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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Indomethacin inhibits prostaglandin synthesis and interferes with renin release; these effects were studied in rabbit renovascular hypertension. 2. Ten intravenous injections (3 mg day-1 kg-1 after two initial doses of 9 mg/kg) of indomethacin were given daily to ten normal rabbits, ten rabbits with two-kidney Goldblatt hypertension (2KH), tension (1KH). Twelve appropriate control rabbits received diluent phosphate buffer without indomethacin. Plasma renin activity and plasma prostaglandin E2 were measured by radioimmunoassay. 3. In the normal group, indomethacin significantly decreased plasma prostaglandin E2 (1-15 to 0-2 ng/ml, SEM 0-2; P less than 0-01) and plasma renin activity (20 to 3 ng h-1 ml-1, SEM 1, P less than 0-01). Plasma creatinine increased slightly but the mean blood pressure was not significantly changed by indomethacin. 4. Six of ten rabbits with 2KH showed results similar to those in the normal rabbits. In four of ten rabbits in which development of 2KH was accompanied by increments in plasma renin activity (18 to 31-5 ng h-1 ml-1, SEM 3 and 4 respectively; P less than 0-01) and plasma prostaglandin E2 (1-2 to 3-4 ng/ml, SEM 0-2 and 0-4 respectively; P less than 0-05), treatment with indomethacin produced renal failure (plasma creatinine increasing to 7-6 mg/100 ml), oliguria, malignant hypertension (mean blood pressure, 168 mmHg, SEM 7-7) and death within 5 days. 5. In 1KH, indomethacin decreased plasma renin activity and plasma prostaglandin E2, but caused increased mean blood pressure (102 to 121 mmHg, SEM 4 and 6 respectively; P less than 0-01) and decreased renal function (plasma creatinine 0-9 +/- 0-04 to 3-5 +/- 1 mg/100 ml, SEM 0-04 and 1 respectively; P less than 0-01). 6. Aggravation of hypertension was conditioned by pre-existing levels of renal function and, to a lesser extent, by plasma renin activities. 7. These results suggest that prostaglandins exert a protective effect on renal function in renovascular hypertension.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Effects of indomethacin in rabbit renovascular hypertension. 107 20

1. The role of renal medullary prostaglandin E has been examined in rats with hypertension induced by sodium chloride and deoxycorticosterone (salt-DOC). 2. Synthesis of prostaglandin E was normal in early salt-DOC hypertension. Indomethacin exacerbated the hypertension, and depressed synthesis of prostaglandin E equally in hypertensive and control rats. 3. Synthesis of prostaglandin E was depressed in rats with late salt-DOC hypertension. 4. The results lend support to the concept that prostaglandin E is involved in the regulation of arterial pressure.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Renal prostaglandin synthesis in hypertension induced by deoxycorticosterone and sodium chloride in the rat. 107 21

1. Urinary kallikrein, sodium, potassium and water excretion, and plasma renin activity were measured before and during the reversal of experimental hypertension produced by unclamping the renal artery in rats. 2. Kallikrein excretion decreased significantly after unclamping, suggesting that it does not play a significant role in the reversal of hypertension. 3. A decrease in plasma renin activity coupled with a slight increase of sodium excretion was observed, indicating that these might participate in the reversal of hypertension.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Urinary kallikrein and plasma renin during the reversal of renovascular hypertension in rats. 107 24

1. The free deoxycorticosterone pool in the rat was measured by means of a radioimmunoassay in vivo. 2. The free deoxycorticosterone pool in rats with adrenal regeneration with normal or high blood pressure was similar. 3. In rats with adrenal regeneration, the free deoxycorticosterone pool 21 days post-operatively was significantly lower than that in sham-operated control rats and returned to control values at 60 days.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Deoxycorticosterone measured by a radioimmunoassay in vivo in rats undergoing adrenal regeneration. 107 30

1. The arteriolar lesions of rats with deoxycorticosterone (DOCA)-salt hypertension have been studied by colloidal carbon injection and light- and electron-microscopy. 2. Colloidal carbon particles enter the media of arterioles to form focal deposits when hypertension develops. 3. The focal lesions are similar to those seen after angiotensin infusion or renal artery constriction. They are characterized by endothelial damage and plasma deposition in the media. 4. Heavy deposition of carbon in the glomeruli of DOCA-treated animals was found to be caused by increased mesangial uptake and not by hypertensive vascular damage. 5. Angiotensin II concentrations fell during the development of hypertension and vascular lesions. The renin-angiotensin system was not implicated in the development of vascular damage in this form of hypertension.
Clin Sci Mol Med Suppl 1976 Dec
PMID:The arteriolar lesions of steroid hypertension in rats. 107 33

1. Using a newly developed and validated radioassay method, we have measured plasma 11-deoxycorticosterone concentrations in a wide spectrum of human hypertensive states. 2. Patients with essential and renovascular hypertension have normal plasma concentrations of 11-deoxycorticosterone. 3. Elevated concentrations are seen in some patients with primary aldosteronism, Cushing's syndrome, low-renin hypertension, and in adult hypertensive subjects with elevated urinary 17-ketosteroid excretion. 4. An aetiological role for deoxycorticosterone in certain forms of human hypertension appears likely.
Clin Sci Mol Med Suppl 1976 Dec
PMID:The role of 11-deoxycorticosterone in human hypertension. 107 34

1. Renal hypertensive rats with a normal or suppressed activity of the renin-angiotensin system develop vascular lesions which are similar to those observed in spontaneously hypertensive rats on high sodium diet. 2. Exposure of a vascular bed to high blood pressure results in a rapid damage of the vascular wall, irrespective of the state of the renin-angiotensin system.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Does the renin-angiotensin system contribute to the vascular lesions in renal hypertensive rats? 107 39

1. The autonomic and local control of the circumflex coronary bed evoked through acute rises in aortic pressure (aortic balloon inflation) was analysed in conscious, normotensive and hypertensive dogs in complete heart block with ventricles paced at 100 beats/min. 2. In normotensive dogs there was an initial rise (6-12 s) in circumflex conductance preceding a fall in conductance as aortic pressure increased and was sustained. The initial rise, but not the later fall, in circumflex conductance was partly due to a cholinoreceptor and partly due to alpha-adrenoreceptor mechanisms. Local constrictor mechanisms were responsible for the later fall in conductance. 3. The initial cholinoreceptor component of the rise in circumflex conductance is initiated through arterial baroreflex mechanisms. 4. The initial autonomic mechanisms regulating circumflex conductance appear to be absent in renal hypertension. 5. The absence of the transient autonomic rise in circumflex flow and conductance in response to rapid elevations in aortic pressure in certain forms of hypertension, e.g; during tachyarrhythmias and behavioural disturbances, may result in myocardial ischaemia when it is least appropriate.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Baroreflex control of coronary conductance in normotensive and renal hypertensive conscious dogs with complete heart block. 107 46

1. Hypertension was produced experimentally in three groups of rabbits by atherosclerosis, meical sclerosis and renal encapsulation. 2. The sensitivity of afferent baroreceptor fibre recordings, obtained from an isolated perfused aortic arch preparation, was reduced in all three treated groups. 3. The reduction of baroreceptor sensitivity was directly related to the increase in the lability of the blood pressure in the intact animal and to the reduction of the distensibility of the perfused region. 4. There was a closer relationship between the length of time of rabbits had been hypertensive and the reduction in the baroreceptor sensitivity, than to the level of their blood pressure. 5. The reduction of baroreflex sensitivity obtained by the infusion of phenylephrine was also directly correlated with the period of the hypertension. 6. Baroreceptor resetting occurred to a higher pressure in the renal hypertensive group.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Time-course of the reduction of baroreceptor sensitivity in experimental hypertensive rabbits. 107 47

1. A new experimental system has been used to analyse factors involved in the initiation of atherosclerosis in rats. 2. Arterial fat deposition in the cerebral arteries was affected by blood pressure, serum cholesterol concentrations, strain difference and age, of which high blood pressure was the most important. 3. A genetic factor independent of hypertension was shown to be involved in acute arterial fat deposition in spontaneously hypertensive rats.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Importance of hypertension and genetic factors for atherogenesis in rats. 107 48


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