Measurement of Concentrations of Angiotensin I in Human Blood by Radioimmunoassay

Waite, Marion

doi:10.1042/cs0450051

Cited by 53 publications

(26 citation statements)

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“…On days 1 and 8 at times 0 and again 6 h and 24 h after drug administration, measurements were made of plasma active renin concentration (normal range 10-50 mu/l) (Millar et al, 1978), blood angiotensin I (normal range 3-15 pmol/l) (Waite, 1973), plasma angiotensin II (normal range 5-35 pmol/l) (Atkinson et al, 1980), plasma aldosterone (normal range < 500 pmol/l) (Fraser et al, 1973), plasma cortisol (normal range 140-700 nmol/l) and serum converting enzyme activity (ACE) (Cushman & Cheung, 1971;Anderson et al, 1981). As (Miller, 1966 Supine heart rate did not change with treatment and there were similar rises of pulse rate with both compounds and with placebo on standing.…”

Section: Introduction Methodsmentioning

confidence: 99%

Enalapril (MK421) and its lysine analogue (MK521): a comparison of acute and chronic effects on blood pressure, renin‐angiotensin system and sodium excretion in normal man.

Hodsman¹,

Zabludowski²,

Zoccali³

et al. 1984

Brit J Clinical Pharma

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The immediate and long‐term effects of enalapril (MK421) and its lysine analogue (MK521) in once‐daily dosage, were compared in a study of 12 normal subjects. Both compounds lowered blood pressure equally throughout 24 h without causing tachycardia. The biochemical changes with MK521 were more sustained than with MK421, but this did not affect the magnitude of blood pressure reduction. Twenty‐four hours after the previous dose, with both active drugs, plasma renin concentration was significantly higher on day 8 than on day 1, though angiotensin I did not increase in proportion; this probably reflects a fall in renin‐ substrate with prolonged converting enzyme inhibition. There was an early natriuresis with each compound but this effect was no longer apparent after 8 days of continuous therapy. Both MK421 and MK521 were well tolerated with no serious side effects.

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Section: Introduction Methodsmentioning

confidence: 99%

Enalapril (MK421) and its lysine analogue (MK521): a comparison of acute and chronic effects on blood pressure, renin‐angiotensin system and sodium excretion in normal man.

Hodsman¹,

Zabludowski²,

Zoccali³

et al. 1984

Brit J Clinical Pharma

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“…The characteristics of these methods in our laboratory have been described previously . Angiotensin I levels were determined using a method which is a modification of that described by Waite (1973). The serum drug concentrations were measured by radioimmunoassay (Hichens et al, 1981).…”

Section: Methodsmentioning

confidence: 99%

Enalapril maleate and a lysine analogue (MK‐521) in normal volunteers; relationship between plasma drug levels and the renin angiotensin system.

Biollaz¹,

Jl²,

Combes³

et al. 1982

Brit J Clinical Pharma

112

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1 Two single doses of 10 mg each of the converting enzyme inhibitor enalapril maleate or MK-421 and of its lysine analogue (MK-521) were administered p.o. to twelve male volunteers. 2 The active diacid metabolite of MK421 and the lysine analogue were determined by radioimmunoassay and MK-421 by the active metabolite method following in vitro hydrolysis. 3 Peak serum levels of MK-421, active metabolite and lysine analogue were reached within 1, 3 to 4, and 6 h respectively. Practically all MK-421 had disappeared from serum within 4 h. 4 A close correlation between percent inhibition of plasma converting enzyme activity and the serum concentration of active metabolite was observed (r = 0.98, n = 171, P < 0.001). Similarly, converting enzyme blockade as expressed by the ratio plasma angiotensin II/angiotensin I was closely correlated with serum active metabolite levels (r = 0.93, n = 15, P < 0.001).

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“…Thus, this revised concept predicts that plasma levels of angiotensin largely represent a spillover from the tissue sites of production (15). That plasma angiotensins predominantly result from the action of kidney-derived renin on plasma (liver-derived) angiotensinogen is shown by the fall in plasma angiotensin levels that follows nephrectomy (16)(17)(18)(19), and by the hypotensive effect of anti-angiotensinogen antibodies when injected into either sodium-replete or sodium-deplete rats (20). Given this local production ofAl and All by the circulating RAS, it is apparent that such local production may be subject to tissue-specific mechanisms of regulation, which cause changes in local All concentration that are not reflected in the plasma concentrations of renin or All.…”

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confidence: 99%

Circulating and tissue angiotensin systems.

Campbell¹

1987

J. Clin. Invest.

564

167

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Angiotensin has many different actions, most of which relate, either directly or indirectly, to the regulation of blood pressure, fluid, and electrolyte homeostasis (1, 2). In addition to potent vasoconstrictor effects, actions ofangiotensin on vasculature include the stimulation ofprostaglandin release (3), the modulation of angiotensin receptor number (4), and the stimulation of angiogenesis (5). Angiotensin also has important actions on the central and peripheral nervous systems, the adrenal, kidney, intestine, and heart (6-1 1). Given these multiple diverse actions of angiotensin, two important questions are (a) which of these actions represent normal physiological events, and (b) whether such actions may assume a pathogenic role. These questions have recently been placed in sharper focus by the clinical application of inhibitors of the renin-angiotensin system (RAS),' and in particular, the use of converting enzyme inhibitors (CEIs) for the treatment of hypertension. Any attempt to answer these questions requires an accurate concept ofthe RAS. The purpose ofthis review is to discuss new concepts concerning angiotensin production by the circulating RAS, how these relate to angiotensin production within tissues, and the possible mechanisms by which CEIs lower blood pressure. The study of tissue angiotensin systems is still at an early stage. In this review I have attempted to synthesize a coherent model of the interaction between the circulating and tissue angiotensin systems, which might assist in the interpretation of new developments in this area. Circulating RASAt the present time, the prevailing view holds that the circulating RAS is primarily an endocrine system designed for the general mediation, through the systemic circulation, of the effects of renin on angiotensin production in plasma (12,13). This concept can be summarized as follows: renin released by the kidney circulates in plasma, where it cleaves angiotensinogen to generate angiotensin I (Al).

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Measurement of Concentrations of Angiotensin I in Human Blood by Radioimmunoassay

Cited by 53 publications

References 0 publications

Enalapril (MK421) and its lysine analogue (MK521): a comparison of acute and chronic effects on blood pressure, renin‐angiotensin system and sodium excretion in normal man.

Enalapril (MK421) and its lysine analogue (MK521): a comparison of acute and chronic effects on blood pressure, renin‐angiotensin system and sodium excretion in normal man.

Enalapril maleate and a lysine analogue (MK‐521) in normal volunteers; relationship between plasma drug levels and the renin angiotensin system.

Circulating and tissue angiotensin systems.

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