Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Primary aldosteronism is a relatively uncommon etiology of hypertension. Plasma renin activity is suppressed in the majority of the cases but not always. Plasma renin activity has been associated with increased vascular injury. The occurrence of vascular complications has rarely been reported with low plasma renin activity. The authors report a case of long-standing secondary hypertension due to primary aldosteronism with coronary artery aneurysms and aortic dissection. Diagnosing is important, for therapeutic intervention can be curative.
 ...
PMID:Coronary artery aneurysms, aortic dissection, and hypertension secondary to primary aldosteronism: a rare triad. A case report. 1037 27

Since its initial description in 1955, primary aldosteronism was thought to be a rare cause of hypertension. However, with improved screening methodologies, it appears that primary aldosteronism is the most common form of secondary hypertension. Diagnosis of this disorder results in either the cure of hypertension or targeted pharmacotherapy. In addition, recent evidence suggests that aldosterone excess may have specific cardiotoxicity that is reversible with treatment. Patients with hypertension and hypokalemia and most patients with treatment-resistant hypertension should undergo screening for primary aldosteronism. A random and ambulatory ratio of plasma aldosterone concentration (ng/dl) to plasma renin activity (ng/ml per hour) >20 and a plasma aldosterone concentration >15 ng/dl is a positive screen for primary aldosteronism. A plasma aldosterone concentration/plasma renin activity ratio >20 alone is not diagnostic of primary aldosteronism; primary aldosteronism must be confirmed by demonstrating inappropriate aldosterone secretion with either the intravenous saline suppression test or measurement of 24-hour urinary aldosterone while on a high-sodium diet. The 2 major subtypes of primary aldosteronism are unilateral aldosterone-producing adenoma and bilateral idiopathic hyperplasia. Patients with aldosterone-producing adenoma are usually treated with unilateral adrenalectomy, and patients with idiopathic hyperplasia are treated medically. The subtype evaluation may require one or more tests, the first of which is imaging the adrenals with computed tomography (CT). When CT reveals a solitary unilateral macroadenoma (>1 centimeter) and normal contralateral adrenal morphology in a patient with primary aldosteronism, unilateral laparoscopic adrenalectomy is a reasonable therapeutic option. However, in many cases, CT imaging may reveal normal-appearing adrenals or ambiguous findings. Adrenal venous sampling helps solve these clinical dilemmas.
 ...
PMID:Primary aldosteronism: A common and curable form of hypertension. 1042 72

Glucocorticoid-remediable aldosteronism (GRA) is a rarely recognised cause of arterial hypertension. We report the features of a 13-year-old boy with hypertension (casual blood pressure (BP) 140-180/95-110 mm Hg) discovered during a routine paediatric check. Ambulatory BP monitoring (ABPM) revealed significant hypertension with an abolished nocturnal BP fall (mean daytime BP 155/108 mm Hg, mean night-time BP 156/104 mm Hg, nocturnal BP fall 0/4%) which was indicative of secondary hypertension. Despite triple antihypertensive drug therapy the hypertensive control was unsatisfactory. Laboratory tests revealed hypokalaemia (3.0 mmol/l), suppressed plasma renin activity (0.012 nmol/l/h) and high plasma aldosterone (1.190 nmol/l). The diagnosis of primary hyperaldosteronism was established and GRA was further confirmed by the presence of the chimaeric GRA-gene and dexamethasone therapy was initiated. During the next 2 months of dexamethasone therapy all three antihypertensive drugs were discontinued and BP remained under control with restoration to a normal nocturnal BP fall (mean daytime BP 129/77 mm Hg, mean night-time BP 113/64, nocturnal BP fall 12/17%). A change of therapy from dexamethasone to spironolactone was necessary due to the side effects of corticosteroids after 3 months. Spironolactone alone (0.8-2 mg/kg/day) was able to control the BP sufficiently. In conclusion, to our knowledge, this is the first reported case of abolished nocturnal BP fall in a patient with genetically proven GRA. This study indicates that GRA can cause severe hypertension even in children, associated with an abolished nocturnal BP fall. GRA thus should be excluded in all hypertensive patients with circadian BP rhythm disturbances.
 ...
PMID:Abolished nocturnal blood pressure fall in a boy with glucocorticoid-remediable aldosteronism. 1061 71

The circadian rhythm of arterial pressure (AP) is not a passive consequence of the impact of exogenous factors. Endogenous mechanisms play an important role in the generation and maintenance of AP rhythm. The adaptation of the exogenous components of AP rhythm to the demands of the environment is modulated by the circadian-time-dependent responsiveness of the biologic oscillator. A neuronal network in the rostral hypothalamus including the suprachiasmatic nucleus is implicated in the generation of AP rhythm, in the modification of the rhythm amplitude (possibly due to homeostatic constraints), and in the regulation of its phase. The central sympathoexcitatory pathway to the upper thoracic cord plays a crucial role in the maintenance of normal circadian AP rhythm. The circadian pattern of AP is influenced also by hormonal factors such as the hypothalamic-pituitary-adrenal and the hypothalamic-pituitary-thyroid axes, the renin-angiotensin-aldosterone system, opioids, and various vasoactive peptides. The circadian variations of AP depend on physiological state--sleep and wakefulness, pregnancy, work, and senescence (primary aging). In some essential hypertensive patients and in patients with secondary hypertension the nocturnal fall in AP is reduced or absent (nondippers). Target-organ damage is more advanced in nondippers than in dippers. The occurrence of cardiovascular events exhibits a prominent circadian pattern, with events more frequent in the morning (06:00-12:00 h).
 ...
PMID:Circadian rhythms of arterial pressure: basic regulatory mechanisms and clinical value. 1073 7

Structural alterations of small arteries in patients with essential hypertension are characterized by inward eutrophic remodeling. However, small arteries in patients with secondary hypertension, as well as in experimental models of hypertension with high circulating renin, are characterized by inward hypertrophic remodeling, which is characterized by smooth muscle cell hypertrophy in animal models. The aim of our study was to determine whether remodeling of subcutaneous small arteries in patients with secondary forms of hypertension is associated with smooth muscle cell hypertrophy and/or alterations in the elastic modulus of the vessel wall. Fifteen patients with renovascular hypertension, 9 with primary aldosteronism, and 13 with essential hypertension and 9 normotensive subjects were included in the study. A biopsy of subcutaneous fat was taken from all subjects. Small arteries were dissected, and morphology was determined on a micromyograph. Unbiased estimates of cell volume and number were made in fixed material. From the resting tension-internal circumference relation of the small arteries, the incremental elastic modulus was calculated and plotted as a function of wall stress. Blood pressure was greater in patients with essential hypertension, renovascular hypertension, or primary aldosteronism than in normotensive subjects, but no significant difference was observed among the 3 groups of hypertensive patients. The media/lumen ratio, the medial cross-sectional area, and the smooth muscle cell volume were significantly greater in patients with renovascular hypertension than in normotensive subjects and patients with essential hypertension. No difference in cell number or in the elastic properties was observed among the 4 groups of subjects. In conclusion, our data demonstrate for the first time that a pronounced activation of the renin-angiotensin-aldosterone system is associated with vascular smooth muscle cell hypertrophy in human hypertension in a manner similar to that found in animal models.
 ...
PMID:Cellular hypertrophy in subcutaneous small arteries of patients with renovascular hypertension. 1077 64

We studied 1,020 patients with hypertension visiting our outpatient clinic during a five-year period, from 1995 until 1999. Those subjects were screened by determining plasma renin activity (PRA) and plasma aldosterone concentration (PAC) after testing routine laboratory examinations in order to differentiate secondary hypertension from essential hypertension. All patients with low-reninemic hypertension were examined by furosemide plus the upright test. This led to an increase in diagnoses of primary aldosteronism (PA) (confirmed by captopril-loading test). Our studies demonstrated that the incidence of PA is 5.4%, and also that the plasma potassium level is not always beneficial for suspecting the presence of PA, because 28% of the patients with PA show only hypokalemia. We would like to emphasize that adrenal venous sampling plays a critical role in establishing the optimal management for patients with PA, because CT imaging is limited to detection of adrenal masses.
 ...
PMID:Clinical characteristics of primary aldosteronism: its prevalence and comparative studies on various causes of primary aldosteronism in Yokohama Rosai Hospital. 1091 99

This prospective multicenter study included 1,205 patients, who were referred for difficult-to-treat hypertension or analysis of possible secondary hypertension. After a standardized selection protocol based on sharply defined drug-resistant hypertension or renal function impairment during angiotensin-converting enzyme inhibition, patients underwent renal scintigraphy and a captopril-renin challenge test. A set of clinical characteristics was also recorded. Sensitivity and specificity of renal scintigraphy for diagnosing renal artery stenosis were 0.72 and 0.90 and of the captopril-renin test 0.77 to 0.91 and 0.69 to 0.75 depending on the criterion used. The clinical characteristics were used to construct a clinical prediction rule for renal artery stenosis, which had a sensitivity of 0.68 and a specificity of 0.87 at a cut-off level of 30% predicted probability. However, with the prediction rule a sensitivity of 0.90 could be reached by performing arteriography only in patients with a predicted probability of stenosis of > or =10%, resulting in a considerable reduction of the number of arteriograms to be made. A diagnostic strategy is advocated starting with drug-resistant hypertension and continuing to renal arteriography only in patients with increased probability of stenosis. Patients with atherosclerotic renal artery stenosis were then randomized to balloon angioplasty (n = 56) versus antihypertensive medication (n = 50). Three months after randomization 22 patients from the medication group underwent balloon angioplasty in second instance. In an intention-to-treat analysis, no difference in blood pressure was found between the groups after 3 months, nor after 12 months of follow-up, although there was a small medication-sparing effect of balloon angioplasty. The lack of a beneficial effect of balloon angioplasty compared with medication could not be attributed to the high stenosis recurrence rate after angioplasty, nor to the fact that the inclusion criterion was set at a stenosis level of > or =50% so that patients with relatively mild stenosis were also included. Renal function after angioplasty was slightly better in the angioplasty group than in the medication group, and improvement of the renal scintigram occurred more often after angioplasty. Apart from the treatment of patients with specific characteristics, the presented therapeutic approach starts with extending the antihypertensive drug therapy to control blood pressure. Only if blood pressure cannot be controlled or if renal function deteriorates, balloon angioplasty (with stent placement) is indicated.
 ...
PMID:Prospective studies of diagnosis and intervention: the Dutch experience. 1102

Primary aldosterone excess or hyperaldosteronism is an important cause of hypertension which, when associated with an aldosterone secreting adenoma, is amenable to surgical cure. The biochemical hallmarks of the condition are a relative excess of aldosterone production with suppression of plasma levels of renin (a proxy for angiotensin II, the major trophic substance regulating aldosterone secretion). This combination of a high aldosterone and a low renin is however more commonly associated with 'nodular hyperplasia' of the adrenal glands, a condition not improved by surgery and variably responsive to the effects of the mineralocorticoid antagonist, spironolactone. Until recently the prevalence of either form of secondary hypertension has been thought to be low such that few clinicians 'hunted' for it in the absence of hypokalaemia (the traditional clue for the syndrome). This view has been challenged, firstly by the realisation that no more than 50% of such patients will have a low plasma potassium and secondly by the assumption that a 'normal' plasma aldosterone is in fact inappropriately elevated if the renin level is low. A single measurement of the ratio of aldosterone to renin levels is claimed to be highly predictive of patients who will have primary aldosterone excess. This paper examines the logic behind such claims and presents evidence from the literature that an abnormal ratio is simply a different description of the low renin state and that such patients do not necessarily have mineralocorticoid hypertension. Most patients 'discovered' by this test will have what many call low-renin hypertension, a condition not amenable to specific therapy. Claims that they are peculiarly sensitive to the hypotensive effects of spironolactone have not been tested in controlled trials. The test would however be expected to pick up those individuals with true Conn's syndrome but such patients remain too few in number to justify widespread use of an expensive screening test.
 ...
PMID:Primary aldosteronism, a common entity? the myth persists. 1208 Apr 39

The ratio of serum aldosterone to plasma renin activity (PRA) has been proposed as sensitive screening method in the diagnosis of primary aldosteronism under random conditions. However, the method for determination of renin activity is hampered by the necessity of ice cooling during storage and transport. The present study was therefore conducted to examine the ratio of serum aldosterone to plasma renin concentration (ARR) and its usefulness in diagnosis of primary aldosteronism under ambulatory conditions and given antihypertensive medication. 146 patients with arterial hypertension who consecutively attended the outpatient clinic were studied prospectively. Patients with secondary hypertension besides primary aldosteronism were not included in the series. 37 normotensive patients served as control. Also, 17 patients with known primary aldosteronism were retrospectively examined. Among the hypertensive group 2 patients with Conn's syndrome were newly detected (1.4%). ARR was 7.92 +/- 6.04 [pg/ml]/[pg/ml] in normotensive controls (range from 2.03 to 26.98), 14.61 +/- 18.50 [pg/ml]/[pg/ml] in patients with essential hypertension (n = 144, range from 0.41 to 115.45) and 155.92 +/- 127.84 [pg/ml]/[pg/ml] in patients with primary aldosteronism (n = 19, range from 6.75 to 515). 17 of the 19 patients with Conn's syndrome had an ARR of more than 50. Under ongoing drug treatment this represents a sensitivity of 89% and a specificity of 96%. Sensitivity decreased to 84% and specificity increased to 100% when a second criteria (aldosterone > or = 200 pg/ml) was included. In summary, ARR using renin concentration is a useful screening parameter for primary aldosteronism.
 ...
PMID:Ratio of serum aldosterone to plasma renin concentration in essential hypertension and primary aldosteronism. 1192 71

Von Euler characterised the sympathetic neurotransmitter noradrenaline (NA) and postulated that excessive neural tone was a cause of primary hypertension (PH). Thirty years ago, we found raised NA levels in 30-40% of young patients with PH. Laragh found plasma renin activity (PRA) a risk marker for coronary artery disease. With Esler, Miura, and Campese, a close association was found of plasma NA with PRA. We found raised tyrosine hydroxylase activity (AC) in the hearts of a rabbit model of sinoaortic denervated hypertension and in PH with raised plasma NA. Esler utilised titrated NA infusion and described increased spillover of NA from heart, kidney and subcortical areas of brain of patients with PH. With Eide we found raised cerebrospinal fluid (CSF) NA in PH (not secondary hypertension) and with Kolloch and Miura, we found raised plasma/CSF NA in conjunction with reduced dopaminergic tone. With Shkvatsabaya, Yurenev and Davison, we found that relaxation therapy improved the anger ambience and blood pressure of PH with raised plasma NA vs those with normal NA levels. Campese found a hypothalamic source of raised blood pressure in two rat models - microphenol treated and ischaemic kidney. The resulting hypertension was associated with raised NA turnover of their hypothalamic centres. Finally, with Hsueh and Hodis, we found raised plasma NA in association with insulin resistance increased left ventricular mass and intimal medial hypertrophy in Mexican-American diabetics and their yet unaffected offspring. Reliable estimates of human sympathetic AC, including levels of plasma NA in the effluent of selected organs and peripheral venous and arterial sites, may eventually be displaced by techniques using genetic analysis and molecular biology. Never the less, the sympathetic nervous system appears to play an important role in the pathogenesis, sequelae and therapy of PH.
 ...
PMID:The sympathetic nervous system: the muse of primary hypertension. 1198 98


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>