Familial, Dexamethasone-Suppressible, Normokalemic Hyperaldosteronism

PEDIATRICS ◽  
1980 ◽  
Vol 65 (3) ◽  
pp. 597-604
Author(s):  
C. E. Grim ◽  
M. H. Weinberger
Keyword(s):  
Blood Pressure ◽  
Adrenocorticotropic Hormone ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Saline Infusion ◽  
Elevated Blood ◽  
Aldosterone Production ◽  
Renin Level ◽  
Dexamethasone Therapy ◽  
Low Levels

An 8-year-old boy was found to be hypertensive on routine exam (144/88). His brother (age 6) and father (age 31) were also found to have elevated blood pressure. Detailed investigations first revealed a low renin level without hypokalemia. Further study revealed that all three patients had low plasma renin activity and nonsuppresible plasma aldosterone levels after saline infusion. Serum potassium was almost always normal. A trial of dexamethasone therapy normalized blood pressure, and plasma and urinary aldosterone decreased to low levels and renin levels increased. Therapy with spironolactone and prednisone also normalized blood pressure. However, the amount of prednisone required to maintain normotension resulted in Cushingoid features and has been discontinued. Studies in the father suggest that the aldosterone production by his adrenals is hyperresponsive to adrenocorticotropic hormone (ACTH). Renin levels should be determined in all hypertensive children and their hypertensive parents. If renin is low and plasma aldosterone fails to be suppressed by saline infusion, a trial of dexamethasone would seem indicated before other investigations are carried out.

Adenovirus-mediated human prostasin gene delivery is linked to increased aldosterone production and hypertension in rats

2003 ◽  
Vol 284 (4) ◽  
pp. R1031-R1036 ◽  
Author(s):  
Cindy Wang ◽  
Julie Chao ◽  
Lee Chao
Keyword(s):  
Blood Pressure ◽  
Gene Transfer ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Sodium Reabsorption ◽  
Elevated Plasma ◽  
Aldosterone Production ◽  
Renal Kallikrein

Prostasin has been demonstrated to be an activator of epithelial sodium channels in cultured renal and bronchial epithelial cells. In this study, we evaluated the effects of adenovirus-mediated gene transfer of human prostasin on blood pressure regulation and sodium reabsorption in Wistar rats. Expression of human prostasin mRNA was identified in rat adrenal gland, liver, kidney, heart, lung, and aorta, and immunoreactive human prostasin was detected in the circulation and urine of rats receiving prostasin gene transfer. A single injection of adenovirus carrying the prostasin gene caused prolonged increases in blood pressure for 3–4 wk. Blood pressure increase was accompanied by elevated plasma aldosterone levels and reduced plasma renin activity. The increase in blood pressure and plasma aldosterone levels as well as the reduction of plasma renin activity correlated with the expression of human prostasin transgene. Elevated plasma aldosterone levels were detected at 3 days after gene transfer before the development of hypertension, indicating that stimulation of mineralocorticoid production is the primary target of prostasin. Prostasin gene transfer significantly reduced urinary K+ excretion but increased urinary Na+ and kallikrein excretion. Elevated renal kallikrein levels promote natriuresis, which may lead to sodium escape and prevent further increases of blood pressure after prostasin gene transfer. In summary, these results suggest that prostasin participates in blood pressure and electrolyte homeostasis by regulating the renin-angiotensin-aldosterone and kallikrein-kinin systems.

Hormonal responses to synthetic atrial natriuretic peptide in patients on regular hemodialysis

1988 ◽  
Vol 119 (2) ◽  
pp. 257-262 ◽  
Author(s):  
Sadao Nakajima ◽  
Hiromichi Suzuki ◽  
Yo Kageyama ◽  
Takashi Takita ◽  
Takao Saruta
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Arterial Blood ◽  
Sympathetic Nervous ◽  
Regular Hemodialysis

Abstract. The effects of atrial natriuretic peptide (ANP) on mean arterial blood pressure, heart rate, plasma renin activity, aldosterone, cortisol, norepinephrine, epinephrine and arginine vasopressin were studied in 6 anuric subjects receiving regular hemodialysis. An iv bolus injection of 8 nmol of ANP followed by infusion at 32 pmol·kg−1·min−1 for 1 h in the pre- and posthemodialysis period was performed. Basal plasma ANP was higher before than after hemodialysis. ANP administration produced a reduction in mean arterial blood pressure accompanied by an elevation of norepinephrine and of plasma renin activity (from 2.49 ± 0.52 to 3.39 ± 0.85 nmol·l−1·h−1 predialysis and from 2.78 ± 0.71 to 3.15 ± 0.86 nmol·l−1·h−1 postdialysis, respectively, mean ± sem; P < 0.05). Plasma aldosterone and cortisol were significantly decreased. Plasma epinephrine and AVP remained unchanged. These hemodynamic and hormonal changes were similar in the pre- and the postdialysis period. These results suggest that 1) ANP causes a fall in mean arterial blood pressure, which in turn induces reflex tachycardia and activation of the sympathetic nervous system without diuresis; 2) the activated sympathetic nervous system as reflected in elevation of plasma norepinephrine may increase plasma renin activity; 3) reduced plasma aldosterone is not influenced by enhancement of the reninangiotensin system; therefore, 4) reduction of plasma aldosterone as well as cortisol is probably due to direct action of ANP, and finally 5) AVP had no direct relation with ANP administration.

Atrial natriuretic peptide inhibits the effect of endogenous angiotensin II on plasma aldosterone in conscious sodium-depleted rats

1987 ◽  
Vol 72 (1) ◽  
pp. 31-35 ◽  
Author(s):  
Lynn Chartier ◽  
Ernesto L. Schiffrin
Keyword(s):  
Angiotensin Ii ◽  
Atrial Natriuretic Peptide ◽  
Plasma Renin Activity ◽  
Natriuretic Peptide ◽  
Adrenocorticotropic Hormone ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Aldosterone Secretion ◽  
Atrial Natriuretic

1. Previous studies have shown that atrial natriuretic peptide (ANP) inhibits the secretion of aldosterone by isolated adrenal glomerulosa cells stimulated by angiotensin II, adrenocorticotropic hormone and potassium in vitro. We have also demonstrated that this inhibitory effect of ANP on plasma aldosterone induced by angiotensin II and adrenocorticotropic hormone can be reproduced in vivo in conscious unrestrained rats. In this study, we have investigated the effect of an intravenous infusion of ANP on plasma aldosterone in conscious unrestrained sodium-depleted rats. 2. During sodium depletion, the rise in plasma renin activity which determines an increment in the circulating concentration of angiotensin II was accompanied by a rise in aldosterone secretion as expected. ANP infused intravenously at a dose which increased the plasma concentration of the peptide three- to five-fold, produced a significant decrement in the concentration of aldosterone in plasma after an infusion period of 120 min. There was no significant effect of ANP on plasma renin activity and plasma corticosterone concentration. 3. Since the increase in plasma aldosterone levels in sodium-depleted rats is mainly dependent on the activation of the renin–angiotensin system, we conclude that ANP may modulate the effect of endogenous as well as exogenous angiotensin II on plasma aldosterone secretion.

Acromegaly and hypertension: role of the renin-angiotensin-aldosterone system

1982 ◽  
Vol 100 (4) ◽  
pp. 581-587 ◽  
Author(s):  
Bengt E. Karlberg ◽  
Anna-Maria Ottosson
Keyword(s):  
Blood Pressure ◽  
High Frequency ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Substantial Part ◽  
Volume Factor ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Before And After

Abstract. The incidence of arterial hypertension was evaluated in a partly retrospective study of patients with active acromegaly. Of 37 patients studied, 18 (48%) had hypertension, i.e. a supine blood pressure of > 160/95 mmHg. The type of hypertension was explored further by measuring plasma renin activity and, in some patients plasma aldosterone concentrations before and after stimulation (upright posture or furosemide 80 mg given orally). Urinary 24 h excretion of aldosterone was also determined. About half of the patients with hypertension but also a substantial part of normotensive acromegalics had inappropriately low plasma renin levels both during basal conditions and after stimulation. On the other hand urinary aldosterone excretion was either normal or (in 2 patients) slightly elevated. There was no other evidence of coexistent primary aldosteronism. Our results confirm previous reports of a high frequency of alterations in the renin-angiotensin-aldosterone system in acromegalic patients with growth hormone excess which in some instances may lead to an elevated blood pressure. The biochemical changes have many similarities to low renin essential hypertension. A volume factor may be operating in acromegalic patients with hypertension since in 10 patients treatment with the aldosterone antagonist, spironolactone, with doses between 50–200 mg daily lowered blood pressure to near normal levels. Thus, spironolactone seems to be a worthwhile alternative in the treatment of hypertensive acromegalics.

Differential Effects of Acute and Chronic β-Adrenoreceptor Blockade on Blood Pressure and the Renin—Angiotensin—Aldosterone System in Essential Hypertension

1976 ◽  
Vol 51 (s3) ◽  
pp. 537s-540s
Author(s):  
R. Kolloch ◽  
K. O. Stumpe ◽  
H. Vetter ◽  
W. Gramann ◽  
F. Krück
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Chronic Administration ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Receptor Blockade ◽  
Plasma Aldosterone Concentration ◽  
Group 2 ◽  
Β Receptor ◽  
Group 1

1. Serial measurements of plasma renin activity (PRA), plasma aldosterone concentration (PA) and blood pressure were performed overnight in patients with borderline (group 1) and sustained essential hypertension (group 2) before and after acute and chronic administration of either propranolol or pindolol. 2. Group 1 patients exhibited a typical rhythm of recumbent PRA with low values before midnight and large increases early in the morning. 3. In contrast, no rhythm and very low PRA values were observed in patients of group 2. Blood pressure was higher in group 2 than in group 1. There was a significant correlation between the hyporeninaemic and hypotensive effect of either acute (r = 0·79) or chronic (r = 0·4) β-receptor blockade. 4. In group 1, after β-receptor blockade the day—night profile of renin was similar to that observed in group 2 before treatment. Thus, in this latter subgroup, low-renin profiles might reflect reduced β-adrenoreceptor activity. 5. Plasma aldosterone was lower in group 2 but appeared to be inappropriately high relative to renin. 6. The data suggest that in hypertensive patients classified according to their blood pressure and recumbent PRA profiles a significant relationship exists between changes in PRA and arterial pressure. Thus patients with high PRA respond better to treatment than patients with low renin. We conclude that in the patients studied sympathetic nervous system activity mainly determined renin values as well as anti-hypertensive effectiveness of the β-blocking drugs.

Urinary Prostaglandin E2 and Kallikrein Excretion in Glucocrticoid Hypertension in Rats

1983 ◽  
Vol 65 (1) ◽  
pp. 37-42 ◽  
Author(s):  
Michiko Handa ◽  
Kazuoki Kondo ◽  
Hiromichi Suzuki ◽  
Takao Saruta
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Prostaglandin E2 ◽  
Urine Volume ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Concurrent Administration ◽  
Angiotensin System

1. Oral administration of dexamethasone (about 2.5 × 10-7 mol/day) caused hypertension in rats. The blood pressure rose from 108 ± 6 (mean ± sd) to 156 ± 17 mmHg on the seventh day. The urine volume and urinary excretion of sodium were increased. The plasma renin activity and plasma aldosterone were unchanged. However, the urinary excretions of prostaglandin E2 (UPGE2V) and kallikrein (Ukall.V) were markedly decreased throughout the experiment. 2. With concurrent administration of captopril, the elevation of blood pressure was partially prevented. in this group of rats, the plasma renin activity was elevated and the reductions in UPGE2V and Ukall.V were partially prevented. 3. Based on these results, it is suggested that suppression of the kallikrein—kinin and prostaglandin systems, in addition to involvement of the renin-angiotensin system, is one of the factors contributing to the hypertensive action of dexamethasone.

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