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

Genain, Claude P.; Reddy, S. Raghupathi Rami; Ott, Cobern E.; Loon, Glen R. Van

doi:10.1161/01.hyp.12.6.568

Cited by 29 publications

(19 citation statements)

References 32 publications

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“…The mean systolic pressure was slightly higher in the DS compared with the DR rats, both before initiation of salt diets and after 5 days on the diets. However, consistent with our previous experience, 9 systolic pressure in DS rats after 5 days on the 7% NaCl diet was not increased above that in DS rats on the normal salt diet.…”

Section: Resultssupporting

confidence: 92%

“…9 Thus, the differences in sensitivity observed could represent significant factors in the initiation of hypertension but are not secondary to elevated pressure.…”

Section: Discussionmentioning

confidence: 98%

“…In addition, DS rats demonstrate a greater rate of adrenal synthesis of catecholamines in comparison with DR rats. 12 Genain et al 9 reported that salt loading fails to inhibit norepinephrine turnover in heart and brown fat of prehypertensive DS rats but not in that of DR rats.…”

Section: Discussionmentioning

confidence: 99%

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Specific supersensitivity of the mesenteric vascular bed of Dahl salt-sensitive rats.

1991

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Dahl salt-sensitive (DS) and salt-resistant (DR) rats were maintained on a diet containing normal (0.45%) or high (7%) salt for 5 days. The DS rats had slightly higher systolic blood pressures than DR rats, although a high salt diet failed to significantly elevate pressure in either group when compared with their appropriate (low salt diet) controls. The sensitivity of the isolated, perfused mesenteric vasculature from DS rats fed a high salt diet to nerve stimulation was greater when compared with all other groups in the presence or absence of cocaine (1 fiM). A similar difference in sensitivity between high salt DS rats and high salt DR rats to bolus injections of norepinephrine was observed only in the presence of cocaine. The change in sensitivity was characterized by a leftward shift of the dose-response curve without a change in maximum response. No difference in sensitivity between the high salt DS group and any other treatment group was observed in response to the pressor agents KC1, angiotensin II, 5-hydroxytryptamine or the depressor agent acetylcholine. These data indicate that DS rats on a short-term, high salt diet possess a significant and specific elevation in sensitivity to nerve stimulation and norepinephrine in the absence of an increase in blood pressure. Differences in the effectiveness of cocaine among the groups suggest that differences may exist in neuronal . uptake (uptake 1). Although the greater neuronal uptake in preparations from high salt DS rats masks a greater sensitivity of the vascular smooth muscle to exogenous norepinephrine, supersensitivity of the smooth muscle may contribute to the enhanced responses to nerve stimulation since neuronal uptake has less influence on responses to neurally released norepinephrine. The specificity of the sensitivity difference suggests that the vascular smooth muscle of DS rats on high salt diets for 5 days possesses an abnormality either at the level of the «,-adrenoceptor or in the sequelae that develop after adrenoceptor occupation. This could be an early event in the induction of hypertension in the Dahl rat (Hypertension 1991;17: 349-356) T he literature is often conflicting regarding the existence and characteristics of altered sensitivity of vascular smooth muscle in animal models of hypertension. The reasons are multiple and include differences in the 1) choice of model, 2) choice of preparation (large artery, small artery, vascular bed), 3) degree of hypertension (and changes in arterial morphology or physiology secondary to the elevated pressure), and 4) control conditions. It is the long-range goal of our laboratory to use the same isolated vascular bed to examine the responsiveness to a variety of agonists in several rat

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Section: Resultssupporting

confidence: 92%

“…9 Thus, the differences in sensitivity observed could represent significant factors in the initiation of hypertension but are not secondary to elevated pressure.…”

Section: Discussionmentioning

confidence: 98%

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Specific supersensitivity of the mesenteric vascular bed of Dahl salt-sensitive rats.

1991

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“…This discrepancy may be due to the use of anesthetized animals in these earlier reports. The results from the present experiments are consistent with investigations reporting that increases in dietary sodium are associated with diminished SNS drive in rats (3,13) and in humans (21,30).…”

Section: Discussionsupporting

confidence: 92%

Increased dietary sodium alters neural control of blood pressure during intravenous ANG II infusion

Bealer

2003

American Journal of Physiology-Heart and Circulatory Physiology

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Bealer, Steven L. Increased dietary sodium alters neural control of blood pressure during intravenous ANG II infusion. Am J Physiol Heart Circ Physiol 284: H559-H565, 2003. First published October 24, 2002 10.1152/ajpheart.00628.2002Increased dietary sodium enhances both excitatory and inhibitory blood pressure responses to stimulation of the central sympathetic nervous system (SNS) centers. In addition, long-term (hours to days) administration of ANG II increases blood pressure by activation of the SNS. These studies investigated the effects of increased dietary sodium on SNS control of blood pressure during 0-to 24-h infusion of ANG II in conscious, male rats consuming either tap water or isotonic saline (Iso) for 2 to 3 wk. The SNS component (evaluated by ganglionic blockade with trimetaphan) of both control blood pressure and the pressor response to intravenous ANG II was reduced in Iso animals. Furthermore, although the pressor response to intravenous ANG II infusion was similar between groups, the baroreflexinduced bradycardia during the initial 6 h of ANG II infusion was significantly greater, whereas the tachycardia accompanying longer infusion periods was significantly attenuated in Iso animals. These data suggest that in normal rats increased dietary sodium enhances sympathoinhibitory responses during intravenous ANG II. baroreflex; heart rate; sympathoexcitation; sympathoinhibition; hypertension INCREASED DIETARY SODIUM has been associated with the enhanced risk of high blood pressure (4, 12) because increased salt intake induces and/or increases hypertension in several experimental animal models (1,15,34,40). However, the mechanisms of the hypertensinogenic effects of increased dietary sodium have not been completely defined. Several studies (37,38,47) have suggested that elevated sodium ingestion is associated with activation of the sympathetic nervous system (SNS), and it has been proposed that increasing dietary salt alters the SNS circuits that regulate SNS control of cardiovascular function (37,41).In support of this proposal, recent studies (19, 39) show that animals on a high-salt diet demonstrate enhanced pressor responses to microinjection of several excitatory neurotransmitters into the rostral ventrolateral medulla. These authors suggest that although dietary sodium does not increase blood pressure alone, it may contribute to development of hypertension by potentiating the actions of other hypertensive stimuli on SNS centers. However, in addition to enhancing sympathoexcitatory responses to stimulation of medullary pressor sites, increased dietary sodium also potentiates the depressor responses to both glutamate injections in the nucleus tractus solitarius (19) and aortic nerve stimulation (39) and enhances baroreflex-induced bradycardia (39). Therefore, it appears that both sympathoexcitatory and sympathoinhibitory responses are sensitized by increased dietary sodium. However, the physiological significance of these observations has not been completely defined.Systemic ANG II has been im...

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“…We have previously reported that plasma volume is greater in Dahl salt-sensitive than in Dahl salt-resistant rats maintained on a "normal" NaCl diet. 17 Other investigators have also found either transient or sustained elevations of plasma volume in the Dahl salt-sensitive rat. 18 -20 Studies of selective sodium loading support the hypothesis that volume mechanisms contribute to the pathogenesis of salt-sensitive hypertension.…”

Section: Volume Mechanismsmentioning

confidence: 95%

Importance of dietary chloride for salt sensitivity of blood pressure.

Boegehold

1991

Hypertension

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

Cited by 29 publications

References 32 publications

Specific supersensitivity of the mesenteric vascular bed of Dahl salt-sensitive rats.

Specific supersensitivity of the mesenteric vascular bed of Dahl salt-sensitive rats.

Increased dietary sodium alters neural control of blood pressure during intravenous ANG II infusion

Importance of dietary chloride for salt sensitivity of blood pressure.

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