Angiotensin II, aldosterone and arginine vasopressin in plasma in congestive heart failure

Abstract

Angiotensin II (AII), aldosterone (Aldo) and arginine vasopressin (AVP) in plasma were determined during basal conditions in seventeen patients with congestive heart failure and in seventeen control subjects. The same parameters were measured before and 1, 2 and 3 h after an oral water load of 20 ml (kg body weight)-1 together with urine volume (V) and free water clearance (CH2O) in seven patients with congestive heart failure and in seven control subjects. AII, Aldo and AVP were significantly higher in heart failure than in control subjects (AII:81 and 12 pmol l(-1) (medians), P less than 0.01; Aldo: 411 and 103 pmol l(-1), P less than 0.01; AVP: 5.3 and 2.0 pmol l)-1), P less than 0.01). AVP was positively correlated to Aldo in both heart failure (p = 0.593, n = 17, P less than 0.02) and control subjects (p = 0.511, n = 17, P less than 0.05), but in neither of the groups to AII. V and CH2O were significantly lower in heart failure when compared to control subjects (maximum increase in CH2O 3.55 and 5.86 ml min-1, P less than 0.02), but did not correlate directly with either A II, Aldo or AVP. Creatinine clearance was reduced in heart failure. It is concluded that the activity of both the renin-angiotensin-aldosterone system and the osmoregulatory system is enhanced in congestive heart failure, presumably as a compensatory phenomenon in order to maintain arterial blood pressure. It is suggested that the decrease in free water clearance may be attributed to both an elevated level of vasopressin and a reduced glomerular filtration rate.

Endothelin-A Receptors Mediate Renal Hemodynamic Effects of Exogenous Angiotensin II in Humans

“…27 Previous human studies performed under similar experimental conditions have shown that plasma Ang II may increase from 15 to 57 pmol/L after a 2-hour infusion of 1.5 ng/kg per minute 29 or from 20 to 25 to 50 to 70 pmol/L with stepwise increasing doses of Ang II from 0.3 to 3.0 ng/kg per minute each for 30 minutes. 28 Such levels of plasma Ang II were roughly the same observed in human pathophysiological conditions such as CHF 31 and renovascular hypertension. 32 Thus, although we could not measure plasma Ang II, our infusion protocol was designed in the assumption that a stepwise increasing rate of 0.625 to 2.5 ng/kg per minute Ang II would have produced a progressive elevation in plasma Ang II from low baseline levels toward physiological and, later, pathophysiological concentrations.…”

Effects of ACE inhibition with cilazapril on splanchnic and systemic haemodynamics in man.

“…Thus, the sensitivity to AI within the splanchnic vascular bed, as indicated by SVR increase, was diminished to a value of 0.2 ± 0.1 after cilazapril, indicating that at AII plasma concentrations comparable with those in congestive heart failure (Staroukine et al, 1984;Pedersen et al, 1986) the splanchnic vasoconstriction was strongly suppressed. It therefore appears that the ACE inhibition may be beneficial in avoiding splanchnic (mesenterial) vasoconstriction and that this may be of clinical importance in haemodynamic conditions accompanying congestive heart failure (Staroukine et al, 1984;Menge, 1986;Bailey et al, 1987).…”

“…Thus, RAS-dependent vasoconstriction reaches greatest importance in patients with congestive heart failure and other low cardiac output states (McNeill et al, 1970(McNeill et al, , 1982Staroukine et al, 1984;Bailey et al, 1987). It was demonstrated that in most patients with myocardial pump failure not only were increased catecholamine plasma levels found (Vignerat et al, 1985), but also plasma renin activity and AII plasma concentrations were elevated (Pedersen et al, 1986), AII being positively correlated with PCWP and negatively correlated with CO, thus, reflecting the severity of myocardial failure (Staroukine et al, 1984).…”

“…As a controlled study in severely ill patients with established pronounced mesenterial vasoconstriction was not feasible we investigated in a clinical pharmacological model the influence of cilazapril on AI-dependent changes in splanchnic haemodynamics by raising AII plasma concentrations to levels comparable with those in patients with severe heart failure (Staroukine et al, 1984;Pedersen et al, 1986). In our experimental model the splanchnic circulation was, rather simplistically, treated as a single hypothetical vascular bed; the blood flow control mechanisms to individual splanchnic organs being ignored.…”

Association between plasma concentration of tolvaptan and urine volume in acute decompensated heart failure patients with fluid overload

“…Neurohumoral factors including RAAS factors increase fluid retention [17]. Angiotensin-II, in particular, increases vasopressin, which weakens the effect of TLV somewhat, and aldosterone, which is the final product of the RAAS, increases retention of sodium and water in the renal tubules and is thus thought to act against the effects of TLV [18][19][20]. Neither carperitide nor any inotropic agent that would enhance RAAS activity in patients with ADHF was used in this study.…”