The response of plasma aldosterone to exogenous angiotensin II was evaluated in five normal volunteers on three occasions, once without endogenous ACTH or angiotensin II suppression (control), once with ACTH suppression (dexamethasone) and once with ACTH and angiotensin II suppression (dexamethasone and captopril). Plasma aldosterone concentration (PAC) fell from a control of 6.8 +/- 1.6 (mean +/- SEM) to 4.4 +/- 0.4 ng/dl with dexamethasone (p less than 0.05) and to 1.8 +/- 0.2 ng/dl with dexamethasone and captopril (p less than 0.001). PAC increased dose-dependently upon infusion rates of angiotensin II (0.2, 0.4, 0.8, 1.0, 1.2, 2.5 and 5.0 ng/kg/min) on each occasion, but aldosterone responsiveness to infused angiotensin II (change and percentage from base line levels) was not altered by the suppression of endogenous ACTH secretion with dexamethasone with each incremental infusion of the octapeptide. However, change in PAC caused by angiotensin II in the suppression of ACTH and angiotensin II was greater than that in the control at an infusion rate of 0.2 ng/kg/min (p less than 0.05), 1.2 ng/kg/min (p less than 0.05) and 2.5 ng/kg/min (p less than 0.01), and it was also greater than that in the suppression of ACTH at an infusion rate of 0.2 ng/kg/min (p less than 0.05) and 2.5 ng/kg/min (p less than 0.01). These results demonstrate that in normal men, base line aldosterone levels are controlled not only by the renin-angiotensin system, but also, in part, by ACTH. The aldosterone response to angiotensin II, however, does not depend upon endogenous ACTH secretion, an action of angiotensin II on the pituitary to release ACTH. Simultaneous administration of dexamethasone and captopril may be a useful tool to assess the sensitivity of aldosterone production in the adrenal glomerulosa with exogenous angiotensin II since endogenous ACTH and angiotensin II can be suppressed by these medications.

Adult↗

PubMed1981

[The correlation between serum angiotensin I-converting enzyme activity and the renin-angiotensin-aldosterone system in hypertensive patients (author's transl)].

In order to investigate the role and origin of serum angiotensin I-converting enzyme activity (ACEA) in hypertension, the correlation between serum ACEA and the renin-angiotensin-aldosterone system was evaluated in hypertensive patients of whom 36 had essential hypertension, five had hypertension associated with chronic renal failure, three had renovascular hypertension, and one had primary aldosteronism. Serum ACEA was 17.0 +/- 3.3 U (mean +/- sd) in the normotensive control, 20.1 +/- 7.1 U in patients with essential hypertension, 11.6 +/- 3.4 U in patients with chronic renal failure, 31.7 +/- 1.1 U in patients with renovascular hypertension, and 9.7 U in primary aldosteronism in a recumbent state. There was a significant correlation between serum ACEA and plasma renin activity (PRA) (r = 0.615, p less than 0.001, n = 45) and plasma aldosterone concentration (PAC) (r = 0.599, p less than 0.001, n = 34) in a recumbent state. However, there was no significant correlation between serum ACEA and mean blood pressure. Serum ACEA elevated with furosemide and an upright posture significantly correlated with elevation in PRA (r = 0.369, p less than 0.05, n = 32) but did not significantly correlate with elevation in PAC. It is suggested, therefore, that the kidney is the suspected source of the plasma activity of the enzyme and that serum ACEA plays a possible role in the regulations of blood pressure and electrolyte metabolism modulating the renin-angiotensin-aldosterone system.

Adult↗

PubMed1981

[A simple and rapid assay for the determination of plasma, urine and tissue catecholamine concentrations by high pressure liquid chromatography with fluorescent reaction (author's transl)].

The method of determining catecholamines has been studied, and such sensitive methods as radioenzymatic assay and gas chromatography are used for their measurement, but these techniques are not widespread because of their complexity. In this study, we developed a high pressure liquid chromatographic method with a fluorescent reaction system for the determination of plasma, urine and tissue catecholamine concentration. The eluates from plasma, urine and tissue were chromatographied on a Hitachi #3011C Gel (2.6 x 250mm) and reacted to the mixed solution of 0.1M KH2PO4, 0.2M K2HPO4 and 0.0075% K3Fe(CN)6 (the first solution), followed by the mixture of 0.1% ascorbic acid and 5N NaOH. A stock solution (0.1mg/ml of norepinephrine, 0.1mg/ml of epinephrine and 2.0mg/ml of dopamine) was stored in 0.2N CH3COOH at 4 degrees C, and was diluted at 1/5,000-1/40,000 when needed. Recovery of norephinephrine after extraction was 54.3-58.9% and that of epinephrine was 49.2-55.8%. The accuracy was acceptable and sensitivity was 30-50pg. The mean plasma norepinephrine concentrations (p-NE) were 105.6 +/- 6.8pg/ml in normal subjects and 157.7 +/- 74.5pg/ml in essential hypertensives (EH). The mean epinephrine concentrations (p-E) were 30.8 +/- 16.3pg/ml in normals and 20.0 +/- 11.9pg/ml in EH. PNE increased after standing or after furosemide plus 2-hour standing, but p-E did not increase as much as p-NE. Catecholamine concentration in the rat brain and adrenal medullary tissue could be determined by the use of this method.

Animals↗

PubMed1981

Effect of sodium intake on angiotensin-converting enzyme activity of aorta in rats.

1. The effect of sodium intake on angiotensin-converting enzyme activity in subcellular fractions of aorta (homogenate, mitochondria, microsomes and supernatant) was studied in normotensive and spontaneously hypertensive rats. 2. Angiotensin-converting enzyme activity was extremely high in the supernatant fraction in normotensive and spontaneously hypertensive rats. 3. Total converting enzyme activity in spontaneously hypertensive rats was 34% higher than that in normotensive rats. 4. Increased sodium intake resulted in a marked reduction, almost to zero, of converting enzyme activity in each fraction of aorta in normotensive and spontaneously hypertensive rats. 5. Converting enzyme, widely distributed in subcellular fractions of the aorta, may play a possible rôle in the local control of vascular tone. It is likely that sodium intake inhibits production of the enzyme in vascular tissue.

Animals↗

PubMed1981

A possible role of the brain angiotensin II receptor binding in development of hypertension.

To clarify a role of brain angiotensin II receptor binding in development of hypertension, the regional distribution and extent of specific angiotensin II binding were studied in salt-loaded normotensive (NTR) and spontaneously hypertensive (SHR) rats, and Goldblatt one-kidney hypertensive rat (GB). Further, angiotensin-converting enzyme activity was measured in these rats' brains. In control rats, angiotensin Ii receptor binding was consistently lower in the thalamus, hypothalamus, midbrain, striatum and cortex of SHR rats than in NTR rats. In GB rats, the binding capacity in the thalamus was greater than that of NTR rats. Sodium intake resulted in a rise in the receptor binding capacity in the hypothalamus, thalamus and striatum of SHR rat, whereas it did in a fall in the binding capacity in the hypothalamus, thalamus, striatum, midbrain and cortex of NTR rats. Angiotensin-converting enzyme activity was significantly elevated in the midbrain of salt-loaded SHR rats.

Angiotensin II↗

PubMed1981

Methacholine, a cholinergic agent, stimulates catecholamine release in man.

To study the effect of cholinergic stimulation on catecholamine release, methacholine, a choline ester, was injected im into normal subjects. Significant increases in plasma norepinephrine and plasma epinephrine concentrations were observed in response to methacholine administration with significant haemodynamic changes, but there was no correlation between the rise in plasma catecholamines and the haemodynamic changes. These results suggest that the increases in plasma catecholamines induced by methacholine did not result from reflex responses to haemodynamic changes and thus could be a direct effect of methacholine on sympathetic nerves and the adrenal medulla.

Adult↗

PubMed1981

Effect of sodium intake on the brain and the aortic angiotensin-converting enzyme activity in spontaneously hypertensive rat.

Effect of sodium intake on angiotensin-converting enzyme activity was studied in five areas of the brain (cerebral cortex, midbrain, striatum, thalamus and hypothalamus) and in subcellular fractions of the aorta (homogenate, mitochondria, microsomes and supernatant) in normotensive, spontaneously hypertensive, and stroke-prone spontaneously hypertensive rats. Angiotensin-converting enzyme activity was significantly higher in the hypothalamic area than in the other areas of the brain in spontaneously hypertensive rat. The enzyme activity of subcellular fractions of the aorta showed an extremely high value in the supernatant in normotensive, spontaneously hypertensive, and stroke-prone spontaneously hypertensive rats. Sodium intake resulted in a marked decrease in the aortic converting enzyme activity, while it did in a significant rise of the enzyme activity in the midbrain area in spontaneously hypertensive rat, and in the midbrain and striatum areas in stroke-prone spontaneously hypertensive rat. It is likely therefore that sodium intake lowers the converting enzyme activity of the aorta. Increased converting enzyme activity of the brain in spontaneously hypertensive rats may play a possible role in hypertension induced by sodium intake.

Animals↗

PubMed1981

Antihypertensive effect of the oral angiotensin I-converting enzyme inhibitor in long-term treatment of hypertensive patients.

Antihypertensive effect of an orally active angiotensin I-Converting enzyme inhibitor, SQ 14225 (Captopril) was assessed in 18 hypertensive patients, of whom 13 had essential hypertension, 2 had malignant hypertension, 2 had hypertension associated with chronic renal failure, and 1 had renovascular hypertension. Blood pressure decreased markedly not only in patients with high renin levels but also in those with low renin levels. Nevertheless, the magnitude of blood pressure reduction was correlated with the pre-treatment plasma renin activity (r =-0.64, p less than 0.01 systolic, r =- 0.60, p less than 0.05 diastolic). There was a significant correlation between the fall in mean blood pressure and the decrease in plasma aldosterone concentration 3 weeks after treatment (r = 0.64, p less than 0.05). The serum potassium elevated from 4.2 +/- 0.4 to 4.8 +/-0.9 mEq/L (p less than 0.05), and the change correlated inversely with the reduction of plasma aldosterone concentration (r = 0.71, p less than 0.02), while serum sodium slightly decreased from 140-+/- 2 to 138 +/- 3 mEq/L. There was neither finding of orthostatic hypotension nor escape from the antihypertensive effect. These results indicate that chronic inhibition of angiotensin I-converting enzyme with an orally active compound offers an effective and well-tolerated approach to treatment of hypertension.

Adult↗

PubMed1981

Effect of sodium intake on brain angiotensin-converting enzyme activity in spontaneously hypertensive rat.

The effect of sodium intake on angiotensin-converting enzyme activity in five areas of the brain (the cerebral cortex, midbrain, striatum, thalamus and hypothalamus) was studied in normotensive, spontaneously hypertensive and stroke-prone spontaneously hypertensive rats. The enzyme activity was significantly higher in the hypothalamus than in other areas of the brain of spontaneously hypertensive rats. Sodium intake resulted in a significant rise of the enzyme activity in the midbrain of spontaneously hypertensive rats and also in the midbrain and the striatum of stroke-prone spontaneously hypertensive rats. In normotensive rats, however, there was no significant difference in the enzyme activity in any area of brain between the control and the salt-treated group. It is likely therefore that a high circulating sodium level increases angiotensin-converting enzyme content of the brain in spontaneously hypertensive rats, and it is suggested that the increased converting-enzyme activity may play a role in development of hypertension induced by sodium loading.

Animals↗

PubMed1981

Brain angiotensin-converting enzyme activity in experimental hypertensive rats.

Angiotensin-converting enzyme (ACE) activity was measured in six areas of the brain of normotensive and experimental hypertensive rats; one-clip, one-kidney (1-c, 1-k) and one-clip, two-kidney (1-c, 2-k) Goldblatt hypertensive (GH) rats. ACE activity was consistently high in the thalamus of normotensive and both 1-c, 1-k and 1-c, 2-k GH rats. However, the enzyme activity in the hypothalamus of 1-c, 2-k GH rats was significantly higher than that of normotensive rats, while there was no significant difference in the enzyme activity between normotensive and 1-c, 1-k GH rats. These results demonstrate that in 1-c, 2-k GH rats, increased ACE activity in the brain may play a central role in the hypertension.

Animals↗

PubMed1981

[Effect of sodium intake on the brain and the aortic angiotensin-converting enzyme activity in spontaneously hypertensive rat (author's transl)].

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Animals↗

PubMed1981

[A case report of so-called postoperative erythroderma after aorto-coronary bypass (author's transl)].

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Coronary Artery Bypass↗