Effects of Chronic Excess Salt Ingestion. Experimental Hypertension in the Rat, Correlation With Human Hypertension

Dahl, Lewis K.

doi:10.2172/4079421

Cited by 81 publications

(111 citation statements)

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“…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 However, we have observed (unpublished observation) that DS and DR fed 0.4% NaCl gain weight at a slower rate than animals fed 1% NaCl.…”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: 95%

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: Discussionmentioning

confidence: 95%

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

et al. 1988

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“…Detailed reports on breeding, feeding, care, and blood pressure measurements have been published (6)(7)(8) so that only details pertinent to the present studies will be included here. Standard Purina rat chow with a special low sodium content (0.4% NaCI dry weight) and tap water were used in all experiments.…”

Section: Methodsmentioning

confidence: 99%

Genetic Influence on the Development of Renal Hypertension in Parabiotic Rats

Iwai

Knudsen

Dahl

et al. 1969

The Journal of Experimental Medicine

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The relative roles of renal pressor and antihypertensive factors in the pathogenesis cf experimental renal hypertension remain a central, and disputed, issue.In our laboratory, we have evolved two strains of rats with opposite genetic predispositions to different forms of experimental hypertension including those produced by salt and unilateral renal artery constriction (1-4). But when a rat from each of the two strains was united in parabiosis, it was found that the reaction pattern to salt hypertension could be changed, i.e., the normally resistant animal not only developed significant hypertension but did so prior to its susceptible partner (5). This was interpreted to indicate that the genetic factors might act via a humoral agent, transmittable between rats from the two strains. The studies did not settle whether such factors were of a pressor or anti-pressor nature.In the current study, we have explored the effects of a variety of renal manipulations in single and parabiotic animals. Our results suggest that, although intact renal tissue has an antihypertensive action, the loss of this function is not alone sufficient to explain renal hypertension; a pressor agent must be involved. Since only animals from the sensitive strain were able to induce experimental hypertension in their intact parabiotic partners, we have speculated that, in animals from the sensitive strain there are two pressor principles: One agent is present in animals from this strain as well as in the one resistant to hypertension and is not transmitted through the parabiosis junction; a second agent is peculiar to the strain predisposed to hypertension and will traverse the junction. Material and MethodsThe rats belonged to two strains developed in this laboratory, called R and S because of their resistance or sensitivity, respectively, to experimental hypertension.

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“…Nevertheless, the interactions of all these factors have seldom been studied under the same experimental conditions. Dahl salt-sensitive (DS) rats with their age-dependent susceptibility to salt hypertension 1 represent an experimental model that appears to be suitable for such an analysis.…”

Section: With the Technical Assistance Ofjutta Kronauermentioning

confidence: 99%

Kinetics of Na+ and K+ transport in red blood cells of Dahl rats. Effects of age and salt.

Zicha¹,

Duhm²

1990

Hypertension

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Blood pressure response to chronic high salt intake and kinetics of red blood cell Na + and K + (Rb + ) transport were studied in salt-sensitive (DS) and salt-resistant (DR) Dahl rats fed a high salt diet (8% NaCl) for 7 weeks from the fifth (young), 12th (adult), or 23rd (old) week of age. The kinetics of ouabain-sensitive Rb + uptake and Na + extrusion were determined in Na + media as a function of both intracellular Na + (Na + ,, 2-8 mmol/1 cells) and extracellular Rb + (Rb + 0 ). In addition, the kinetics of furosemide-sensitive Rb + uptake (related to Rb + 0 ) and the magnitude of the Na + and Rb + leaks were assessed. High salt intake induced hypertension in young and adult but not in old DS rats although red blood cell Na + was slightly increased in all age groups of DS rats fed a high salt diet The kinetic parameters of the Na + -K + pump were similar in DS and DR rats fed a low salt diet Ouabain-sensitive transport rates were not suppressed in erythrocytes of salt hypertensive Dahl rats. Maximal velocities of the Na + -K + pump (related to Na + ,) decreased significantly with age in all groups except in DS rats fed a high salt diet This was compensated by an age-dependent increase in the affinity for Na + , so that no substantial differences in transport rates between young and old rats were seen at physiological cell Na + and plasma K + levels. The maximal velocity of furosemide-sensitive Rb + uptake rose with age in all groups without changes in the affinity for Rb + 0 . High salt intake increased its maximal activity only in DS rats. The Rb + leak was higher in DS relative to DR rats irrespective of salt intake, age, or blood pressure. The Na + leak was elevated in DS rats in which it was augmented by high salt intake. Salt hypertension was, however, not associated with a significant increase of the Na + leak, which was responsible for most alterations of cell Na + content (Hypertension 1990;15:612-627) M any previous studies have indicated the role of genetic factors, salt intake, agedependent susceptibility, and ion transport alterations in the development of hypertension. Nevertheless, the interactions of all these factors have seldom been studied under the same experimental conditions. Dahl salt-sensitive (DS) rats with their age-dependent susceptibility to salt hypertension 1 represent an experimental model that appears to be suitable for such an analysis.From the Institute of Physiology, University of Munich, Munich, Germany.J.Z. was the recipient of a research fellowship from the Alexander von Humboldt Foundation.Presented in part at the 66th Meeting of the German Physiological Society in Wurzburg, September 1988, and published in abstract form (Pflugcrs Arch 1988;412(suppl 1):R51).Address for reprints: Prof. J. Duhm, Institute of Physiology, University of Munich, Pettenkoferstr. 12, D-8000 Munchen 2, FRG.Received May 16, 1989; accepted in revised form February 12, 1990. The information on ion transport in vascular smooth muscle and red blood cells of DS and saltresistant rats (DR) is rath...

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Effects of Chronic Excess Salt Ingestion. Experimental Hypertension in the Rat, Correlation With Human Hypertension

Cited by 81 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.

Genetic Influence on the Development of Renal Hypertension in Parabiotic Rats

Kinetics of Na+ and K+ transport in red blood cells of Dahl rats. Effects of age and salt.

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