Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0011570 (depression)
172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of diltiazem on hemodynamics, plasma catecholamine and plasma renin activity were studied during treadmill exercise test in 9 cases with moderate essential hypertension. Diltiazem of 120 mg/day was orally administered for 4 weeks. At maximum exercise, significant decrease in systolic blood pressure (-32 mmHg), heart rate (-16/min), pressure-rate product (-7,883 mmHg/min), plasma norepinephrine (-195 ng/L) and plasma epinephrine (-11 ng/L) were observed; while, diastolic blood pressure, ST depression and plasma renin activity showed no significant change. Also, a significant correlation between systolic blood pressure and plasma norepinephrine (r = 0.57, p < 0.001), especially after diltiazem therapy (r = 0.68, p < 0.001), was observed. These findings indicated that diltiazem can reduce the secretion of catecholamine from the sympathetic nerves during exercise in patients with essential hypertension.
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PMID:[Effects of diltiazem on hemodynamics, plasma catecholamine and renin activity during exercise in hypertension]. 184 25

Epidemiologic studies have shown that insulin is a risk factor for coronary heart disease (CHD). Clinical studies have also demonstrated positive correlations between insulin and blood pressure, triglycerides, total cholesterol, fibrinogen, and plasminogen activator inhibitor. Moreover, there is an inverse correlation between insulin and high-density lipoprotein (HDL). These studies have provided evidence in support of the biologic plausibility of epidemiologic observations, but they have not clearly established insulin's role in the pathogenesis of human cardiovascular diseases (CVD) such as hypertension. In fact, there is considerable evidence that insulin resistance (abnormal nonoxidative glucose disposal), not hyperinsulinemia, is the primary insulin-related abnormality in human hypertension, and that hyperinsulinemia occurs as a response to insulin resistance. Skeletal muscle appears to be the primary site of insulin resistance in essential hypertension, although other organs, such as the kidneys and liver--key sites for cell and water homeostasis and lipoprotein regulation, respectively--may respond normally to insulin. Adipocytes also appear to be a site of insulin resistance. Thus, the putative interrelationship between hyperinsulinemia and insulin resistance, on the one hand, and with blood pressure and lipoproteins, on the other, is a complex one and may involve organ-specific insulin resistance. Altered cation transport is one of several mechanisms by which insulin resistance might raise blood pressure. The Na+, K(+)-ATPase and Ca(2+)-ATPase pumps are insulin sensitive. Thus, when insulin resistance is present, the activity of these pumps in the smooth muscle of the arterial wall might be reduced. This would lead to an intracellular accumulation of sodium and calcium, thereby sensitizing the vascular wall to pressor substances. Moreover, secondary hyperinsulinemia will occur, and insulin has been shown to stimulate sympathetic nervous system activity and to increase renal tubular absorption of sodium. Insulin is also a growth factor and therefore might have a trophic effect on the vessel wall, one that could initiate and/or sustain hypertension as well as atherosclerosis. Abnormal lipoprotein metabolism is yet another possible explanation for the accelerated atherosclerosis that has been observed in persons with abnormal carbohydrate tolerance and insulin resistance. Hyperinsulinemia and insulin resistance both play a role in the expression of elevated very-low-density lipoprotein (VLDL) and low-density lipoprotein (LDL) levels as well as in the depression of HDL levels. Coronary risk reduction has been disappointing when blood pressure has been lowered with treatment regimens based on thiazide diuretics and/or beta blockers. Thiazides and some beta blockers may further impair tissue insulin sensitivity and often cause blood lipoprotein abnormalities.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Epidemiologic and clinical aspects of insulin resistance and hyperinsulinemia. 186 24

In order to clarify the role of renal dopaminergic activity in renal sodium-water metabolism, the effects of oral administration of L-DOPA (400 mg), were studied on blood pressure (BP), plasma renin activity (PRA), plasma aldosterone concentration (PAC), urinary volume (UV), urinary excretion of sodium and lithium (UNa and ULi) in 11 normal subjects (N) and 32 patients with essential hypertension (EH). EH were divided into the salt sensitive (SS) and non salt-sensitive (NSS) groups by response of mean blood pressure (10% increase) after administration of NaCl. The change of UNa, PRA, and PAC after administration of NaCl were lower in SS than in NSS. After administration of L-DOPA, BP falled and UV, UNa, FENa, FELi and Ccr increased in both N and EH. The change of these factors were greater in SS as compared with those in NSS. These results suggest that in SS patients the suppression of water-sodium handling in the kidney might be due to depression of renal dopaminergic activity. Renal dopaminergic activity may play an important role in the pathogenesis of EH.
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PMID:[Significance of renal dopamine on pathogenesis of essential hypertension]. 206 17

ECG evidence of silent ischemia occurs commonly in patients with systemic hypertension, but its relationship to left ventricular hypertrophy (LVH), large-vessel coronary artery disease (CAD), and neurohumoral factors remains unclear. Accordingly we validated the results of the echocardiographic method used to measure left ventricular (LV) mass in the Soviet Union by comparison with necropsy measurements in 30 patients, and we examined the relationships in 46 men with essential hypertension among ST segment depression during ambulatory monitoring, exercise stress and transesophageal pacing (n = 38), and LV mass, catheterization evidence of CAD (n = 25), and neurohumoral factors (plasma catecholamines and platelet aggregability). Echocardiographic measurements of LV mass by both the Soviet and Penn methods were closely correlated with necropsy values (r = 0.78 and 90, respectively; both p less than 0.001). During ambulatory monitoring from 1 to 17 episodes of greater than or equal to 1 mm ST depression occurred in 26 of 46 (65%) patients with hypertension; ischemia was also provoked by exercise or pacing stress in most but not all of these patients (65% and 80%, respectively). Neither ST depression nor the occurrence of additional episodes of symptomatic angina was related to the presence of coronary obstruction at catheterization; patients with and without ST depression did not differ in age, blood pressure, or LV mass.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypertensive heart disease: relationship of silent ischemia to coronary artery disease and left ventricular hypertrophy. 214 35

Twenty consecutive, chronic low back pain patients admitted to our pain treatment unit completed the Attributional Style Questionnaire (an instrument that detects a cognitive style that is correlated with, and that predicts, depression) and the Beck Depression Inventory. An age, sex, and education-matched group of normal subjects, a group of patients with asymptomatic essential hypertension, and a group of patients with end-stage renal disease receiving dialysis treatment served as controls. The majority of the chronic-pain and renal-dialysis patients had elevated depression scores, whereas none of the normal subjects or hypertensive patients were outside the nondepressed range. The Attributional Style scores of the pain and renal dialysis patients were significantly deviant from the normal control group, but no more so than those of the patients with hypertension. The results of this study suggest that individuals with a chronic medical condition, either symptomatic (chronic low back pain or renal disease) or asymptomatic (essential hypertension) in nature, develop an attributional style characteristic of depression. These data neither lend support nor refute the thesis that chronic pain syndromes are a variant of, or a masked, depression. Rather, this research implies that a more important question is what identifiable risk factors (for example, attributional style) predispose patients with chronic pain to develop a depressive illness.
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PMID:Chronic low back pain, depression, and attributional style. 215 7

A sample of family practice patients with essential hypertension (N = 106) who were predominantly elderly, black, and disadvantaged were studied to determine psychosocial and physiological side effects from antihypertensive therapy regimens. Patients were assigned randomly to one of four monotherapy treatment groups: Hydrochlorothiazide-triamterene, metoprolol, captopril, and methyldopa. These medications have been reported to have contrasting effects on quality of life. Measurements of quality of life, physical symptoms, and depression taken at baseline and during therapy revealed few significant changes in these indicators. Changes in mean levels of diastolic and systolic hypertension over time were clinically and statistically significant. Findings raise issues regarding medication effectiveness and cost given the disadvantaged population studied.
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PMID:Antihypertensive regimen and quality of life in a disadvantaged population. 229 9

Effects of submaximal exercise were studied on the unipolar esophageal electrocardiogram recorded at ventricular level in 15 patients with essential hypertension who complained of chest discomfort on effort but had negative exercise stress tests using standard leads and lead CM5. Six patients developed horizontal or downsloping depression of the ST segment in the esophageal lead. The ischemic response might result from subcritical coronary stenosis in face of the increased myocardial oxygen demand of hypertrophied myocardium.
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PMID:Early detection of myocardial ischemia in hypertensive patients using exercise esophageal electrocardiography. 230 6

In asymptomatic patients with essential hypertension, electrocardiographic changes suggestive of myocardial ischemia can be elicited by rapid pressure lowering or by pronounced coronary arteriolar dilation. The aim of this study was to assess whether dipyridamole infusion might induce ischemic-like electrocardiographic changes in asymptomatic essential hypertensive patients and to describe the clinical and echocardiographic correlates possibly associated with this response. We therefore studied a control group of 20 normotensive individuals and a group of 28 asymptomatic patients with mild-to-moderate essential hypertension. All underwent dipyridamole-echocardiography testing (12-lead electrocardiogram and two-dimensional echocardiographic monitoring with dipyridamole infusion, 0.84 mg/kg over 10'). No patient showed transient regional dyssynergy during dipyridamole infusion. None of the normotensive and 10 of 28 of the hypertensive participants had horizontal or downsloping ST segment depression more than 0.1 mV during dipyridamole (0% versus 36%, p less than 0.01). Hypertensive patients with ("responders") (n = 10) and without ("nonresponders") (n = 18) ST segment depression showed similar values of percent fractional shortening in baseline conditions (32 +/- 5 versus 33 +/- 6, p = NS) and at peak dipyridamole infusion (45 +/- 8 versus 43 +/- 5, p = NS). The peak early to peak late velocity ratio values (evaluated from transmitral flow tracings by Doppler technique) were also similar in baseline conditions (0.86 +/- 0.14 versus 0.94 +/- 0.30, p = NS) and at peak dipyridamole (0.72 +/- 0.15 versus 0.78 +/- 0.32, p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:ST segment depression elicited by dipyridamole infusion in asymptomatic hypertensive patients. 236 45

Patients with hypertension in the clinic but not during daily activities ("white coat" hypertension) may be at lower risk of hypertensive morbidity and mortality than patients with hypertension in both settings ("persistent" hypertension). We hypothesized that the white coat phenomenon was due to greater blood pressure reactivity to the stress of a clinic visit and that, as a consequence, white coat hypertensive patients would display greater blood pressure reactivity to exercise and mental stress, as well as increased emotional reactivity and higher levels of anger, anxiety, or depression. We studied 89 patients with essential hypertension between 29 and 59 years old with ambulatory blood pressure monitoring, treadmill exercise testing with oxygen consumption measurement, mental stress testing (including mental arithmetic, public speaking, and video game tasks), and psychological testing (State-Trait Anxiety Scale, Cook-Medley Hostility Scale, Center for Epidemiologic Studies Depression Scale, emotional reactivity scale). We defined white coat hypertension as a mean ambulatory systolic blood pressure of 135 mm Hg or less and diastolic 85 mm Hg or less and persistent hypertension as a mean ambulatory systolic blood pressure of 140 mm Hg or more or diastolic 90 mm Hg or more. Forty-nine patients were classified as persistent hypertensives and 20 as white coat hypertensives. No significant differences were seen in demographic or clinical characteristics, fitness level, blood pressure response to exercise or mental stress, or psychological characteristics, except that white coat hypertensive patients had lower systolic blood pressures in the clinic and during exercise and greater variability of clinic diastolic blood pressures.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Physiological, psychological, and behavioral factors and white coat hypertension. 237 47

Since the cardinal hemodynamic disorder in essential hypertension is an increased total peripheral resistance, drugs that can lower resistance without reducing blood flow would be particularly useful. The calcium antagonists seem to fulfill this criterion. The purpose of this work was to study the hemodynamic effects at rest and during exercise of three calcium channel blockers, verapamil, nifedipine, and nisoldipine, in patients with mild to moderate essential hypertension. Fifty-four patients aged 20-64 years with pretreatment diastolic blood pressures of between 95 and 120 mm Hg were studied at rest and during exercise on an ergometer bicycle. Blood pressure was recorded intraarterially and cardiac output was measured by Cardiogreen. After the initial study, 10 patients were treated with verapamil (40-80 mg three times daily), 15 with nifedipine (long-acting form, 20-80 mg daily), and 19 with nisoldipine (10-40 mg daily). After 1 year the hemodynamic study was repeated. The immediate response to the first dose was studied in the patients taking nisoldipine and in 10 patients after taking placebo tablets. Placebo induced no significant changes in central hemodynamics during the first 3 h after tablet intake. The calcium antagonists induced a reduction in blood pressure and in total peripheral resistance (in the order of 10-18%) without any reduction in cardiac index. Reflex tachycardia and an increase in cardiac output were seen in the first 2 h after the first dose of nisoldipine, but after 1 year the heart rate was unchanged compared with the pretreatment rate at rest and during exercise. In contrast, heart rate was reduced on verapamil treatment, particularly during exercise (about 10% of patients), but this was compensated for by an increase in the stroke volume. The hemodynamic profiles of the three calcium channel blockers were slightly different, especially with respect to the heart rate response. Total peripheral resistance was reduced, acutely as well as chronically, and no depression in cardiac pump function was seen, either at rest or during exercise.
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PMID:Central hemodynamic changes of calcium antagonists at rest and during exercise in essential hypertension. 244 6


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