The effects of varying sodium diets on haemodynamics and fluid balance in the spontaneously hypertensive rat

Ely, Daniel; M, Norlander; Friberg, Peter; Folkow, Björn

doi:10.1111/j.1748-1716.1986.tb07806.x

Cited by 20 publications

(9 citation statements)

References 17 publications

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“…However, it is unlikely that animals consuming Iso in the present experiments were volume expanded. Although there are reports (19,24) of increased plasma and/or blood volume with large increases in dietary sodium (8% diet), other studies (10,18,20) report no effects of this diet on vascular volumes in normotensive salt-resistant animals. Furthermore, we could find no studies demonstrating increased fluid volumes in animals consuming a more moderate 4% NaCl diet.…”

Section: Discussionmentioning

confidence: 95%

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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Section: Discussionmentioning

confidence: 95%

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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“…However, their growth is then slightly retarded and although cardiac output, blood volume and exchangeable Na space are within normal limits, they show increased vulnerability to, for example, blood loss (Gothberg et al 1983, Ely et al 1986a), which at least in part seems to be due to a reduced transmitter release per impulse . However, their growth is then slightly retarded and although cardiac output, blood volume and exchangeable Na space are within normal limits, they show increased vulnerability to, for example, blood loss (Gothberg et al 1983, Ely et al 1986a), which at least in part seems to be due to a reduced transmitter release per impulse .…”

Section: Discussionmentioning

confidence: 99%

Sodium appetite as well as 24‐h variations of fluid balance, mean arterial pressure and heart rate in spontaneously hypertensive (SHR) and normotensive (WKY) rats, when on various sodium diets

Ely

Thorén

Wiegand

et al. 1987

Acta Physiologica Scandinavica

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Young SHR and WKY rats were compared, first, concerning sodium (Na) appetite during 'rest', mild social stress and ACTH injections, second, concerning the diurnal patterns of water intake, urine output, mean arterial pressure (MAP) and heart rate (HR) while on various Na diets: 0.5 mmol Na(LNa), 5 or 12-13 mmol Na (CNa), 50 (HNa) or 120 mmol Na (vHNa) per 100 g food. Sodium appetite and water intake were about 50% higher in SHR than in WKY (4-4.5 vs 2.5-3 mmol Na per 100 g body wt day-1). It was modestly increased by both social stress and ACTH, and more so in WKY, thereby approaching that in SHR. Concerning the various Na diets and their influences, daytime resting MAP was modestly lowered in LNaSHR and slightly increased in vHNaSHR compared with CNaSHR but largely equal in all WKY groups. Food-water consumption was concentrated to the active night period, but even high Na-water intakes caused no signs of sustained hypervolaemia, because each intake bout was in both SHR and WKY eliminated by urine within 30-40 min. However, particularly the vHNa diet in SHR also increased the frequency of drinking, and each bout caused transient, evidently neurogenic MAP and HR increases which occurred too rapidly to be consequences of blood volume expansion. As a result, the diurnal MAP-HR patterns in SHR varied markedly with the Na diets, in vHNa group resulting in considerably raised average diurnal MAP levels even though resting daytime MAP was here nearly the same as in CNaSHR. These findings illustrate how largely continuous diurnal recordings are needed to judge correctly the relationships between, for example, Na intake, volume equilibrium and MAP. Finally, the relevance of these results in rats for also judging the control of Na balance in man is discussed.

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“…For example, Norman et al 5 showed that the RFC in adult SHR was nearly vertical over the range of sodium intakes used in the present study, and other investigators have shown the relative insensitivity of arterial pressure in adult SHR to changes in dietary sodium. 12 ' 13 In addition, captopril is known to decrease the slope of the RFC in normotensive dogs, 14 and the effect of captopril in increasing the sensitivity of arterial pressure to dietary sodium has been reported in SHR during the development of hypertension. 15 Finally, the parallel shift of the RFC produced by hydralazine in this study agrees with the effect of this drug on the RFC of rats with established deoxycorticosterone acetatesalt hypertension.…”

Section: Effect Of Chronic (2 Wk) Administration Of Captopril or Hydrmentioning

confidence: 99%

Effect of captopril and hydralazine on arterial pressure-urinary output relationships in spontaneously hypertensive rats.

Kline

Mercer

1987

Hypertension

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SUMMARY Angiotensin I converting enzyme inhibitors are typically classified as peripheral vasodilators. We studied the effect of captopril and a known vasodilator, hydralazine, on arterial pressure-urinary output relationships in adult spontaneously hypertensive rats to determine whether these drugs produced similar changes in this relationship. Tail-cuff pressure and 24-hour urine output and sodium excretion were measured under steady state conditions during ingestion of tap water or saline (1% NaCI) ad libitum. Sodium intake increased seven to nine times when rats drank saline, but in the absence of drug treatment, tail-cuff pressure was not altered significantly (water, 213 ± 3 vs saline, 220 ± 5 mm Hg). Daily administration of captopril (100 mg/kg p.o.) or hydralazine (15 mg/kg p.o.) for 2 weeks lowered tail-cuff pressure significantly (175 ± 3 and 166 ± 3 mm Hg, respectively; p<0.01) while rats drank tap water. Continued administration of hydralazine plus 2 weeks of drinking saline did not alter tail-cuff pressure (162 ± 4 mm Hg), but with the addition of saline during captopril treatment, tail-cuff pressure was elevated significantly (210 ± 5 mm Hg; p<0.01). Thus, hydralazine produced a parallel shift of the arterial pressure-urinary output relationship along the pressure axis. In contrast, captopril produced a marked change in the slope of this relationship, making arterial pressure extremely salt-sensitive. The results suggest that the two drugs have different effects on the mechanisms that contribute to the long-term control of arterial pressure. The changes associated with captopril treatment are consistent with the removal of the normal renal effects of the renin-angiotensin system, rather than with a nonspecific peripheral vasodilation. (Hypertension 10: 590-594, 1987) KEY WORDS • renal function curve • sodium excretion • sodium sensitivity antihypertensive drugs • captopril • spontaneously hypertensive rats A LTHOUGH numerous types of drugs are effec-/ \ tive in treating primary hypertension, the A. \ -physiological changes leading to the decrease in arterial pressure during administration of these drugs are not well documented. One of the major obstacles to understanding the mechanism of action of antihypertensive agents is the failure to adequately describe the pathophysiology of hypertension. Using a systems analysis approach, Guyton et al.1 have provided a useful conceptual framework for understanding the long-term control of the circulation in normal and abnormal conditions, including hypertension. According to the predictions of their model, the ability of Received March 27, 1987; accepted July 15, 1987. the kidneys to excrete sodium and water is a primary determinant of the long-term steady state level of arterial pressure. 2 -3 The importance of pressure-diuresis and pressure-natriuresis to the long-term control of arterial pressure has recently been reviewed. 4 This relationship between arterial pressure and excretion of sodium and water by the kidneys, called the renal function curve...

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The effects of varying sodium diets on haemodynamics and fluid balance in the spontaneously hypertensive rat

Cited by 20 publications

References 17 publications

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

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

Sodium appetite as well as 24‐h variations of fluid balance, mean arterial pressure and heart rate in spontaneously hypertensive (SHR) and normotensive (WKY) rats, when on various sodium diets

Effect of captopril and hydralazine on arterial pressure-urinary output relationships in spontaneously hypertensive rats.

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