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

The antihypertensive effect of a new vasodilator with betablocking properties (SK & F 92657) was investigated in 10 patients with mild to moderate essential hypertension. After a mean treatment period of 26,5 weeks (6,5-49 weeks) blood pressure was significantly reduced, from 168 +/- 22/106 +/- 6 mmHg to 144 +/- 19/94 +/- 12 mmHg (p less than 0.05 and 0.025). The mean dose was 410 mg (100-700 mg). Heart rate decreased slightly from 77 +/- 12 to 70 +/- 8 beats/min. Plasma renin activity and plasma aldosterone showed only minor changes. Nausea, heavy dreams, facial and hand flushing and mild depression were reported as side effects. In most patients the symptoms disappeared without reduction in the dose. In one patient anaemia developed after 7 weeks and treatment with prizidilol was stopped. A slight but statistically significant decrease in haemoglobin concentration of 1.1 +/- 0.6 g/dl was observed in 5 of the 10 patients (p less than 0.02). Thus, a mean dose of prizidilol of 410 +/- 242 mg/day had a mean blood pressure lowering effect of 24/12 mmHg. In 7 of the 10 patients (70%) diastolic blood pressure could be reduced to 95 mmHg or less. However, the observed haematological side-effects should be carefully monitored in further studies and may limit the clinical use of prizidilol.
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PMID:Prizidilol (SK & F 92657), a new vasodilator with beta-blocking properties in the treatment of essential hypertension. 612 80

Sixty four patients with essential hypertension were studied by phonocardiographic systolic time intervals. Prolongation of the pre-ejection period (PEP) at expense of the isovolume contraction time and of the true isovolume contraction time, which suggests myocardial contractile depression due to the increase in after-load. The significant increase, in rise of mean velocity of ventricular pressure suggests that the Anrep phemomena is used by the human heart as a compensatory mechanism in systemic hypertension. Ejection fraction in hypertensives was significantly lower (P less than 0.001) than that of normal controls, which indicates subclinical depression of ventricular function in the former. Myocardial hypertrophy can be considered as a compensatory mechanism which appears late in systemic hypertension and helps normalize ventricular performance and MVO2. It is clinically detected by an s-4 (registered by phonocardiographic tracings) and by an increase in the "A" index and the apexcardiogram (14.5 +/- 8%). The authors conclude that hypertensive heart disease can be identified early through the functional adaptations wich produce detrimental physiopathological reactions to the heart compensated initially by homeometric autorregulation and latter by myocardial hypertrophy.
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PMID:[Hypertensive cardiopathy. Phonomechanocardiographic study and review of its physiopathological mechanisms]. 622 4

Hormonal and mean arterial pressure (MAP) responses to posture, isometric handgrip, angiotensin II (AII), adrenocorticotrophic hormone (ACTH), and metoclopramide (MCP), a dopamine (DA) antagonist, were examined in nine men with essential hypertension and nine age- and weight-matched normotensive men on a constant 100 mEq sodium and 80 mEq potassium intake before and after 4 days of administration of the DA agonist, bromocriptine (BEC; 2.5 mg three times a day). BEC depressed supine basal MAP in the hypertensives, and decreased MAP response to posture and isometric exercise in both groups. Hypertensives displayed greater (p less than 0.01) NE responses to posture and exercise than the normotensives. BEC decreased the NE response to 10 minutes of upright posture and exercise more in hypertensives (p less than 0.01) than in normotensives, but following BEC, the responses were similar. BEC did not affect basal PRA or PRA responses to posture and exercise in the two groups. PA responses to ACTH and MCP were similar in both groups, but the hypertensives displayed greater (p less than 0.01) PA responses to AII. BEC suppressed PA responses to AII (p less than 0.01) and to high dose ACTH (p less than 0.05) to a similar extent in both groups. The prolactin as well as the PA response to DA antagonism with MCP was similar in the two groups. These results suggest that dopaminergic control of NE secretion may be altered in essential hypertension. Blood pressure lowering effects of BEC in patients with essential hypertension may be related, in part, to depression of sympathetic nervous system activity.
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PMID:Dopaminergic modulation of pressor and hormonal responses in essential hypertension. 627 98

The concurrent administration of tricyclic antidepressants has been shown in man to result in a clinically significant impairment of the antihypertensive effect of clonidine. This interaction is thought to be related to competition for central alpha 2 receptors where clonidine acts as an agonist and the tricyclics act as antagonists. Although it seems to cause less cardiovascular effects than tricyclic antidepressants, the tetracyclic antidepressant, mianserin also has been reported to be an alpha receptor antagonist and may, therefore, also interfere with the antihypertensive activity of centrally-acting drugs. This study investigates the effects of acute and chronic mianserin administration in patients with essential hypertension established on long term treatment with either clonidine or methyldopa. The first dose of mianserin was not associated with an increase in blood pressure and during a further two weeks of mianserin therapy there were no significant alterations in blood pressure, supine or erect. Similarly, mianserin did not alter heart rate either after acute or after chronic administration. Mianserin itself had a sedative effect but there was no interference with the sedation attributable to clonidine or methyldopa. Mianserin caused no reduction salivary flow and did not influence the reduced saliva production caused by clonidine. Both clonidine and methyldopa are associated with a reduction in sympathetic outflow but there was no evidence in this study of any further change in plasma noradrenaline or 24 h urinary catecholamine excretion. This study demonstrates that if mianserin is given acutely or chronically, it does not interfere with the effects of the centrally acting anti-hypertensive drugs, clonidine and methyldopa. Mianserin may therefore be a suitable antidepressant for patients receiving these antihypertensive agents if drug treatment for depression is indicated.
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PMID:Absence of an effect of mianserin on the actions of clonidine or methyldopa in hypertensive patients. 629 52

Serum angiotensin-converting enzyme activity (s-ACE) was measured spectrophotometrically in a variety of renal disorders. In 111 renal patients not on dialysis, s-ACE was slightly lower (22.9 +/- 5.9 U/ml; mean +/- SD) than in 116 controls 24.4 +/- 6.2 U/ml). In 52 patients on chronic hemodialysis s-ACE was 24.1 +/- 4.7 U/ml; serial analyses done before initiation of chronic dialysis showed a significant increase in s-ACE levels towards normal values. In 38 renal allograft recipients s-ACE was relatively low (22.0 +/- 5.0 U/ml); a significant decrease in s-ACE was observed in patients followed from the time of transplantation (24.6 +/- 6.4 U/ml) to two weeks after transplantation (20.2 +/- 4.5 U/ml). S-ACE was also depressed (17.4 +/- 2.6 U/ml) in 12 patients with acute renal failure, and it increased in parallel with normalization of renal function. S-ACE was normal (24.4 +/- 5.7 U/ml) in 14 patients with essential hypertension. Elevated s-ACE (above mean of controls + 2 SD) was observed in only one patient of the total series. We could not confirm previous reports on elevated s-ACE in dialysis patients, but several factors invalidate a direct comparison between series. Thus, the deviations in s-ACE in renal disorders seem to be discrete: depressed levels in acute renal failure and a relative depression in undialyzed patients with chronic renal disorders. The low activity after transplantation may be secondary to the immunosuppressive treatment.
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PMID:Angiotensin-converting enzyme activity in renal disorders: influence of disease pattern, hemodialysis and transplantation. 632 76

Leucocytes were isolated from venous blood of 11 normotensive volunteers with no family history of hypertension and the sodium efflux rate constants determined both alone and in the presence of increasing physiological concentrations of noradrenaline. There was a significant dose dependent reduction of total sodium efflux rate constant due to a reduction in ouabain sensitive sodium pump activity, glycoside insensitive efflux rate constants being unaffected. The magnitude of this effect was similar to the reduction in leucocyte sodium efflux rate constants observed in hypertensive patients (and their normotensive relatives). The noradrenaline induced depression of sodium pump activity was prevented by propranolol in a further seven experiments, suggesting that the effect was mediated by beta adrenoceptors. Catecholamines possibly functioning as circulating inhibitors of sodium transport may contribute to some of the disturbances in membrane electrolyte handling both in essential hypertension in man and in some experimental models of hypertension.
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PMID:Noradrenaline: a circulating inhibitor of sodium transport. 643 58

The effect of local infusion of ouabain into the forearm vascular bed has been examined in 15 normotensive male volunteers in an attempt to define the nature of the functional abnormalities of the resistance vessels in primary hypertension. Ouabain and other drugs were infused into the brachial artery and forearm blood flow was measured by venous occlusion plethysmography. Infusion of ouabain at 2 micrograms/min for 1 h caused a 26% reduction in forearm blood flow with a small rise in systemic arterial pressure; the increase in vascular resistance was unaffected by prior treatment with phentolamine. After infusion of ouabain the dilator response to potassium was reduced by 33% but the responses to verapamil and sodium nitroprusside were unchanged. The results show that acute depression of sodium pump activity by ouabain reproduces the increased resting resistance and impaired response to potassium that are seen in hypertension. It does not reproduce the relative enhancement of responsiveness to verapamil that is also observed in the resistance vessels of patients with hypertension and this abnormality must have some other cause.
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PMID:Effect of local infusion of ouabain on human forearm vascular resistance and on response to potassium, verapamil and sodium nitroprusside. 668 Oct 36

Atenolol has been studied prospectively in the management of ten patients with essential hypertension during pregnancy. Median supine BP fell significantly from 156/98 mmHg before treatment to 128/82 mmHg at term. Atenolol did not suppress cardiotocographic signs of foetal distress. Although there was one intrauterine death, the remaining nine babies had a median Apgar score at birth of 9 and a median weight which was 82% of the gestational mean. There were no cases of neonatal bradycardia or respiratory depression and the only case of hypoglycaemia was in a dysmature baby. These findings justify a formal study of beta-adrenoceptor blocker therapy in hypertensive diseases of pregnancy.
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PMID:Atenolol in the treatment of essential hypertension during pregnancy. 710 79

To determine whether basal blood pressure or pressor responses to stress are related to sympathetic nerve tone or to psychological factors in hypertensives, 15 hypertensives and 13 normotensives were studied by mean of a self-administered questionnaire, isometric handgrip exercise (IHE), and the mental stress of serial subtraction. Plasma norepinephrine (NE), epinephrine (E), blood pressure (BP) and heart rate (HR) were measured before and at the end of IHE and mental stress. A greater number of hypertensives had suppressed anger (p less than 0.01) and scored higher on anxiety trait (p less than 0.01) and depression (p less than 0.05). Prestress (IHE and mental) BP and NE values were significantly greater in hypertensives (all p less than 0.01). During IHE, both groups had a significant increase of BP, HR, and NE (all p less than 0.01) but E rose in hypertensives only (p less than 0.05). The percentage change of BP, HR, NE, and E during IHE was similar in both groups. The changes of BP and HR were not related to NE or E. During mental stress, HR (p less than 0.01) and E (p less than 0.05) increased in both groups. However, BP (systolic and diastolic) increased in normotensives only (p less than 0.01). Plasma NE contents were unchanged in both groups. There were significant positive correlations of anxiety trait with systolic BP (p less than 0.05), diastolic BP (p less than 0.05), and NE (p less than 0.05) and E (p less than 0.05). Although hypertensives had increased neurogenic tone related perhaps to inward anger and anxiety, the percentage responses of neurogenic tone and BP to IHE were equivalent to those of normotensives. The challenge of serial subtraction did not elicit further noradrenergic or pressor responses in hypertensives. Suppressed anger and anxiety, via increased basal neurogenic tone, may be pathogenic factors in some patients with primary hypertension.
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PMID:Anxiety, anger, and neurogenic tone at rest and in stress in patients with primary hypertension. 729 29

This study examines the influence of dopamine on recumbent circadian mean arterial blood pressure (MAP) levels and secretory patterns of norepinephrine (NE) in essential hypertension. Nine patients with sustained essential hypertension were studied after they had reached metabolic equilibrium of a constant 100-mmol sodium and 80-mmol potassium intake. MAP measurements and plasma NE determinations were made at 30-min intervals over 24 h during a control (no medication) and a bromocriptine (BEC) period (2.5 mg, three times a day for 5 days). In the control period, a clear circadian rhythm in blood pressure was evidenced in these hypertensive patients, with lowest MAP occurring during sleep. NE was secreted in an episodic manner, with most secretory peaks occurring between 0600-1800 h. Sleep was characterized by lower levels of NE than in waking hours and a paucity of secretory peaks. During the control period, recumbent 24-h MAP was strikingly correlated with plasma NE (gamma = 0.67; P less than 0.001). BEC treatment was associated with a depression in MAP throughout the 24-h cycle and a lessening of the relationship between MAP and plasma NE (gamma = 0.35; P less than 0.025). BEC eliminated much of the circadian variation in plasma NE secretion in these hypertensives. Thus, circadian variations in sympathetic nervous system activity and blood pressure in patients with essential hypertension appear to be modulated by a central and/or peripheral dopaminergic mechanism.
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PMID:Dopaminergic control of circadian norepinephrine levels in patients with essential hypertension. 729 97


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