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)

The presence of left ventricular hypertrophy (LVH) in either hypertensives -H- or in normotensives -N-, suggests that not only blood pressure is determining this anatomic change, but various factors, as neural or endocrine ones, could be involved in its genesis. In order to evaluate the role of sympathetic dys-reactivity on LVH, we studied three groups of subjects: a) 12 -H- (SBP 159+/-9; DBP 99.6+/-7; FC 80+/-7) with LVH, diagnosed by echocardiogram. b) 12 -N- (SBP 138.2+/-8; DBP 83+/-2; FC 75.6+/-4) with LVH. c) 12 -N- (SBP 136.6+/-11; DBP 81.8+/-5; FC 76.3+/-5) without LVH. Using computer interfaced equipment, we measured beat to beat, hemodynamic and extra-cardiovascular autonomic functions, during a session of stressors (Mental Arithmetic, Color Word Stroop, Cold Pressure and Handgrip Tests), preceded and followed by 10' of observation. Among the various considered indexes, we evaluated the Percentual Total Activity Index (PTAI), as percentual total activity change + percentual total recovery change. Our findings point out that the PTAI of N with LVH is significantly higher for SCL, PHT, HR, SV, CO, TPR than either in H with LVH or N without LVH. These data seem to demonstrate a prolonged reactivity in N without LVH and are according to the hypothesis that LVH could also be supported by a hyper-adrenergic state with sympathetic dys-reactivity, independently from high blood pressure values.
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PMID:[Left ventricular hypertrophy: physiopathological signs using a hemodynamic and cardio-autonomic approach]. 146 95

We evaluated the effect of verapamil therapy on left ventricular hypertrophy and left ventricular diastolic function in 13 patients with mild to moderate hypertension. Left ventricular hypertrophy was determined by M-mode echocardiographic measurements of interventricular septal thickness (IVST), posterior wall thickness (PWT) and left ventricular mass index (LVMI) both before (T0) and after 3 months (T3) of verapamil therapy. Left ventricular diastolic transmitral flow was measured by pulsed Doppler indices of early (E) and atrial (A) velocity, E/A ratio, total area (Ta), A area (Aa), Aa/Ta ratio, E-pressure half-time (E-PHT). A-pressure half-time (A-PHT) and E-PHT/A-PHT ratio both before and after 3 months of verapamil therapy. No significant changes occurred in mean heart rate, systolic function or body weight. We conclude that 3 months' therapy with verapamil resulted in an improvement in left ventricular hypertrophy and left ventricular diastolic function and a normalization of blood pressure, without a corresponding deterioration in left ventricular systolic function.
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PMID:Improvement in left ventricular hypertrophy and left ventricular diastolic function following verapamil therapy in mild to moderate hypertension. 214 51

The blood pressure, heart rate, and plasma catecholamine (CA) response to standing and mental stresses were studied in 14 normotensive subjects with normotensive parents (PNT group), 14 normotensive subjects with hypertensive parent(s) (PHT group), and eight borderline hypertensive patients (BHT group). Mean basal plasma norepinephrine (NE) concentration in BHT group (302 +/- 94 pg/ml) and PHT group (289 +/- 167 pg/ml) were significantly higher than in PNT group (205 +/- 76 pg/ml). Significant differences in the mean basal plasma epinephrine (E) were found only between the PNT and BHT groups (22 +/- 12 vs 43 +/- 18 pg/ml, p less than 0.01). Both plasma NE and E increased significantly on standing in all groups. With mental stress, plasma E increased significantly, though plasma NE did not change significantly in all three groups. The mean changes in blood pressure, heart rate, and plasma CA in response to standing and mental stresses were not different in the three groups. However, a higher incidence (50%) of high blood pressure responders (greater than or equal to 20 mmHg in systolic blood pressure) to mental stress was found in the PHT group compared with PNT (14%) and BHT (12%). The high responders in the PHT group had significantly higher mean plasma E concentrations throughout the experiment. Also, their increases in plasma NE and E in response to mental stress were higher than those of the low responders. The results indicate that genetic predisposition to hypertension plays a significant role in determining plasma catecholamine levels and the responsiveness to stress, especially to mental stress.
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PMID:The adreno-sympathetic system, the genetic predisposition to hypertension, and stress. 400 25

The blood pressures (BP) of the parents of a group of students were determined and two subgroups of students were defined, one with (PHT group) and one without (PNT group) a familial predisposition to hypertension. Observations were made in both groups during three periods of modified dietary electrolyte intake: (i) no-added sodium (low Na), (ii) no added sodium with potassium supplementation (low Na/high K), and (iii) sodium supplementation (high Na). The diets were given in random order. At the start of the trial, while the students continued their customary diet, the PHT group had higher systolic and diastolic pressures and plasma noradrenaline levels than the PNT group. At the end of 4 weeks of the high Na diet, the BP levels of both groups were significantly higher than those after the low Na diet. In contrast, when the low Na diet was supplemented for 2 weeks with potassium, BPs of the PHT group fell significantly, while those of the PNT group rose slightly. BP in the PHT group was significantly lower during the low Na/high K than during the high Na diet (systolic 10.5 mm Hg +/- 2.3 SE; diastolic 11.2 +/- 2.5, the changes being significantly different from those in the PNT group. The changes in plasma renin and aldosterone were similar in both groups during the different diets. Plasma noradrenaline fell in the PHT group, but rose in the PNT group when the low Na diet was supplemented with potassium. This fall in plasma noradrenaline in the PHT group during the low Na/high K diet correlated with the falls in systolic and diastolic BP. It is concluded that whereas young adults with a familial predisposition to hypertension behave similarly to those without such a predisposition in having a pressor response to a high sodium intake, they are peculiar in showing a depressor response to a high potassium intake.
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PMID:Blood pressure and hormonal changes following alteration in dietary sodium and potassium in young men with and without a familial predisposition to hypertension. 610 98

Some of the relatively easily measurable and possibly hypertension-associated parameters were evaluated in thirty normotensive young subjects divided into the PHT (either parent hypertensive) group and the PNT (both parents normotensive) group. In subjects of the PHT group, the platelet aggregating sensitivity to the arachidonic acid and the ratio of total cholesterol to HDL cholesterol were significantly (p less than 0.05) increased while urinary kallikrein excretion was decreased without simultaneously significant elevation of blood pressure. The enhanced platelet aggregating sensitivity to the arachidonic acid and the increased ratio of total cholesterol to HDL cholesterol suggest that subjects with a positive family history of hypertension might have a greater tendency to atherosclerosis and could contribute to the development of essential hypertension. Decreased urinary kallikrein excretion suggests that the vasodepressive activity of the kallikrein-kinin system might be inhibited in subjects with a positive family history of hypertension.
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PMID:Relation of family history of hypertension to platelet aggregation, ratio of total cholesterol to HDL cholesterol and urinary kallikrein excretion. 643 May 81

We investigated the relation between home blood pressure (BP) and body weight in 38 young normotensive men (mean age, 16 years) whose parents were normotensive (PNT group) and 34 age- and sex-matched normotensive men, one or both of whose parents were hypertensive (PHT group). Although causal BP measurements were similar in both groups, home systolic BP was significantly higher in the PHT group (123 +/- 1 mm Hg) than in the PNT group (116 +/- 1 mm Hg). Body weight was significantly greater in the PHT group (66.0 +/- 1.4 v 61.8 +/- 1.3 kg, P < .05) and body mass index (BMI) was not significantly higher in the PHT group (22.4 +/- 0.5 v 21.3 +/- 0.5 kg/m2, P = .09). Body weight (r = 0.38) and BMI (r = 0.42) were significantly correlated with home systolic BP in the PHT group. There were no differences in serum lipid or uric acid concentrations between the two groups. Our results showed that young normotensive subjects with a genetic predisposition to hypertension weighed more and had higher home systolic BPs compared with subjects without a family history of hypertension. Our observations further indicated a close relationship between a family history of hypertension and increased body weight, even in young normotensive men.
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PMID:Relation of home blood pressure to body weight in young normotensive men with or without family history of hypertension. 791 46

Hypertension which is part of the metabolic syndrome has frequently a family background. The authors investigated therefore indicators of insulin sensitivity by the method of a hyperinsulinaemic euglycaemic clamp in the offspring of hypertensive probands. In conjunction with the increased interest in the role of muscles in influencing insulin sensitivity the authors were also interested in serum amino acid levels. They examined a group of 15 healthy offspring of hypertonic subjects (PHT) and compared them with a group of 18 healthy volunteers without a family-history of hypertension. PHT had as compared with controls a higher systolic pressure (117 +/- 7.2 mm Hg vs. 106.1 +/- 11.7 mm Hg p < 0.01). In the clamp examination in PHT significantly lower indexes of tissue insulin sensitivity were recorded, SI (46.51 +/- 11.8% vs. 54.3 +/- 7.79%, p = 0.02) and ISI (6.6 +/- 3.99 vs. 9.88 +/- 5.05, p < 0.01). In the PHT group were, in addition to the different ratio of some branched chain amino acids and tyrosine, also relations between indicators of insulin sensitivity and arginine. It is thus obvious that signs of reduced insulin sensitivity are present in PHT already in the preclinical stage. Relations between the altered insulin sensitivity and arginine, the precursor of nitrogen oxide, apparent only in PHT could be a stimulus for seeking associations with endothelial damage described in insulin resistant conditions.
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PMID:[Relation between serum amino acids and insulin sensitivity (results of a clamp study in offspring of hypertensive patients]. 960 33

37 patients with obvious pregnancy-induced hypertension, 56 normal pregnant women and 40 nonpregnant women in the same age groups were tested on their serum calcium(Ca), phosphorus(P) alkaline phosphatase(AKP), parathyroid hormone(PHT) and calcitonin(CT). Results indicated that the respective means of serum Ca and CT were statistically lower (P < 0.05), while AKP and PTH were higher (P < 0.01) than that of normal pregnant women. It was also confirmed that Ca metabolism of patients with pregnancy-induced hypertension was obviously abnormal. In addition, pathogenesis of pregnancy-induced hypertension was also discussed.
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PMID:[Observation and analysis on metabolism of serum calcium and phosphorus in patients with pregnancy-induced hypertension]. 1092 Nov 21

This review describes the ionic heterogeneity manifest in the pulmonary circulation, particularly as it pertains to hypoxic pulmonary vasoconstriction (HPV) and pulmonary arterial hypertension (PAH). Heterogeneity in potassium (K(+)) channels, key regulators of vascular tone, cell proliferation, and apoptosis rates, contribute to the diverse response of vascular segments to hypoxia and to the localization of pathological changes in PAH. Pulmonary artery (PA) and pulmonary vein (PV) smooth muscle cells (SMC) express several K(+) channel families, including calcium-sensitive (KCa), voltage-gated (K(v)), inward rectifier (Kir), and 2-pore channels. Diversity is created by heterogeneous occurrence of alternatively spliced, mRNA species, assembly of heterotetrameric channels from diverse alpha-subunits, and association of channels with regulatory beta-subunits. Local heterogeneity in transcription factor activity may underlie differences in channel expression. Enrichment of resistance PASMCs with O(2)-sensitive K(+) channels, such as K(v)1.5, partially explains the greater HPV in resistance versus conduit PAs. In addition, resistance PAs are unique in having mitochondria which dynamically alter production of reactive O(2) species (ROS) in proportion to PO(2), thereby regulating K(+) channel activity and controlling expression through transcription factors, such as HIF-1alpha. In intraparenchymal PVs, a coaxial layer of cardiomyocytes encompasses a media of typical vascular SMCs. PV cardiomyocytes have rhythmic contraction and their Kir-enriched channels may be relevant to genesis of atrial arrhythmias and pulmonary edema. K(v) channel expression is decreased in PAH, leading to elevations of cytosolic K(+) and Ca(2+) that impair apoptosis and increase proliferation. Understanding ionic diversity may allow development of therapies that locally increase K(+) channel current and expression to treat PHT.
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PMID:Potassium channel diversity in the pulmonary arteries and pulmonary veins: implications for regulation of the pulmonary vasculature in health and during pulmonary hypertension. 1758 56

Some studies suggest a higher risk of hypertension in people with epilepsy. Captopril, a potent and selective angiotensin-converting enzyme (ACE) inhibitor, is a well known antihypertensive drug. Besides the peripheral renin-angiotensin system (RAS), ACE inhibitors are also suggested to affect the brain RAS which might participate in the regulation of seizure susceptibility. The purpose of the current study was to evaluate the effect of captopril on the protective action of numerous antiepileptic drugs (carbamazepine [CBZ], phenytoin [PHT], valproate [VPA], phenobarbital [PB], oxcarbazepine [OXC], lamotrigine [LTG] and topiramate [TPM]) against maximal electroshock-induced seizures in mice. This study was accompanied by an evaluation of adverse effects of combined treatment with captopril and antiepileptic drugs in the passive avoidance task and chimney test. Captopril (25 and 50 mg/kg i.p.) did not influence the threshold for electroconvulsions. Among the tested antiepileptics, captopril (25 and 50 mg/kg i.p.) potentiated the antiseizure action of CBZ, decreasing its ED(50) value from 12.1 to 8.9 and 8.7 mg/kg, respectively. Moreover, captopril (50 mg/kg i.p.) enhanced the anticonvulsant activity of LTG. ED(50) value for LTG was lowered from 5.1 to 3.5 mg/kg. The observed interactions between captopril and CBZ or LTG were pharmacodynamic in nature as captopril did not alter plasma and total brain concentrations of these antiepileptics. The combinations of captopril with antiepileptic drugs did not lead to retention deficits in the passive avoidance task or motor impairment in the chimney test. Based on the current preclinical data, it is suggested that captopril may positively interact with CBZ and LTG in epileptic patients. The combinations of captopril with the remaining antiepileptics (PHT, VPA, PB, OXC and TPM) seem neutral.
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PMID:Captopril potentiates the anticonvulsant activity of carbamazepine and lamotrigine in the mouse maximal electroshock seizure model. 2071 8


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