Subpressor angiotensin infusion, renal sodium handling, and salt-induced hypertension in the dog.

DeClue, J W; Guyton, Arthur C.; Cowley, Allen W.; Coleman, Thomas G.; Norman, Roger A.; McCaa, R E

doi:10.1161/01.res.43.4.503

Cited by 82 publications

(79 citation statements)

References 33 publications

(27 reference statements)

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“…Previous experiments have demonstrated that hypertension associated with systemic ANG II administration is enhanced with concurrent administration of increased dietary sodium (1,8,9). Although not directly tested in all of these earlier studies, the data are consistent with increased SNS tone contributing to the increase in blood pressure (7).…”

Section: Discussionmentioning

confidence: 69%

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: 69%

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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“…For example, several studies show that long-term infusion of angiotensin II (ANG II) causes salt-dependent hypertension in experimental animals (1,7,9,11,12,16). However, the precise nature of the relationship between plasma ANG II and long-term salt sensitivity of arterial pressure remains unclear.…”

mentioning

confidence: 99%

Responsiveness vs. basal activity of plasma ANG II as a determinant of arterial pressure salt sensitivity

Osborn¹,

Ariza-Nieto²,

Collister³

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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.-Infusion of angiotensin II (ANG II) causes salt-sensitive hypertension. It is unclear whether this is due to the body's inability to suppress ANG II during increased salt intake or, rather, an elevated basal level of plasma ANG II itself. To distinguish between these mechanisms, SpragueDawley rats were instrumented with arterial and venous catheters for measurement of arterial pressure and infusion of drugs, respectively. The sensitivity of arterial pressure to salt was measured in four groups with the following treatments: 1) saline control (Con, n ϭ 12); 2) administration of the angiotensin-converting enzyme inhibitor enalapril to block endogenous ANG II (ANG-Lo, n ϭ 10); 3) administration of enalapril and 5 ng ⅐ kg Ϫ1 ⅐ min Ϫ1 ANG II to clamp plasma ANG II at normal levels (ANG-Norm, n ϭ 10); and 4) administration of enalapril and 20 ng ⅐ kg Ϫ1 ⅐ min Ϫ1 ANG II to clamp ANG II at high levels (ANG-Hi, n ϭ 10). Rats ingested a 0.4% NaCl diet for 3 days and then a 4.0% NaCl diet for 11 days. Arterial pressure of rats fed the 0.4% NaCl diet was lower in ANG-Lo (84 Ϯ 2 mmHg) compared with Con (101 Ϯ 3 mmHg) and ANG-Norm (98 Ϯ 4 mmHg) groups, whereas ANG-Hi rats were hypertensive (145 Ϯ 4 mmHg). Salt sensitivity was expressed as the change in arterial pressure divided by the change in sodium intake on the last day of the 4.0% NaCl diet. Salt sensitivity (in mmHg/meq Na) was lowest in Con rats (0.0 Ϯ 0.1) and progressed from ANG-Lo (0.8 Ϯ 0.2) to ANG-Norm (1.5 Ϯ 0.5) to ANG-Hi (3.5 Ϯ 0.5) rats. We conclude that the major determinant of salt sensitivity of arterial pressure is the basal level of plasma ANG II rather than the responsiveness of the renin-angiotensin system.renin-angiotensin system; sympathetic nervous system LONG-TERM SALT SENSITIVITY of arterial pressure is a significant clinical problem in both the normotensive and hypertensive human populations. It is currently estimated that 25% of the normotensive population is "salt sensitive" in that their arterial pressures are abnormally sensitive to changes in dietary NaCl intake (29). This is clinically significant, because the salt sensitivity of arterial pressure may be a more accurate predictor of future cardiovascular disease and morbidity than the basal level of arterial pressure (29). Salt sensitivity is more prevalent in humans with essential hypertension; estimates are that 50-75% of these patients exhibit increased salt sensitivity of arterial pressure (28). Despite the clinical importance of salt-dependent hypertension, its pathogenesis is poorly understood.Previous studies support the idea that impaired regulation of the renin-angiotensin-aldosterone system (RAAS) increases the salt sensitivity of arterial pressure. For example, several studies show that long-term infusion of angiotensin II (ANG II) causes salt-dependent hypertension in experimental animals (1,7,9,11,12,16). However, the precise nature of the relationship between plasma ANG II and long-term salt sensitivity of arterial pressure remains unclear. It is logical to conclude that the ...

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“…This assumption has led us to suggest that the circulating levels of angiotensin are inappropriate or in excess when compared with the level of extracellular fluid volume. This hypothesis is largely supported by the studies of DeClue et al (52) who showed that when sodium intake is increased without allowing the circulating levels of angiotensin to be decreased because of continuous intravenous infusion, then the levels of blood pressure become strictly determined by the level of sodium intake. The observations of DeClue et al (52) have many physiological and clinical implications.…”

Section: Isoprostanesmentioning

confidence: 89%

Oxidative stress may explain how hypertension is maintained by normal levels of angiotensin II

Romero

Reckelhoff

2000

Braz J Med Biol Res

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It is well known that essential hypertension evolves in most patients with near normal levels of plasma renin activity. However, these levels appear to be responsible for the high levels of arterial pressure because they are normalized by the administration of angiotensin II converting inhibitors or angiotensin receptor antagonist. In experimental animals, hypertension can be induced by the continuous intravenous infusion of small doses of angiotensin II that are not sufficient to evoke an immediate pressor response. However, this condition resembles the characteristics of essential hypertension because the high levels of blood pressure exist with normal plasma levels of angiotensin II. It is suggested that small amounts of angiotensin whose plasma levels are inappropriate for the existing size of extracellular volume stimulate oxidative stress which binds nitric oxide forming peroxynitrite. The latter compound oxidizes arachidonic acid producing isoprostaglandin F2a (an isoprostane) which is characterized by a strong antinatriuretic vasoconstrictor renal effect. In this chain of reactions the vasoconstrictor effects derived from oxygen quenching of nitric oxide and increased isoprostane synthesis could explain how hypertension is maintained with normal plasma levels of renin. Correspondence

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Subpressor angiotensin infusion, renal sodium handling, and salt-induced hypertension in the dog.

Cited by 82 publications

References 33 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

Responsiveness vs. basal activity of plasma ANG II as a determinant of arterial pressure salt sensitivity

Oxidative stress may explain how hypertension is maintained by normal levels of angiotensin II

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