Stimulation of renal sodium reabsorption by angiotensin II

Johnson, Michael D.; Malvin, Richard L.

doi:10.1152/ajprenal.1977.232.4.f298

Cited by 59 publications

(42 citation statements)

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“…Inhibiting AT 1 receptors markedly increased the FENa in the presence of a modest fall in MAP, suggesting that the increase in FENa can be attributed to the withdrawal of the antinatriuretic effect of Ang II. Indeed, low doses of Ang II are well known to directly increase proximal tubular reabsorption of sodium 9,24,25 and also stimulate distal reabsorption through stimulation of aldosterone secretion. 26 However, since AT 1 blockade also increased RBF and GFR, the increased FENa may have also been due to increased renal interstitial pressure subsequent to the elevation in RBF and GFR.…”

Section: Relative Role Of Ang II Through Its At 1 Receptor Et No Amentioning

confidence: 99%

Interactions Between Vasoconstrictors and Vasodilators in Regulating Hemodynamics of Distinct Vascular Beds

Gómez-Alamillo¹,

Juncos²,

Cases³

et al. 2003

Hypertension

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Abstract-We examined whether interactions between angiotensin II (Ang II), endothelin (ET), nitric oxide (NO), and prostaglandins (PGs) differentially regulate perfusion to distinct vascular beds. For this, we blocked either angiotensin AT 1 or ET receptors or both and then sequentially inhibited NO and PG synthesis in anesthetized dogs. Blocking Ang II or ET had similar effects on systemic hemodynamics: Mean arterial pressure fell slightly without altering cardiac output. Blocking both caused a synergistic fall in mean arterial pressure and increased cardiac output. Pulmonary vascular resistance was not altered by blocking Ang II, ET, or both but progressively increased during NO and PG blockade in group 2 (which had unblocked ET receptors), suggesting that endogenous ET exerts pulmonary vasoconstriction that is tempered by NO and PGs. In the kidney, blocking Ang II increased regional blood flow (RBF), glomerular filtration rate (GFR), and fractional excretion of sodium (FENa). In contrast, blocking ET did not alter RBF, and it decreased GFR and FENa. Combined Ang II and ET blockade markedly increased RBF without altering GFR, and FENa was maintained at the levels as when only ET was blocked. Sequentially inhibiting NO and PGs decreased RBF when Ang II or ET were blocked but had little effect when both were blocked. Finally, Ang II or ET blockade did not alter iliac blood flow. Inhibiting NO and PGs decreased iliac blood flow when Ang II or ET but not both were blocked. These results suggest that regional differences in the interactions between endogenous Ang II, ET, NO, and PGs are important determinants in systemic, pulmonary, and regional hemodynamics. Key Words: endothelin Ⅲ angiotensin II Ⅲ nitric oxide Ⅲ prostaglandins Ⅲ hemodynamics Ⅲ natriuresis T he maintenance of mean arterial pressure (MAP) depends on a critical equilibrium between renal perfusion and systemic blood pressure. 1 In general, increments of renal perfusion pressure trigger compensatory mechanisms that tend to lower MAP, whereas the opposite occurs when renal perfusion pressure is decreased. To a large extent, these cardiorenal interactions are enacted by the participation of humoral systems such as renin angiotensin, prostaglandins (PGs), nitric oxide (NO) and as revealed in more recent studies by endothelin (ET). Because of this, numerous studies have evaluated the effects of angiotensin II (Ang II), ET, NO donors, and PGs by infusing 2-5 or blocking one or more of these vasoactive factors. 6 -10 However, the relative role that each one of these vasoactive factors plays in regulating regional hemodynamics remains incompletely understood. Therefore, the aim of the present study was to determine the relative role of endogenous Ang II, ET, NO, and PGs (as well as their interactions) in regulating systemic and regional hemodynamics (with particular emphasis on renal function) in normal anesthetized dogs. For this purpose, we blocked the effects of either Ang II with the intravenous administration of L158,810 (a selective AT 1 receptor antag...

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Section: Relative Role Of Ang II Through Its At 1 Receptor Et No Amentioning

confidence: 99%

Interactions Between Vasoconstrictors and Vasodilators in Regulating Hemodynamics of Distinct Vascular Beds

Gómez-Alamillo¹,

Juncos²,

Cases³

et al. 2003

Hypertension

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“…Kimbrough et al 41 have indicated that intra-renal angiotensin II may promote the conservation of salt and water. Johnson and Malvin 43 have suggested that angiotensin II exerts a direct stimulatory effect on tubular sodium reabsorption independent of changes in renal blood flow or glomerular filtration rate. We would like to speculate that the 50% greater PRA values observed in the relatives before, and 33% greater PRA values immediately after, the intravenous sodium loads may have resulted in increased angiotensin II levels, which may have impeded the natriuretic responses of the relatives.…”

Section: -41mentioning

confidence: 99%

An approach to the evaluation of genetic influences on factors that regulate arterial blood pressure in man.

Grim¹,

Luft²,

Miller³

et al. 1980

Hypertension

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SUMMARY To assess the influence of heredity on factors that help regulate the arterial blood pressure in man, we conducted sodium-loading and depletion studies in monozygotic and dizygotic twins, normotensive first-degree relatives of essential hypertensives, and in nonnotenslve control subjects matched for age, sex, and race. Following sodium-loading, we found evidence for the influence of genetic variance on the natriuretic responses, plasma renin activity (PRA), plasma aldosterone concentrations (PA), and plasma and urinary norepinephrine. Relatives of hypertensives differed from controls in that they had higher blood pressures, greater renin values, and relatively sluggish natriuretic responses. Since renin and fractional sodium excretion values were inversely correlated in all subject groups, it is possible that the heritable influences we observed on sodium excretion were mediated by the renin-angiotensin-aldosterone system. 79 the nature of these influences has not been defined clearly. To examine inherited mechanisms that may contribute to the development of essential hypertension in some individuals, or the resistance to hypertension in others, we conducted detailed studies of monozygotic and dizygotic normotensive twins, normotensive firstdegree relatives of essential hypertensives, and large numbers of normotensive white and black subjects by means of a standardized protocol incorporating both sodium-loading and depletion. "14 In these studies we examined electrolyte balance, components of the renin-angiotensin-aldosterone system, and humoral indicators of sympathetic nervous system activity. The studies in twins 1-34fluences in each of these areas. The studies in normotensive, first-degree relatives of essential hypertensives indicated the existence of important differences in electrolyte excretion and peripheral renin values that may contribute to the susceptibility to hypertension of this high-risk group." We present these findings in light of their bearing on the importance of heredity in regulating blood pressure in man. Methods Studies in TwinsData from monozygotic (MZ) and dizygotic (DZ) twins provide a unique opportunity to test for the existence of genetic variation in traits. Since MZ twins are genetically identical and DZ twins are related as full siblings, a given trait would be expected to exhibit smaller twin-pair differences for MZ than DZ twins if genetic influences are present. On the other hand, if the trait is only influenced by environmental variability, the MZ and DZ twin-pair differences should be approximately equal.The statistical methods involved in the analysis of MZ and DZ twin data have been recently reviewed by Christian. 16 We chose the comparison of MZ and DZ twins as the most efficient method for the initial investigation of heritable components in quantitative by guest on May 11, 2018 http://hyper.ahajournals.org/ Downloaded from

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“…However as we have not measured renal blood flow in our study we cannot exclude intrarenal haemodynamic changes. Nevertheless it has been demonstrated that low doses of AII can decrease sodium excretion in animals and man without changes in GFR or renal plasma flow (Johnson & Malvin, 1977;Ljungman et al, 1983), and without changing the intrarenal distribution of blood flow in animals (Johnson & Malvin, 1977). Similarly low dose infusion of NA and low frequency renal SNS stimulation in animals can reduce sodium excretion without affecting GFR, renal blood flow or distribution of intrarenal blood flow (Slick et al, 1975;DiBona, 1978;Johnson & Barger, 1981).…”

Section: Discussionmentioning

confidence: 99%

The effect of angiotensin II and noradrenaline alone and in combination on renal sodium excretion in man.

Seidelin

McMurray

Brown

et al. 1989

Brit J Clinical Pharma

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1 The renin-angiotensin-aldosterone-system is important for the maintenance of sodium balance in man. Recent animal evidence suggests the anigiotensin II can modulate the effect of the renal sympathetic nervous system on renal function. We have investigated the possible interaction of physiological doses of angiotensin II and noradrenaline on sodium excretion in man. 2 Seven normal volunteers were studied on four occasions during maximum water diuresis sustained by oral hydration. Samples were obtained during a baseline and four subsequent 20 min periods (A-E). Placebo or noradrenaline was infused over periods B-E, and angiotensin II infused over period C. 3 There was no change in systemic blood pressure, heart rate or creatinine clearance caused by infusion of either angiotensin II, noradrenaline or both in combination. 4 Noradrenaline alone caused a significant fall in absolute and fractional sodium excretion. Angiotensin II when infused with placebo caused a 37% fall in absolute sodium excretion and a 32% fall when infused with noradrenaline (no significant difference between the 2 days). Similar changes were seen for urinary flow and fractional sodium excretion. 5 We have therefore found no evidence to support a postsynaptic interaction of low doses of angiotensin II and noradrenaline on renal sodium excretion in man.

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Stimulation of renal sodium reabsorption by angiotensin II

Cited by 59 publications

References 0 publications

Interactions Between Vasoconstrictors and Vasodilators in Regulating Hemodynamics of Distinct Vascular Beds

Interactions Between Vasoconstrictors and Vasodilators in Regulating Hemodynamics of Distinct Vascular Beds

An approach to the evaluation of genetic influences on factors that regulate arterial blood pressure in man.

The effect of angiotensin II and noradrenaline alone and in combination on renal sodium excretion in man.

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