Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To clarify the precise function of incidentally discovered adrenocortical adenoma, immunohistochemical and dispersed adrenal cell studies were performed. We have recently seen five patients with so-called nonfunctioning adrenocortical adenoma. Diurnal variation in plasma cortisol and suppression of plasma cortisol and urine 17-hydroxycorticosteroids in response to dexamethasone administration revealed adrenocortical function within normal limits in all cases, and no signs or symptoms of adrenal steroid hormone excess were evident. Since a high uptake of iodomethylnorcholesterol was recognized in each adrenal mass, it was supposed that these adrenal tumors produced steroid hormone to a certain extent, and each patient received unilateral adrenalectomy. P450c17, a key enzyme involved in cortisol production, was expressed in the tumor region in all cases in an immunohistochemical study. Upon in vitro steroidogenesis with dispersed adrenal cells in two cases, all steroid hormones measured except for aldosterone (progesterone, 17 alpha-hydroxyprogesterone, pregnenolone, 17 alpha-hydroxypregnenolone, 11-deoxycortisol, cortisol, 11-deoxycorticosterone, corticosterone, 18-hydroxydeoxycorticosterone, dehydroepiandrosterone and androstenedione) were produced in a culture medium. The results indicated that these tumors possessed the capacity for cortisol production, which was in agreement with the results of an iodomethyl-norcholesterol scintigraphy. All patients with mild hypertension or diabetes mellitus had no signs or symptoms of steroid hormone excess, but they could potentially develop a steroid excess syndrome such as Cushing's syndrome in the future.
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PMID:Incidentally discovered adrenocortical adenomas are not fully nonfunctioning: immunohistochemical and dispersed adrenocortical cell study. 873 56

Arterial hypertension is a serious and common complication of cyclosporine administration in humans. The prevalence of arterial hypertension in patients following orthotopic heart transplantation ranges from 38% to 92%. There are several characteristic features of this form of hypertension, including very early onset--usually within 4 to 6 weeks after transplantation and persistence with little alteration overtime. Diurnal profile shows the lack of normal nocturnal decline in blood pressure (BP) and appearance of the highest values of BP early in the morning. This phenomenon is caused by altered regulation of BP due to cardiac denervation. There was shown no correlation between the dose of cyclosporine and development of posttransplant arterial hypertension. It develops also independently of many investigated pretransplant and posttransplant cardiovascular risk factors. A great deal of attention has been focused on explantation of cyclosporine influence leading to hypertension occurrence. suggested mechanisms of this action are: elevation of systemic vascular resistance, prostaglandines and tromboxance production imbalance, hypomagnesemia, increased intravascular volume, modulation of sympathetic activity, nephrotoxicity. Reninangiotensin system seems to be not significantly associated with posttransplant hypertension, whereas the role of corticosteroides is still controversal. Hypertension remains the most common complication associated with cyclosporine administration in heart transplant recipients. Mechanisms of cyclosporine action leading to development of hypertension are still unknown. Further investigation is also needed into clinical significance of posttransplant hypertension and its influence on long-term survival after heart transplantation as they remain undefined.
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PMID:[Hypertension in patients after heart transplantation]. 883 36

The progression of IgA-NP is influenced unfavourably by development and existence of hypertension. The treatment of hypertension (HTN) has an important role in these patients. Both short- and long-acting formulations of angiotensin convertase enzim inhibitors (ACEi) and calcium channel blockers (CCB) lower blood-pressure, however long-acting preparations may provide better control and may have more renoprotective effect. Verifying this hypothesis, 22 IgA-NP patients were followed for 7.25 +/- 2.36 years. The patients were on short-acting ACEi (captopril, n = 9) or dihydropyridine type CCB (nifedipin, n = 2) or both (captopril + nifedipine n = 11), after at least 3 years the medication was changed to long-acting ACEI (enalapril, n = 4; cilazapril, n = 1), or non dihydropyridine type CCB (diltiazem hydrochlorid, n = 1) or both (n = 16). Just before changing the medication these patients underwent 24 hour ambulatory blood pressure monitoring and at the same time the level of proteinuria and the creatine clearance were measured. Values of serum-creatinine were measured in every 3-4 months within a 3 years period before and after the exchange of antihypertensive drugs. The regression of 1/creatinine was a = -5.28.10(-5) +/- 1.16.10(-4) before and a = 1.03.10(-4) +/- 2.05.10(-4) after the change of medication. Using paired t-test there was a significant difference between the regressions of 1/creatine (p < 0.005). Systolic blood pressure (SBP) (128 +/- 81 Hgmm vs. 126.09 +/- 11.67 Hgmm) was not different, however, diastolic blood pressure (DBP) (84.15 +/- 7.94 Hgmm vs. 79.78 +/- 7.17 Hgmm), diastolic percent time elevation index (HTI) (43.58 +/- 23.57% vs. 25.61 +/- 20.1%) and 24-hour diastolic hyperbaric impact (114.71 +/- 81.9 vs. 51.51 +/- 51.4, p < 0.05) was lower with long-acting antihypertensive agents, as was the proteinuria (1.18 +/- 0.94 g/die vs. 0.69 +/- 1.08 g/die, p < 0.05). Diurnal variation and systolic percent time elevation index were not different. We conclude that long-acting ACEi and non dihydropyridine type CCB formulations result in better outcomes in IgA nephropathy patients compared to short-acting drugs, probably because of better and smoother blood pressure control, lowering of proteinuria and better compliance of the patients.
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PMID:[Comparative study of the reno-protective effect of short- and long-acting antihypertensive agents in IgA nephropathy]. 1050 23

Many patients treated with peritoneal dialysis (PD) are overhydrated. We investigated whether hypertension in PD patients is related to ultrafiltration-failure-induced fluid retention. Twenty-four-hour blood pressure measurements were performed in 10 normotensive and 9 hypertensive PD patients, aged 20 to 77 years, and treated with PD for 2 to 125 months. Antihypertensive medication had been discontinued for 3 weeks. Twenty-four-hour blood pressure was monitored with a Spacelabs 90207. Mean 24-hour systolic, mean, and diastolic pressure were calculated, together with the nighttime (23:00-07:00)/daytime (07:00-23:00) ratio. Ultrafiltration was determined separately during a standardized 4-hour peritoneal permeability analysis (SPA) with 1.36% glucose. Based on the SPA, patients were divided into a group with negative net ultrafiltration (NUF) and a group with positive net ultrafiltration (PUF). In 8 patients with NUF, systolic, mean, and diastolic pressures were 142 +/- 16 mmHg, 110 +/- 14 mmHg, and 95 +/- 13 mmHg, compared to 135 +/- 22 (ns), 99 +/- 14 (ns), and 81 +/- 11 (P < 0.05) in 11 patients with PUF. Net ultrafiltration during the test dwell correlated negatively with diastolic blood pressure (r = -0.53, P < 0.05). Diurnal blood pressure variations were not related to ultrafiltration capacity. In conclusion, hypertension in PD patients may in part be explained by fluid retention caused by impaired ultrafiltration.
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PMID:Elevated 24-hour blood pressure in peritoneal dialysis patients with ultrafiltration failure. 1064 5

It is becoming increasingly clear that the intrinsic properties of both the heart and vasculature exhibit dramatic oscillations over the course of the day. Diurnal variations in the responsiveness of the cardiovascular system to environmental stimuli are mediated by a complex interplay between extracellular (i.e., neurohumoral factors) and intracellular (i.e., circadian clock) influences. The intracellular circadian clock is composed of a series of transcriptional modulators that together allow the cell to perceive the time of day, thereby enabling preparation for an anticipated stimulus. These molecular timepieces have been characterized recently within both vascular smooth muscle cells and cardiomyocytes, giving rise to a multitude of hypotheses relating to the potential role(s) of the circadian clock as a modulator of physiological and pathophysiological cardiovascular events. For example, evidence strongly supports the hypothesis that the circadian clock within the heart modulates myocardial metabolism, which in turn facilitates anticipation of diurnal variations in workload, substrate availability, and/or the energy supply-to-demand ratio. The purpose of this review is therefore to summarize our current understanding of the molecular events governing diurnal variations in the intrinsic properties of the heart, with special emphasis on the intramyocardial circadian clock. Whether impairment of this molecular mechanism contributes toward cardiovascular disease associated with hypertension, diabetes mellitus, shift work, sleep apnea, and/or obesity will be discussed.
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PMID:The circadian clock within the heart: potential influence on myocardial gene expression, metabolism, and function. 1637 89

A right adrenal tumor was found incidentally during abdominal computed tomography exam in a 51-year-old female patient, who had had diabetes and hypertension for more than 10 years. The computed tomography scan was arranged for possible pancreatic lesion by a neurologist. Norepinephrine level was high in the plasma and urine. Vanillylmandelic acid level was elevated in the urine. Diurnal cortisol rhythm, plasma adrenocorticotropic hormone and urine free cortisol were all normal,but the plasma cortisol concentration could not be suppressed after a standard low-dose dexamethasone suppression test. Therefore, adrenal cortical adenoma with subclinical Cushing's syndrome was highly suspected; however, further imaging studies, including magnetic resonance image and 131I-6beta-iodomethylnorcholesterol adrenal scintigraphy failed to discriminate an additional tumor. After right adrenalectomy, a small adrenal cortical adenoma and a large pheochromocytoma were noted. This is an extremely rare case of an adrenal incidentaloma consisting of both medullary and cortical tumors in the same gland.
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PMID:Pheochromocytoma and adrenocortical adenoma in the same gland. 1763 66

Questions remain as to whether pediatric sleep disordered breathing increases the risk for elevated blood pressure and blood pressure-dependent cardiac remodeling. We tested the hypothesis that activity-adjusted morning blood pressure surge, blood pressure load, and diurnal and nocturnal blood pressure are significantly higher in children with sleep disordered breathing than in healthy controls and that these blood pressure parameters relate to left ventricular remodeling. 24-hour ambulatory blood pressure parameters were compared between groups. The associations between blood pressure and left ventricular relative wall thickness and mass were measured. 140 children met the inclusion criteria. In children with apnea hypopnea index <5 per hour, a significant difference from controls was the morning blood surge. Significant increases in blood pressure surge, blood pressure load, and in 24-hour ambulatory blood pressure were evident in those whom the apnea hypopnea index exceeded 5 per hour. Sleep disordered breathing and body mass index had similar effect on blood pressure parameters except for nocturnal diastolic blood pressure, where sleep disordered breathing had a significantly greater effect than body mass index. Diurnal and nocturnal systolic blood pressure, diastolic blood pressure, and mean arterial blood pressure predicted the changes in left ventricular relative wall thickness. Therefore, sleep disordered breathing in children who are otherwise healthy is independently associated with an increase in morning blood pressure surge, blood pressure load, and 24-hour ambulatory blood pressure. The association between left ventricular remodeling and 24-hour blood pressure highlights the role of sleep disordered breathing in increasing cardiovascular morbidity.
Hypertension 2008 Jan
PMID:Activity-adjusted 24-hour ambulatory blood pressure and cardiac remodeling in children with sleep disordered breathing. 1807 Oct 53

Sleep apnea syndrome (SAS) is an important risk factor for hypertension and cardiovascular diseases. Diurnal blood pressure (BP) changes are evaluated by 24 h ambulatory blood pressure monitoring (ABPM). The purpose of this study was to clarify the relationship between diurnal BP variation and SAS severity, as well as the impact of antihypertensive therapy on diurnal BP variation. Patients seen at our clinic between April and September 2006 with excessive daytime sleepiness or apnea were enrolled. All patients had polysomnography and ABPM. Mean 24 h BP and nighttime BPs were significantly higher in the SAS group than in the non-SAS group. No significant differences were observed in daytime BPs between the two groups. SAS patients had a high mean 24-h BP and an elevated nighttime BP, both of which increased as SAS severity increased. Nighttime BPs were significantly higher in the moderate SAS group than in the non-SAS group. Nighttime BP and morning BP were significantly higher in the severe SAS group than in the non-SAS group. With respect to antihypertensive agents' effects on diurnal BP changes, there were no significant differences between the SAS and non-SAS groups. In conclusion, compared with non-SAS patients, patients with SAS had a higher 24-h BP, especially nighttime BP. Patients with moderate SAS tended to have elevated nighttime BP. In patients with severe SAS, elevated BP was sustained during the night despite the use of antihypertensive agents.
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PMID:Diurnal blood pressure variation in patients with sleep apnea syndrome. 1836 36

Transient ischemic attack is a medical emergency because early stroke risk after transient ischemic attack is high. Hypertension is the most important modifiable risk factor for stroke and transient ischemic attack. The aims of this review are to provide a summary of the current knowledge concerning the relationship between blood pressure and transient ischemic attack, as well as outline issues regarding diurnal variation and the potential of chronotherapy (timing medications to accord with diurnal patterns of blood pressure). There is a strong relationship between hypertension and the incidence of transient ischemic attack and the subsequent short-term risk for stroke. Ambulatory blood pressure monitoring is a reliable diagnostic and monitoring tool for hypertension and provides additional information about diurnal variation in blood pressure. Different diurnal blood pressure patterns may confer variable stroke risk. Patients with stroke commonly have abnormal diurnal blood pressure patterns and this may relate, in part, to autonomic nervous system dysfunction. However, blood pressure patterns have not been systematically studied in patients with transient ischemic attack. Blood pressure remains poorly controlled in a large proportion of patients after transient ischemic attack and under-treatment and poor adherence are important factors. Chronotherapy for blood pressure may result in more effective blood pressure control. More research is needed in this area. Hypertension is strongly associated with transient ischemic attack. Diurnal blood pressure patterns may influence subsequent stroke risk after transient ischemic attack and more evidence is needed to inform clinical practice to improve blood pressure management for transient ischemic attack patients.
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PMID:Hypertension and TIA. 1965 23

Monitoring arterial pressure (AP) was used to evaluate its daily dynamics in 136 patients with the hypertensive form of chronic glomerulonephritis (CgN) and preserved renal function and in 49 with essential arterial hypertension (EAH). Diagnosis of CGN was verified by the results of clinical, laboratory, and instrumental studies as well as morphological examination of nephrobiopsies. Diurnal AP dynamics was evaluated from the analysis of mean systolic, diastolic, and pulse pressure, their variability, loading time, and daily AP rhythm. It was shown that daily AP dynamics in patients with hypertensive CGN is characterized by high "pressure load" both in daytime and at night. Their daily AP rhythm was much more disturbed than in EAH patients. The normal fall of night AP in these groups occurred in 20 and 40% of the cases respectively and its inadequate decrease in 53 and 39%. Night-time hypertension was documented in 27 vs 9% of the cases. Disturbances of daily AP rhythm in patients with hypertensive CGN were associated with lower pulse pressure than in EAH patients, greater variability of diastolic AP at night, and smaller increase of systolic AP in the morning.
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PMID:[Diurnal dynamics of arterial pressure in patients with chronic glomerulonephritis and preserved renal function]. 1967 Jul 10


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