shows more rapid and severe increases in BP and stroke in almost all animals (31). These three types of hypertensive rat substrains, SHR, SHRSP and M-SHRSP, have been used in multiple investigations of pathophysiology, preventive medicine, pharmacology and drug development worldwide (29)(30)(31)(32). Our facility is one of the original places that bred the three types of SHR substrains and families.…”

Section: Discussionmentioning

confidence: 99%

Whole rat DNA array survey for candidate genes related to hypertension in kidneys from three spontaneously hypertensive rat substrains at two stages of age and with hypotensive induction caused by hydralazine hydrochloride

Kinoshita

Ashenagar

Tabuchi

et al. 2011

Experimental and Therapeutic Medicine

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Abstract. Clarification of the genetic nature and more effective care for hypertension are required, given the high incidences of cardiovascular and cerebrovascular mortality. Thus, we surveyed candidate genes for hypertension with rat whole gene DNA microarrays using three novel methods. Gene expression analyses were conducted as follows: Method 1, three types of spontaneously hypertensive rat (SHR) substrains, SHR, strokeprone SHR (SHRSP) and malignant type of SHRSP (M-SHRSP) were used and compared to normotensive Wistar Kyoto rats; Method 2, the expressed genes between rats of different ages were compared for different blood pressures; and Method 3, genes that were expressed in rats treated with or without an acute hypotensive stimulus, the antihypertensive hydralazine hydrochloride, were compared. This approach identified dozens of genes, including Dusp15, Cyp8b1, Armc 3, Gtpbp4, Mettl2, Mapk14, Prkar2b, frame 12, Anxa13, Ephx2, Myr8 and Pcdh9 by Method 1; Cyp2C and Atp12a by Method 2; and Kcnc3, Vnn1, TC560558 and Gabrq and a number of unknown genes by Methods 2 and 3, as probable candidate genes for hypertension in SHR substrains. Ephx2 was previously reported as a candidate gene in SHRs; however other genes were identified for the first time in this study. Since it was not always possible to completely demonstrate that these genes are responsible for hypertension in SHRs, further research into true candidate genes that participate in the genesis of hypertension in SHR substrains is warranted.

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“…These abnormalities presumably result in the animal's exhibiting a variety ofbiochemical and organ defects related to Ca2+ metabolism (5,(7)(8)(9)14). Besides the SHR's having an apparent dependence upon receiving a sufficient dietary Ca2" exposure, reports have suggested a de-pendence of the SHR on an adequate Na' intake (57,58), as sodium restriction in the young SHR was noted to result in growth retardation and premature mortality (57)(58)(59). Dietary potassium does not appear to be a significant factor in the SHRs' blood pressure responses in this study (60).…”

Section: Discussionmentioning

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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Dietary sodium restriction and development of hypertension in spontaneously hypertensive rats

Cited by 22 publications

References 0 publications

Failure of salt loading to inhibit tissue norepinephrine turnover in prehypertensive Dahl salt-sensitive rats.

Failure of salt loading to inhibit tissue norepinephrine turnover in prehypertensive Dahl salt-sensitive rats.

Whole rat DNA array survey for candidate genes related to hypertension in kidneys from three spontaneously hypertensive rat substrains at two stages of age and with hypotensive induction caused by hydralazine hydrochloride

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

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