Differential Development of Salt-Induced and Renal Hypertension in Dahl Hypertension-Sensitive Rats After Neonatal Sympathectomy

Friedman, Richard A.; Tassinari, Lorraine; Heine, Martha; Iwai, Junichi

doi:10.3109/10641967909068639

Cited by 56 publications

(19 citation statements)

References 22 publications

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“…(1976), causes a profound reduction in cardiac noradrenaline content. The extent of depletion which we measured in the ventricles is within the range reported in the literature for whole hearts (Johnson et al, 1976;Grzanna & Coyle, 1978;Friedman et al, 1979;Overbeck, 1979;Levens et al, 1981). However, we also measured the noradrenaline content of separate right and left atria (which has not been previously done), and found some evidence for reinnervation in these tissues, since there was an increase in their noradrenaline content between 9 and 26 weeks after birth.…”

Section: Discussionsupporting

confidence: 87%

“…In all those studies, evaluation of the extent of the sympathectomy was based on the measurement of 0007-1188/82/080557-08 $01.00 tissue or plasma catecholamine levels (Grzanna & Coyle, 1978;Friedman, Tassinari, Heine & Iwai, 1979;Overbeck, 1979;Levens, Peach & Carey, 1981) or the pressor responsiveness of the anaesthetized rat to noradrenaline and tyramine (Friedman et al, 1979;Simon, 1981). However, there is some discrepancy in the literature regarding the degree of catecholamine depletion caused by the regime of guanethidine treatment outlined by Johnson et al (1976).…”

Section: Introductionmentioning

confidence: 99%

“…However, there is some discrepancy in the literature regarding the degree of catecholamine depletion caused by the regime of guanethidine treatment outlined by Johnson et al (1976). For instance, the levels of noradrenaline in the heart have been reported to be 0-3% (Johnson et al, 1976), 2% (Friedman et al, 1979), 12% (Grzanna & Coyle, 1978) or 22% (Levens et al, 1981) of control levels. Blythe, Hall & Hughes (1976), using a different dose and time course of guanethidine administration, found (8 weeks after the treatment had ended) that whereas the catecholamine content of the ventricles was only (9) The Macmillan Press Ltd 1982 21 % of the control levels, cardiovascular control mechanisms were essentially normal.…”

Section: Introductionmentioning

confidence: 99%

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An Assessment of the Effectiveness of Neonatal Treatment With Guanethidine as a Means of Producing Sympathectomy

Bennett

Gardiner

Kemp

1982

British J Pharmacology

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1 Male Wistar rats were treated neonatally with guanethidine (following a protocol reported to produce a permanent peripheral sympathectomy) and the extent of the sympathectomy was assessed when the rats were mature.2 The noradrenaline content of right and left atria and the ventricles was markedly reduced in 9-and 26-week old rats which had been treated with guanethidine. The extent of depletion in the ventricles was similar at both times but the atrial content increased between 9 and 26 weeks.3 Arterial blood pressures were not significantly different in 24-26-week old conscious rats which had been treated neonatally with guanethidine compared to controls, but the baroreflex sensitivity, assessed by the lengthening of pulse interval in response to a pressor stimulus, was significantly less in the guanethidine-treated rats.4 The blood pressure response to acute bilateral adrenalectomy was similar in control and guanethidine-treated rats. 5 Left atria and hepatic portal veins taken from 20-26-week old rats which had been treated with guanethidine showed classical signs of a denervation supersensitivity, but the chronotropic responses of right atria to noradrenergic nerve stimulation and to noradrenaline were normal.6 Fluorescence histochemical studies on the right atria, irides and hepatic portal veins showed that the neonatal treatment had caused a variable degree of destruction both between and within animals. 7 The findings are consistent with neonatal guanethidine treatment causing extensive damage to peripheral noradrenergic nerves. However, the sympathectomy is neither complete nor permanent.In the heart, there appears to be a selective re-innervation of the atria. 8 Despite the impaired efferent sympathetic nerve activity in rats treated neonatally with guanethidine, compensatory mechanisms permit adequate cardiovascular control in the resting state.

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Section: Discussionsupporting

confidence: 87%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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An Assessment of the Effectiveness of Neonatal Treatment With Guanethidine as a Means of Producing Sympathectomy

Bennett

Gardiner

Kemp

1982

British J Pharmacology

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“…If S rats are treated with either guanethidine 90 or 6-hydroxydopamine 91 -92 to destroy the sympathetic nervous system, then salt-induced hypertension is reduced or fails to occur. Ganglionic blockade abolished the blood pressure difference between S and R rats fed high salt diet for 4 weeks.…”

Section: Nervous Systemmentioning

confidence: 99%

Dahl salt-susceptible and salt-resistant rats. A review.

Rapp¹

1982

Hypertension

342

210

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strain)* to the hypertensive effect of high salt diet. In this review "salt" will always mean NaCl.t Selective BreedingIn the 1950s, Meneely and coworkers studied the effects of high salt diet on the blood pressure of rats. Meneely and Ball 5 reviewed the work, showing that for a large group of rats the average blood pressure of the group was positively and linearly related to the percentage of NaCl in the diet between 0 and 10% NaCl. Moreover, they remarked that "there was quite a marked degree of individual variation" in the response of blood pressure to salt. This work was carried out on Sprague-Dawley rats that were presumably randombred.•A nomenclature committee of the International Society of Hypertension has stated that Dahl salt-sensitive (or salt-susceptible) rats should be designated DS and Dahl salt-resistant rats should be designated DR (see ref. I). This nomenclature is specifically not used in this review, and its use. except as noted below, is discouraged. In DahTs original work in 1962 and for 14 years until his death. Dr. Dahl called the strains S and R. There is no need to replace that historic precedent. The nomenclature committee specifically states that they were naming "hypertensive rat strains with stable hypertension which had been inbred (brother-sister mating) for at least 20 generations" (ref. \>. Apparently they were naming inbred strains under development at Brookhavcn National Laboratory since Dr. Dahl's death in November, 1975. No fully inbred rats were supplied to investigators from the Brookhaven colony because they do not exist (yet). What was supplied were rats from colonies of S and R rats separate from the inbreeding program and maintained as Dahl had done for many years by selective breeding, avoiding inbreeding where possible. Thus, the use of DS and DR implies the use of specific inbred strains which do not exist. If and when such strains from Brookhavcn become available, these specific strains of inbred S and R rats can be referred to as DS and DR. tSodium in the diet is expressed in two ways in the literature, either as % Na+ or % NaCl The latter assumes that all the Na+ is present as NaCl, % NaCl means grams of NaCl per 100 grams of food. In most of the literature reviewed, sodium was expressed as % NaCl, and so this will be used throughout the review. Where the original article gave data in % N a + . this will be given followed by the % NaCl so that diets can always be compared on the same basis (% NaCl = 2.54 times % Na + ).A survey of commercial rat chows shows that they contain close to 1% NaCl, and so "normal salt diet" will refer to l%NaCl in the food. Two diets were introduced by Dahl during his work with S and R rats: 8% NaCl diet referred to as "high salt diet"; and 0.3 to 0.4% NaCl diet referred to as "low salt diet." Note that with this arbitrary nomenclature, low salt diet has only somewhat less than half the salt content of normal diet. Where a diet was fed that contained insufficient salt for optimum growth, this will be called sodium-deficient diet. The m...

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“…6 ' 10 -31 - 32 Reductions in the norepinephrine content in the heart and kidney, as a result of an increase in the rate of turnover of norepinephrine, have been reported in DOC-saline hypertensive rats 34 and in figure-8 renal-wrapped rats with a normal sodium intake. 33 An increase in the rate of norepinephrine turnover has also been reported in the renal cortex and atria of Dahl salt-sensitive rats fed a high sodium diet.…”

Section: Clearance Of [ 3 H]norepinephrine and Apparent Rate Of Norepmentioning

confidence: 99%

Sympathetic nervous system in high sodium one-kidney, figure-8 renal hypertension.

1992

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The contribution of the sympathetic nervous system and vasopressin to the maintenance of arterial pressure was investigated in high sodium-fed rats 4 weeks after the induction of one-kidney, figure-8 renal wrap hypertension. Arterial pressure was significantly greater In renal-wrapped rats than in shamoperated animals. The contribution of the sympathetic nervous system was assessed functionally by measuring the arterial pressure response to ganglionic blockade and estimating the apparent rate of release of norepinephrine. The contribution of vasopressin was assessed by administration of the vascular antagonist

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Differential Development of Salt-Induced and Renal Hypertension in Dahl Hypertension-Sensitive Rats After Neonatal Sympathectomy

Cited by 56 publications

References 22 publications

An Assessment of the Effectiveness of Neonatal Treatment With Guanethidine as a Means of Producing Sympathectomy

An Assessment of the Effectiveness of Neonatal Treatment With Guanethidine as a Means of Producing Sympathectomy

Dahl salt-susceptible and salt-resistant rats. A review.

Sympathetic nervous system in high sodium one-kidney, figure-8 renal hypertension.

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