Self-Sustaining, Post-DCA Hypertensive Cardiovascular Disease

Green, D. M.; Saunders, Francis J.; Wahlgren, Nils; Craig, Rachel

doi:10.1152/ajplegacy.1952.170.1.94

Cited by 39 publications

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“…Hypertension induced by deoxycorticosterone treatment is characterized by cardiac enlargement and is thought to involve a nervous pathway (Green, Saunders, Wahlgren & Craig, 1952). Also an increased cardiovascular reactivity to various pressor agents has been demonstrated (Sturtevant, 1956).…”

Section: Discussionmentioning

confidence: 99%

The contribution of the sympathetic nervous system to the development and maintenance of experimental hypertension in the rat

Finch

Leach

1970

British J Pharmacology

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Summary1. Experimental hypertension in the rat, induced either by renal artery stenosis or by treatment with deoxycorticosterone acetate (DCA) developed maximally over a period of 8 weeks. In both types of hypertension the rate of development was unaffected by immunosympathectomy or by chemical sympathectomy following the administration of 6-hydroxydopamine. 2. The effect of 6-hydroxydopamine on chronic renal hypertensive rats was to produce a hypotensive action of longer duration than when similarly administered to DCA-induced hypertensive or normotensive rats. Reserpine (5-10 mg/kg intraperitoneally) produced a more marked hypotensive effect on both types of hypertensive rats although it was of much shorter duration. 3. It is concluded that experimental hypertension of renal origin or induced by DCA treatment can develop even though most of the sympathetic nervous system has been destroyed. The maintenance of chronic hypertension in these conditions may depend on the adrenal glands or a hormonal system as yet undetected.

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Section: Discussionmentioning

confidence: 99%

The contribution of the sympathetic nervous system to the development and maintenance of experimental hypertension in the rat

Finch

Leach

1970

British J Pharmacology

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“…Kempner also found that in rats with experimental aminonucleoside nephrosis the death rate was eight times as high among those receiving added dietary NaCl (35). Much earlier, Green et al (36) had reported that, among rats with postdeoxycorticosterone acetate (DCA) hypertension, survival rate but not blood pressure was strikingly improved by sodium restriction. Sturtevant (37) quotes some unpublished observations of Salgado who had similar results from sodium restriction also in rats with post-DCA hypertension.…”

Section: Inmentioning

confidence: 99%

FURTHER EVIDENCE OF THE TOXICITY OF NaCl

Dahl

Tuthill

1974

The Journal of Experimental Medicine

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There are now three strains of hypertension-prone rats in which genetic factors are demonstrably involved in setting average blood pressure levels. The first strain was described by Smirk and Hall in 1958 (1), the second by Dahl et al. in 1962 (2, 3), and the third by Okamoto and Aoki in 1963 (4). Formal genetic studies indicated that blood pressure control was multigenic in all three strains (5-7). It is likely that these strains share some genes that control blood pressure but the available evidence is not consistent with the possibility that they share them all. Among a number of differences in these strains that suggest nonidentity of the gene pools controlling blood pressure, none is more evident than the response to excess dietary salt (NaC1). Both the New Zealand strain isolated by Smirk and Hall (1) and the spontaneously hypertensive rat (SHR) 1 separated by Okamoto and Aoki (4) develop significant hypertension without additional dietary salt, whereas the sensitive strain developed by Dahl et al. (2, 3) was originally evolved specifically on the basis of its hypertensive response to NaC1. The fact that some rats develop hypertension spontaneously on normal salt intakes led to the widespread belief that salt intake was therefore unimportant. In the aggregate, our long experience studying both clinical and experimental hypertension by modifying dietary NaC1 is incompatible with such a concept. The belief that dietary NaC1 is unimportant if elevations in blood pressure are insignificantly affected by increments or decrements in salt consumption represents, in our opinion, a simplistic view of such a lethal disease as hypertension. If there is evidence of increased mortality in association with increased salt intake or decreased mortality with decreased salt intake, whatever the effects on blood pressure, this is of consequence: the importance of survival in considerations affecting one of the major cardiovascular diseases is not to be underrated.The present work was done as part of a continuing long-term study in which the relative importance of dietary NaC1 and genetic makeup are being evaluated, in a variety of situations, in both clinical and experimental hypertension.

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“…Blood (Ashkenazi et al, 1983). DOCA-hypertension was produced by unilateral nephrectomy, substitution of 1% NaCl for drinking water, and three times weekly subcutaneous injections of desoxycorticosterone acetate (10 mg/kg) for six weeks essentially as described by Green, Saunders, Wahlgren & Craig (1952). Drugs LM 5008 (Pharmuka) was dissolved in 0.1 M HCl and partially neutralized to pH 6 before injection.…”

Section: Anaesthetized Animalsmentioning

confidence: 99%

“…Behavioural activity was measured with Animax monitors as described previously (Ashkenazi et al, 1983). DOCA-hypertension was produced by unilateral nephrectomy, substitution of 1% NaCl for drinking water, and three times weekly subcutaneous injec-tions of desoxycorticosterone acetate (10 mg/kg) for six weeks essentially as described by Green, Saunders, Wahlgren & Craig (1952).…”

Section: Conscious Ratsmentioning

confidence: 99%

Effects of LM 5008, a selective inhibitor of 5‐hydroxytryptamine uptake, on blood pressure and responses to sympathomimetic amines

Ashkenazi

Finberg

Youdim

1983

British J Pharmacology

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1 LM 5008 (4-[2-(3-indolyl)ethyl]piperidine) (10,20 and 50 mgkg-) had no significant effect on pressor responses to noradrenaline or tyramine in rats anaesthetized with urethane. Desmethylimipramine (1 mg kg-1) blocked the response to tyramine but chlorimipramine (5 mg kg-1) had no significant effect on responses to noradrenaline or tyramine. 2 In the rabbit, anaesthetized with chloralose, LM 5008 (5 mg kg-') had no effect on pressor responses to noradrenaline, tyramine or angiotensin II, while desmethylimipramine (0.25 mg kg-1) inhibited responses to tyramine and potentiated those to noradrenaline.3 LM 5008 (10mg kg-') had no effect on resting blood pressure of conscious normotensive or DOCA-saline hypertensive rats. 4 Tranylcypromine (5 mg kg-) produced a fall in blood pressure in conscious normotensive and in DOCA hypertensive rats.5 Treatment with a combination of LM5008 (10mgkg-t) and tranylcypromine (5mgkg-1) resulted in the appearance of a behavioural hyperactivity syndrome, but blood pressure was not different from that of animals treated with tranylcypromine alone. 6 These results further demonstrate the selectivity of LM 5008 for 5-hydroxytryptamine as opposed to catecholamine uptake.

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Self-Sustaining, Post-DCA Hypertensive Cardiovascular Disease

Cited by 39 publications

References 0 publications

The contribution of the sympathetic nervous system to the development and maintenance of experimental hypertension in the rat

The contribution of the sympathetic nervous system to the development and maintenance of experimental hypertension in the rat

FURTHER EVIDENCE OF THE TOXICITY OF NaCl

Effects of LM 5008, a selective inhibitor of 5‐hydroxytryptamine uptake, on blood pressure and responses to sympathomimetic amines

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