Renin–Angiotensin–Aldosterone System and the Renal Regulation of Sodium, Potassium, and Blood Pressure Homeostasis

Laragh, John H.; Sealey, Jean E.

doi:10.1002/cphy.cp080231

Cited by 40 publications

(30 citation statements)

References 742 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Furthermore, as we observed, such positional change generally increases the natriuresis by about 100%, to be compared with the further 400% natriuresis increase observed after NEP-I in Htx. 3,[37][38][39] Thus, both the magnitude and the time course of natriuresis after moving to the supine position, in view of the length of our baseline period, support that the further natriuresis increase observed after NEP-I is because of the drug activity. Several studies demonstrated that NEP-I, including ecadotril, has either no effect or decreases BP in normal subjects and in heart failure, renal failure, cirrhosis, and hypertensive patients.…”

Section: Study Limitationssupporting

confidence: 57%

Enhanced Natriuretic Response to Neutral Endopeptidase Inhibition in Heart-Transplant Recipients

Gény¹,

Hardy²,

Lonsdorfer³

et al. 1999

Hypertension

View full text Add to dashboard Cite

Abstract-Heart-transplant recipients (Htx) generally present with body fluid and sodium handling abnormalities and hypertension. To investigate whether neutral endopeptidase inhibition (NEP-I) increases endogenous atrial natriuretic peptide (ANP) and enhances natriuresis and diuresis after heart transplantation, ecadotril was given orally to 8 control subjects and 8 matched Htx, and levels of volume-regulating hormones and renal water, electrolyte, and cyclic guanosine monophosphate (cGMP) excretions were monitored for 210 minutes. Baseline plasma ANP, brain natriuretic peptide (BNP), and cGMP were elevated in Htx, but renin and aldosterone, like urinary parameters, did not differ between groups. NEP-I increased plasma ANP (Htx, 20.6Ϯ2.3 to 33.2Ϯ5.9 pmol/L, PϽ0.01; controls, 7.7Ϯ1.2 to 10.6Ϯ2.6 pmol/L) and cGMP, but not BNP. Renin decreased similarly in both groups, whereas aldosterone decreased significantly only in Htx. Enhanced urinary sodium (1650Ϯ370% versus 450Ϯ150%, Pϭ0.01), cGMP, and water excretions were observed in Htx and urinary cGMP positively correlated with natriuresis in 6 of the Htx subjects. Consistent with a normal circadian rhythm of blood pressure, without excluding a possible effect of NEP-I, mean systemic blood pressure increased similarly in both groups at the end of the study (6.9Ϯ2.0% versus 7.4Ϯ2.8% in controls and Htx). Thus, systemic hypertension, mild renal impairment, and raised plasma ANP levels are possible contributory factors in the enhanced natriuresis and diuresis with NEP-I in Htx. These results support a physiological role for the cardiac hormone after heart transplantation and suggest that long-term studies may be useful to determine the potential of NEP-I in the treatment of sodium retention and water retention after heart transplantation.

show abstract

Section: Study Limitationssupporting

confidence: 57%

Enhanced Natriuretic Response to Neutral Endopeptidase Inhibition in Heart-Transplant Recipients

Gény¹,

Hardy²,

Lonsdorfer³

et al. 1999

Hypertension

View full text Add to dashboard Cite

show abstract

“…[23][24][25][26][27] PRA was measured with a standard radioimmunoassay technique to ensure that the hemodilution procedure (see below) had not caused a reduction in circulating blood volume, which would have stimulated renin secretion. 28 This also was ensured through measurements of RA diameter with M-and B-mode echocardiography. 29 Plasma endothelin-1 was measured with radioimmunoassay after extraction from plasma with C18 Sep-Pak Cartridges (Millipore), as described in detail elsewhere.…”

Section: Measurementsmentioning

confidence: 99%

Hemodilution Reduces Clinic and Ambulatory Blood Pressure in Polycythemic Patients

et al. 1998

View full text Add to dashboard Cite

Abstract-Limited information is available for humans on whether blood viscosity affects total peripheral resistance and, hence, blood pressure. Our study was aimed at assessing the effects of acute changes in blood viscosity on both clinic and 24-hour ambulatory blood pressure (BP) values. In 22 normotensive and hypertensive patients with polycythemia, clinic and 24-hour ambulatory BPs were measured before and 7 to 10 days after isovolumic hemodilution; this was performed through the withdrawal of 400 to 700 mL of blood, with concomitant infusion of an equivalent volume of saline-albumin solution. Hematocrit, plasma renin activity, plasma endothelin-1, right atrial diameter (echocardiography), and blood viscosity were measured under both conditions. Plasma renin activity and right atrial diameter were used as indirect markers of blood volume changes. Plasma endothelin-1 was used to obtain information on a vasomotor substance possibly stimulated by our intervention, which could counteract vasomotor effects. Isovolumic hemodilution reduced hematocrit from 0.53Ϯ0.05 to 0.49Ϯ0.05 (PϽ.01). Plasma renin activity, plasma endothelin-1 and right atrial diameter were unchanged. Clinic blood pressure was reduced by hemodilution (systolic, 144.3Ϯ5.4 to 136.0Ϯ3.9 mm Hg[meanϮSEM]; diastolic, 87.0Ϯ2.8 to 82.1Ϯ2.6 mm Hg, PϽ.05 for both) and a reduction was observed also for 24-hour average ABP (systolic, 133.6Ϯ2.9 to 129.5Ϯ2.7 mm Hg; diastolic, 80.0Ϯ2.0 to 77.3Ϯ1.7 mm Hg, PϽ.05 for both). The reduction was consistent in hypertensive patients (nϭ12), whereas in normotensive patients (nϭ10) it was small and not significant. Both clinic and 24-hour average heart rates were unaffected by the hemodilution. Thus, in polycythemia, reduction in blood viscosity without changing blood volume causes a significant fall in both clinic and 24-hour ambulatory BPs; this is particularly true when, as can often happen, blood pressure is elevated. This emphasizes the importance this variable may have in the determination of blood pressure and the potential therapeutic value of its correction when altered. (Hypertension. 1998;31:848-853.)Key Words: blood viscosity Ⅲ hemodilution Ⅲ blood pressure monitoring, ambulatory Ⅲ hemorheology B P is determined by cardiac output and peripheral vascular resistance. The latter depends to a large degree on the caliber and length of arterioles. It also depends, however, on blood viscosity, with which it bears a linear relationship over a wide range of values. 1Although studied extensively in animals, 2-5 the effects of blood viscosity on human BP have received only limited attention except for (1) the epidemiological evidence that there is a relationship between hematocrit and BP levels in both normotensive and hypertensive subjects 6 -15 and (2) the clinical evidence of an increased prevalence of hypertension in subjects with secondary eritrocytosis and polycythemia. 16,17 In particular, no information is available on the BP effects of interventions that reduce blood viscosity (ie, whether this maneuver induces...

show abstract

“…Dietary sodium chloride intake is sensitively tracked by reciprocal changes in renin activity 39 and subsequently by angiotensin II and aldosterone levels. Traditionally, modulation by aldosterone of cortical collecting tubule sodium transport has been held to be important in the renal excretory response to altered dietary salt.…”

Section: Efferent Limb Of Extracellular Volume Regulationmentioning

confidence: 99%

Angiotensin II: a powerful controller of sodium transport in the early proximal tubule.

1990

View full text Add to dashboard Cite

Angiotensin II has recently been shown to exert potent control over sodium and water absorption in the proximal convoluted tubule. This transport stimulation is effected by receptors on both the luminal and basolateral membranes of cells located predominantly in the early, S, proximal tubule. Angiotensin II increases transport primarily by a G f proteinmediated reduction in intracellular cyclic adenosine monophosphate, which enhances the affinity of the Na + -H + antiporter. Change in early proximal acidification ultimately causes alteration in the amount of sodium chloride leaving the proximal tubule and entering the urine. et al 4 was very small. The maximal response was only 16% above the baseline value and was trivial (0.1 nl/mm • min) compared with the normal amount of fluid reabsorbed by the PCT in vivo (18 nl/min). 5The studies described above were performed in the late (S 2 ) subsegment of the PCT. With recent adaptation in micropuncture techniques, it is now recognized that the early (S^ PCT subsegment of the rat has a far more robust capacity for both active and passive transport than the S 2 PCT, or for that matter, any other nephron segment.56 Indeed, although the S, PCT is only a little over 1 mm in length in the rat, it is normally responsible for reabsorbing fully 20% of the solute and water that is filtered by the kidney. 5Were angiotensin II to control this powerful Si PCT transport system, it would obviously have substantial potential for regulating renal sodium and water reabsorption.As shown in Figure 1, angiotensin II does indeed have a potent effect on Si PCT sodium and water transport in the Munich-Wistar rat.7 -9 Angiotensin II infusion (20 ng/kg • min i.v.), which achieves a subpressor, systemic concentration within the physiological range (10~1 2 to 10~n M), augmented S, PCT water absorption by 2.5 nl/mm • min (closed squares) when measured by in vivo microperfusion.

show abstract

Renin–Angiotensin–Aldosterone System and the Renal Regulation of Sodium, Potassium, and Blood Pressure Homeostasis

Abstract: The sections in this article are: Historical Background Renin Aldosterone A Coordinated Renal‐Adrenal Hormonal System: Renin, Angiotensin, and Aldosterone Comparative Aspects Brief Overview of the Renin‐Angiotensin‐Aldosterone System Biochemistry and Molecular Biology o… Show more

Cited by 40 publications

References 742 publications

Enhanced Natriuretic Response to Neutral Endopeptidase Inhibition in Heart-Transplant Recipients

Enhanced Natriuretic Response to Neutral Endopeptidase Inhibition in Heart-Transplant Recipients

Hemodilution Reduces Clinic and Ambulatory Blood Pressure in Polycythemic Patients

Angiotensin II: a powerful controller of sodium transport in the early proximal tubule.

Contact Info

Product

Resources

About