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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma cardionatrine was measured during pregnancy in 14 normotensive non pregnant women, 15 normotensive pregnant women, 35 pregnancy induced hypertension (PIH) and 10 preeclampsia (PE) and again 2 months after delivery in respectively 7, 15 and 7 cases together with plasma volume, PRA and plasma aldosterone. The plasma levels of cardionatrine are higher in pregnant normotensive women than in non pregnant normotensive women suggesting that pregnancy per se stimulates cardionatrine secretion. The higher levels of cardionatrine in PIH and specially in PE during pregnancy and the greater decrease of plasma cardionatrine after delivery in the hypertensive patients than in the normotensive controls exclude a deficiency of cardionatrine secretion in the pathogenesis of hypertension. These data rather suggest a compensatory role of cardionatrine in the prevention of blood pressure increase. Plasma volume was decreased in PIH (-17 p. 100) and in preeclampsia (-25 p. 100). The simultaneous high levels of cardionatrin may explain the inappropriate stimulation of the renin and aldosterone secretion in these hypovolemic hypertensive states.
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PMID:[Pregnancy-induced hypertension and pre-eclampsia develop in spite of high circulating levels of cardionatrin]. 295 37

Patients with untreated essential hypertension had significantly higher plasma atrial natriuretic factor (ANF) levels (92.9 +/- 12.9 pg/ml, mean +/- SE) than those of age-matched controls (37.8 +/- 6.0 pg/ml; p less than 0.01). Plasma ANF levels in essential hypertensive patients showed a significant positive correlation with mean arterial pressure (MAP; r = 0.46, p less than 0.05) and an inverse correlation with plasma renin activity (PRA; r = -0.43, p less than 0.05). Plasma ANF levels after medication showed significant correlation with the decrease in MAP (r = 0.565, p less than 0.05). Patients with primary aldosteronism had significantly higher plasma ANF levels (122.4 +/- 30.2 pg/ml, n = 8) than those of controls (p less than 0.05). The levels returned to normal after extirpation of adrenal tumors. The response of plasma ANF levels in patients with primary aldosteronism to volume expansion with infusion of 2 L of physiological saline in 2 hours was greater than in controls. Such exaggerated response disappeared after surgical treatment. Infusion of angiotensin II (Ang II; 20 ng/kg/min) or norepinephrine (200 ng/kg/min) for 30 minutes to normal volunteers (n = 5) resulted in a rise in MAP (24.9 +/- 3.3 and 15.8 +/- 4.4 mm Hg, respectively) and a twofold increase in plasma ANF level. Infusion of the Ang II antagonist [Sar1, Ile8]Ang II (600 ng/kg/min) for 30 minutes, resulted in a rise in MAP (18.8 +/- 2.1 mm Hg) and more than a twofold increase in plasma ANF level in patients with essential hypertension (n = 6).(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1988 Feb
PMID:Atrial natriuretic factor in essential hypertension and adrenal disorders. 296 1

Basic examination of Mr S., 45 years of age, short in stature and overweight (1.60 m, 76 kg), was carried out because of the mild hypertension (mean AP 125 mm Hg) from which he had suffered for 20 years. The results were as follows: (1) variable hyperkalemia: plasma potassium values were 5.3 to 6.9 mmol/l; (2) normal renal function: serum creatinine 91.5 mumol/l, clearance of inulin 136.6 ml/mn; (3) proximal tubular acidosis: plasma bicarbonate and chloride values were 18.4 and 109 mmol/l, respectively; urinary pH was 7.1 with negative H+ ions urinary excretion (-33 mumol/mn); when plasma bicarbonate level was raised to 26 mmol/l by acute loading, fractional excretion of bicarbonate increased to 19,5 p. 100 while plasma potassium value decreased to 4.2 mmol/l; (4) low PRA (0.29 ng/ml/h) and normal plasma aldosterone concentration (63 pg/ml) with a normal intake of sodium and in a recumbent position. Plasma atrial natriuretic factor (ANF) level was normal: 14 fmol/ml. Intravenous infusion of ANF for 2 h (1 microgram/mn) induced the expected increases in urinary flow rate, and sodium and potassium excretions (+226, +307 and +171 p. 100, respectively). Intravenous infusion of isotonic saline (2 l in 2 h) and oral administration of fludrocortisone acetate for 4 weeks (400 micrograms per day) resulted in a normal decrease in PRA and plasma aldosterone concentration, a normal rise in plasma ANF level (22 and 42 fmol/ml) while slightly increasing AP without improving bicarbonaturia and acidosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Arterial hypertension with hyperkalemia, tubular acidosis and normal renal function: Gordon syndrome and/or pseudohypoaldosteronism type II?]. 297 96

Studies in three families (A, B, and C) revealed five patients with congenital adrenal hyperplasia (CAH) due to partial and combined 21- and 11 beta-hydroxylase deficiency. One patient (A-11 1), a 23-yr-old severely virilized chromosomal female, was reared as a male, and two females (B-11 2 and C-1) complained only of hirsutism, acne, and menstrual abnormalities. Patients A-11 2 and B-11 8 (17 1/2 and 10 yr old) were asymptomatic and detected by finding an HLA genotype identical to that of their respectively affected brother and sister. Three patients (A-11 1, A-11 2, and C-1) had moderate hypertension. In spite of the wide range of clinical manifestations, all individuals had elevated androgen levels, while cortisol secretion was severely impaired only in A-11 2. 21-Hydroxylase deficiency was diagnosed on the basis of markedly increased plasma and urinary levels of 17-hydroxyprogesterone (17-OHP) and 21-deoxycortisol and their respective urinary metabolites pregnanetriol and pregnanetriolone. PRA was elevated in three patients, while urinary aldosterone was normal or increased. 11 beta-Hydroxylase deficiency was diagnosed on the basis of increased 11-deoxycortisol and deoxycorticosterone in plasma and tetrahydro-11-deoxycortisol and deoxycorticosterone in urine, particularly after ACTH administration. In contrast to classical 11 beta-hydroxylase deficiency CAH, urinary 18-hydroxycorticosterone and 18-hydroxy-11-deoxycorticosterone were normal or elevated. The nature and mechanism of a combined enzymatic defect are unknown. The coincidental presence in a single individual of the mutant genes for both 21- and 11 beta-hydroxylase deficiency CAH is very unlikely to occur. Two alternative hypotheses may explain our findings. One is the existence of a genetically inherited abnormal (or aberrant) 11 beta-hydroxylase, whose affinity for its normal substrate is changed for an abnormal one (17-OHP). As a result, 11 beta-hydroxylation of 11-deoxycortisol is deficient while 17-OHP 11 beta-hydroxylation is markedly enhanced. Thus, both 11-deoxycortisol and 21-deoxycortisol as well as their urinary metabolites accumulate. The ability for 18-hydroxylation, however, remains normal. In this case, 21-hydroxylase is not deficient, yet 21-deoxycortisol cannot be further hydroxylated to cortisol, since this steroid is not a suitable substrate for the enzyme. Such a disorder may represent a new allelic variant of 11 beta-hydroxylase deficiency CAH, which, similar to 21-hydroxylase deficiency, is completely linked to the HLA complex.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Combined 21- and 11 beta-hydroxylase deficiency in familial congenital adrenal hyperplasia. 298 4

The present study was designed to clarify the role of serum angiotensin I-converting enzyme (ACE) in the occurrence and maintenance of hypertension in essential hypertension (EH). For this purpose, following experiments were carried out: 1) Correlations between serum ACE activity and renin activity (PRA), aldosterone concentration (PAC) and bradykinin concentration (PBC) in plasma, and blood pressure (BP) as well as serum creatinine levels. 2) Circadian rhythm of serum ACE activity. and 3) Effect of furosemide, upright posture, both furosemide and upright posture, propranolol, indomethacin, 9 alpha-fluorocortisol or angiotensin II (A-II) on the serum ACE activity, PRA, PAC and circulating plasma volume (CPV). The following results were obtained: The serum ACE activity was 30.2 +/- 5.0 U/ml (means +/- SD) in EH as a group, which was significantly higher than that (27.3 +/- 3.9 U/ml) in age matched normotensive subjects (NT) (p less than 0.001). While there was no significant difference in the enzyme activity between low-renin EH (LREH) and NT, a significant difference was found between normal- (NREH) or high-renin EH (NREH) and NT (p less than 0.05 for NREH, p less than 0.01 for HREH). A negative correlation was observed between enzyme activity and age in EH (r = -0.221, 0.05 less than p less than 0.10) as well as in NT (r = -0.306, p less than 0.05). No significant relationships were observed between enzyme activity and BP in either EH or NT. There was a significant positive correlation between enzyme activity and PRA in NT. (r = 0.501, p less than 0.001), NREH (r = 0.658, p less than 0.001) and HREH (r = 0.695, p less than 0.001). However, no significant relationship was found between them in LREH. The enzyme activity was significantly correlated to PAC in NT (r = 0.368, p less than 0.01), NREH (r = 0.567, p less than 0.001) and HREH (r = 0.529, p less than 0.01), but not in LREH. Although no significant correlation was observed between enzyme activity and PBC in NT, NREH and HREH, a significant relationship was found in LREH (r = -0.460, 0.05 less than p less than 0.10). The enzyme activity was not related to serum creatinine levels in EH as well as in NT. In NT, the serum levels of ACE activity reached a maximum values at 6:00 a.m. or 9:00 a.m., and gradually decreased between 6:00 p.m. and 3:00 a.m. An almost similar circadian rhythm of enzyme activity was found in EH.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Clinical significance of serum angiotensin I-converting enzyme in essential hypertension]. 300 63

Patients with idiopathic hyperaldosteronism (IHA) manifest hypertension, hypokalemia, and renin suppression. IHA is thought to have one of three possible etiologies: zona glomerulosa autonomy, an aldosterone secretory factor, or angiotensin-II (A-II) adrenal hypersensitivity. To determine the contribution of A-II adrenal hypersensitivity in IHA, four patients with IHA were treated with a new angiotensin-converting enzyme inhibitor, enalapril, on a controlled diet (sodium [128 mEq/day] and potassium [80 mEq/day]) in a metabolic unit. The results of this study demonstrate that enalapril therapy in three of four patients normalized blood pressure, improved potassium balance, elevated PRA, reversed the postural increment in plasma aldosterone concentration (PAC), and reduced aldosterone secretion to normal. The fourth patient with bilateral macronodular disease, on the other hand, had no improvement in any of the above indices, despite maximal doses of enalapril (80 mg/day). This patient, however, may have had bilateral adrenal adenomas, based on extremely elevated 18-OH-corticosterone levels (greater than 100 ng/dl), and because of a lack of adrenal A-II hypersensitivity, demonstrated by a fall in pre-enalapril, postural-, and lasix-induced PAC. In conclusion, enalapril improved the hypertension, hypokalemia, renin suppression, and hyperaldosteronism in three patients with IHA over 28 days of therapy. The results of this study suggest an etiologic role of A-II adrenal hypersensitivity in IHA.
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PMID:The therapeutic effect of a new angiotensin-converting enzyme inhibitor, enalapril maleate, in idiopathic hyperaldosteronism. 301 6

The acute and long-term efficacy, tolerance and safety of two orally active angiotensin converting enzyme (ACE) inhibitors, captopril (C) and enalapril (E) were compared in patients on regular haemodialysis (RHD). C and E were successively administered for 6 months to 8 RHD patients with hypertension unresponsive to fluid withdrawal and conventional antihypertensive therapy. The fall in blood pressure after a starting dose of 25 mg C or 5 mg E was of the same magnitude. It was not correlated with the initial PRA levels, which were normal in all patients. The mean daily dose of ACE inhibitor was 45 +/- 28 mg during the C period and 19.4 +/- 17.6 mg at the end of the E period. Three patients required additional treatment, comprising beta-blockers and/or calcium antagonists. The individual daily dose of ACE inhibitor, the need for additional treatment and the antihypertensive response achieved were highly correlated during both study periods. During C administration 4 out of 8 patients presented a taste disturbance, which disappeared 2 weeks after substituting E for C. Serum electrolytes, liver enzymes, haemoglobin concentration and white cell and platelet counts remained unchanged throughout both study periods. It is concluded that RHD patients with hypertension are responsive to ACE inhibitors, C and E being equally effective.
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PMID:Intra-individual comparison of captopril and enalapril in patients undergoing regular haemodialysis. 301 37

Renovascular hypertension is the most prevalent form of curable hypertension. Despite some unanswered questions, there is a growing consensus about the need to identify patients with renovascular hypertension so that a specific therapy can be recommended. The renin-angiotensin system is the chief pathophysiologic mechanism responsible for hypertension in patients with renal ischemia but other, yet poorly defined, mechanisms may be operative. Most patients with renovascular hypertension do not present with typical or discriminative clinical features. Thus, many physicians do not perform work-up to uncover renovascular disease even if diagnosis is dictated by patients' clinical course. It is difficult to make the proper diagnosis unless there is a high index of suspicion and certain procedures are performed. How can we, then, select a few patients for the work-up from the vast sea of people with hypertension? The identification of such patients and the pursuit of a renovascular etiology is a matter of clinical judgment. Delineation of renovascular hypertension should be undertaken only after careful deliberation. When clinical clues suggestive of renovascular hypertension are present, appropriate diagnostic tests should be undertaken in patients who are candidates for PTRA or surgery. Captopril-stimulated PRA test is done first. If the test is positive (and in some clinically relevant circumstances even if it is not done or is negative), DSA should be obtained. IV-DSA is being steadily replaced by the superior IA-DSA. The need for renal vein renin determination varies from center to center, but when carefully performed, it yields meaningful information. Ultimately, a conventional arteriogram is done to define the extent of renal artery stenosis and to assess intrarenal vascular anatomy. For selected patients, the benefit-risk ratio clearly outweighs the cost considerations. The spectrum of renovascular hypertension is variable, further compounding the diagnostic indications and contraindications. At one end of this spectrum are those patients in whom surgical therapy is likely to be beneficial, and at the other end are the patients who have relative contraindications to surgery. In between lies the vast gray zone that constitutes a great judgmental challenge in clinical medicine. What is to be done with the patients who have mild to moderate renovascular hypertension whose BP is controlled on medical therapy? There are some patients who may benefit from renovascular repair despite the nonlateralization of renal vein renins. What is the mechanism underlying their hypertension?(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Renovascular hypertension. 306 42

The present study was designed to investigate the involvement of the renal nerve in glucocorticoid hypertension and to assess the role of the renin-angiotensin system in dexamethasone-induced hypertension. The elevated blood pressure in dexamethasone treated rats showing a significant increase in plasma renin concentration (PRC) and activity (PRA) was attenuated dose-dependently by the angiotensin I converting enzyme (ACE) inhibition. Bilateral renal denervation caused a partial decrease in the elevated blood pressure, abolished the increased PRC and PRA, and reduced the dose-dependent decrease in blood pressure with ACE inhibition in dexamethasone treated rats. Although the reduction in body weight and increases in urine volume, urinary sodium excretion and hematocrit were clearly seen following dexamethasone administration, dexamethasone-treated renal denervated rats showed the same degree of change in any of the variables as dexamethasone-treated sham-operated rats. Thus, our results indicate that the stimulation of the renin-angiotensin system through the activation of the renal nerve may be partially responsible for the dexamethasone-induced high blood pressure and, therefore, bilateral renal denervation reduces, partially but significantly, the elevated blood pressure, suggesting that the attenuation of oversecretion of renin contributes to the lowering of the blood pressure.
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PMID:Role of the renal nerve in glucocorticoid hypertension. 307 18

A 38 year-old man was admitted for severe hypertension with hypokalemia. Blood pressure was 180-120 mmHg, funduscopic examination revealed grade II retinopathy and left ventricular hypertrophy was present. Laboratory data disclosed: natremia = 140 mmol/ml, kalemia = 2.8 mmol/l, chloride = 105 mmol/l, bicarbonate = 30 mmol/l, creatinine clearance = 100 ml/mn, natriuresis = 140 mmol/day, kaliuresis = 80 mmol/day. Intravenous pyelography was normal. Angiography revealed a defect in the mid third of the right kidney without arterial abnormalities. Study of renin angiotensin aldosterone system showed: plasma renin activity: peripheric blood = 36 ng/ml/h (normal range I to 2), right renal vein = 30 ng/ml/h. Left renal vein = 18 ng/ml/h, inferior cava vein = 19 ng/ml/h. Plasma aldosterone level = 86 ng/100 ml (normal range 10 to 15). Captopril acute administration was followed by a fall of BP to 70-50 mmHg at 2 hours. Right nephrectomy was performed and revealed an ischemic retracted cortical area without necrosis nor tumoral aspect. The day after BP was 140/80 mmHg. Eight days after, kaliemia was 4.2 mmol/l, PRA was 0.5 ng/ml/h. Light microscopy showed that affected area was sharply delimited from surrounding normal tissue. In this area, glomeruli were present and seemed more numerous as usual; interstitial fibrosis and infiltrates of inflammatory cells were also noted. The main fact was tortuosities of intralobular arteries, thickened, with intimal proliferation. There was a pelvic recess near this cortical tissue. Immunofluorescence findings: antirenin serum fixed on JGA but also on interlobular arterial walls and on peritubular interstitium.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Segmental renal hypoplasia of an adult originating from pseudo-tumor hyperreninism]. 314 6


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