Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Reversal of the normal diurnal blood pressure pattern has been demonstrated in women with severe hypertension and renal impairment in pregnancy (pre-eclampsia). 2. Maximum arterial pressure occurred at night in these women. The phenomenon was not due to hypotensive drug therapy or posture. Patients with uncomplicated essential hypertension in pregnancy retained a normal diurnal blood pressure pattern. 3. Nocturnal hypertension in pre-eclampsia is of theoretical interest and practical importance.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Reversed diurnal blood pressure rhythm in hypertensive pregnancies. 107 9

1. The rate of renal excretion of arginine-vasopressin was determined during unrestricted fluid intake for 24 h and in response to fluid deprivation for 18 h in nine young men with very mild essential hypertension and compared with that in sixteen normotensive men of similar age. 2. Despite an equivalent osmolar stimulus, excretion of arginine-vasopressin was significantly greater in the reference group than in the reference group. This difference increased progressively with increasing dehydration. 3. We suggest that these findings are mainly due to an increased rate of secretion of arginine-vasopressin in response to mild hydropenia in hypertensive patients and that a moderate increase of release of arginine-vasopressin during periods of fluid deprivation may exert vascular effects and thus influence the perpetuation of hypertension.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Increased renal excretion of arginine-vasopressin during mild hydropenia in young men with mild essential benign hypertension. 107 11

1. Vascular resistance at maximal vasodilatation was examined in two vascular beds in two groups of hypertensive patients and in normotensive control subjects before and during anti-hypertensive therapy in the hypertension groups. 2. In one group of twelve untreated patients with essential hypertension, examined with plethysmography and intra-arterial blood pressure recording, a significantly higher vascular resistance at maximal vasodilatation was found in the hands compared with normotensive control subjects matched for age, sex, weight and height. This indicated a structural vascular abnormality in the patient group. 3. After 5 years of anti-hypertensive therapy in the patient group the difference in vascular resistance between patients and control subjects had decreased significantly, indicating a reversibility of the structural vascular abnormality. 4. Vascular resistance at maximal vasodilatation was examined in the calves of twelve untreated patients with essential hypertension and fourteen normotensive control subjects. Plethysmographic technique and indirect blood pressure recordings were used. A significantly higher vascular resistance was found in patients than in control subjects, indicating a structural vascular abnormality also in this vascular bed. 5. Anti-hypertensive treatment for 6 months in the patient group did not change vascular resistance at maximal dilatation, indicating that the structural vascular abnormality remained. 6. During acute reduction of blood pressure in hypertension by means of trimethaphan infusion, blood pressure and blood flow to the hands were reduced proportionally with no change of vascular resistance at maximal vasodilatation. 7. This indicates that resistance at maximal dilatation was unaffected by the acute reduction of blood pressure, in contrast to the findings after prolonged reduction of blood pressure in this vascular bed.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Effects of blood pressure reduction on the structural vascular abnormality in skin and muscle vascular beds in human essential hypertension. 107 15

1. A group of patients with essential hypertension was divided into three categories on the basis of the plasma renin activity. 2. There was no correlation between the plasma renin activity categorized as high, normal or low and the duration of hypertension, the incidence of left ventricular enlargement, the blood urea nitrogen, serum creatinine, cholesterol or uric acid respectively. 3. Analysis of data showed that the incidence of cardiovascular events in the hypertensive population correlated with the plasma renin activity only in combination with known risk factors.
Clin Sci Mol Med Suppl 1975 Jun
PMID:Plasma renin activity and cardiovascular disease. 107 64

1. The role of adrenergic neuronal mechanisms in the development of early hypertension in man and the spontaneously hypertensive rat has been explored. 2. In both, a hyperkinetic circulatory state is associated with reduced parasympathetic and increased adrenergic cardiac influences. 3. Spontaneously hypertensive and normotensive control rats were treated with propranolol from conception until 12 weeks. Although heart rate and output remained reduced, there was no difference in growth or elaboration of pressure with respect to their untreated controls. 4. After another series of spontaneously hypertensive and control rats received cardiac autonomic blockade (atropine and timolol), they sequentially received alpha-adrenergic blockade (phenoxybenzamine), ganglionic blockade (trimethaphan) and smooth-muscle vasodilatation (hydralazine). These studies revealed only a small pressure differential between the two groups before hydralazine and still less thereafter; unlike the control rats, pressure in spontaneously hypertensive rats fell markedly after ganglionic blockade as a result of reduced output, indicating greater adrenergic control mediated through venoconstriction. 5. These findings indicate: increased cardiovascular adrenergic control in young spontaneously hypertensive rats, the hyperkinetic circulation merely reflecting one aspect of increased total cardiovascular input. Structural alterations seem to participate minimally. 6. These experimental observations closely, resemble findings in early hypertensive man, and it is suggested that altered total cardiovascular adrenergic input is responsible for the elaboration, development, and maintenance of essential hypertension in man.
Clin Sci Mol Med Suppl 1975 Jun
PMID:Adrenergic mechanisms in human hypertension and in spontaneously hypertensive rats. 107 70

1. Urinary excretion of dopa, catecholamines and their metabolites (vanillylmandelic acid, methoxycatecholamines, 3-methoxy-4-hydroxyphenylglycol and homovanillic acid) were studied in eighty patients with essential hypertension and in twenty-five healthy control subjects. 2. Increased urinary excretion of catecholamines, dopa and catecholamine metabolites was found in a proportion of cases. 3. The relationship between urinary excretion of catecholamine metabolites and the excretion of dopa and noradrenaline was studied. 4. In view of the suggested significance of 3-methoxy-4-hydroxyphenylglycol as an index of brain catecholamine metabolism, particular attention was paid to urinary excretion of this metabolite in the subjects under study.
Clin Sci Mol Med Suppl 1975 Jun
PMID:Dopa, catecholamines and their metabolites in essential hypertension. 107 80

1. Radioimmunoassay has been used to detect and estimate the urinary excretion of deoxycorticosterone (DOC) in normal, hypertensive and hypokalaemic subjects. The range of excretions in ten healthy normal subjects was 41-232 pmol (13.7-76.7 ng) daily, with a mean of 124 pmol (41 ng). 2. In fourteen subjects with essential hypertension without metabolic disturbance the range found was 29-144 pmol (9.7-47.7 ng) daily, with a mean of 87 pmol (28.8 ng), which is not significantly different from that in normal subjects. 3. In twelve patients with Cushing's syndrome due to adrenal cortical hyperplasia the range found was 26-542 pmol (8.7-179 ng). Ten of these twelve patients had values within normal limits. 4. Of nine subjects showing hypokalaemia, eight had elevated excretion of deoxycorticosterone with values from 263 to 5515 pmol (87-1820 ng) daily. Seven of these were hypertensive and two were normotensive. The elevated excretion of deoxycorticosterone found in hypokalaemic subjects is thus not confined to those with hypertension. 5. No correlation has been found between excretion rates for aldosterone and deoxycorticosterone. Raised excretion of the latter provides an indicator of disturbed adrenal cortical metabolism.
Clin Sci Mol Med 1975 Feb
PMID:Deoxycorticosterone excretion in normal, hypertensive and hypokalaemic subjects. 116 21

1. Intravenous frusemide produced in normal subjects a prompt rise of plasma renin concentration which correlated with urinary sodium. 2. The renin response to frusemide was suppressed in patients with primary hyperaldosteronism. 3. In patients with low-renin hypertension and normal renin essential hypertension, the renin response to frusemide was similarly suppressed. 4. Suppression of the renin response to frusemide is therefore a feature of hypertension not confined to patients with primary hyperaldosteronism and low-renin hypertension. 5. Thus low-renin hypertension does not appear to constitute a distinct diagnostic entity. 6. It is suggested that suppression of the renin response is part of a long-term renal adaptation to high blood pressure.
Clin Sci Mol Med 1975 Oct
PMID:Effect of intravenous frusemide on plasma renin concentration: suppression of response in hypertension. 119 94

1. The effect of physical exercise on blood pressure, plasma catecholamines and plasma renin activity was studied in fourteen patients with essential hypertension and in eight healthy subjects. 2. Resting plasma noradrenaline and adrenaline and plasma renin activity of the hypertensive patients did not differ from those of the control subjects. 3. In response to graded exercise producing successive heart rates of 120, 140 and 160 beats/min, significantly greater increases of blood pressure were found in the patients than in the control subjects. 4. Plasma noradrenaline increased significantly in both groups at all levels of exercise, the responses being significantly greater in the hypertensive patients. 5. The mean arterial blood pressure was significantly correlated with plasma noradrenaline concentration in the control subjects but not in the hypertensive patients. 6. In the hypertensive group plasma adrenaline increased significantly after exercise at all work loads whereas, in the control group, significant increase occurred only at the highest work load. The differences in the response of the two groups were significant at each work load. 7. Plasma renin activity increased significantly after exercise at the heart rate of 120 beats/min, both in the hypertensive patients and in the control subjects. The magnitude of the response was similar in the two groups.
Clin Sci Mol Med 1975 Nov
PMID:Plasma catecholamines and renin activity in response to exercise in patients with essential hypertension. 119 10

1. Nine paatients with clinically unimportant heart disease or benign essential hypertension were given frusemide intravenously during right-heart catheterization. 2. Pressures in both atria decreased rapidly and in parallel. The magnitude of the pressure decrease was clearly related to decrease in plasma volume loss. 3. Plasma renin activity increased significantly after 5 min (P less than 0-01), but did not correlate with plasma volume loss. 4. Venous tone in the forearm was unchanged. 5. It is concluded that the pressure reduction was secondary to plasma volume depletion through diuresis and that increased plasma renin activity was mainly caused by intrarenal changes.
Clin Sci Mol Med 1975 Dec
PMID:The early effects of intravenous frusemide on central haemodynamics, venous tone and plasma renin activity. 120 85


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