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 effect of infusion of the angiotensin II antagonist P113 on blood-pressure (B.P.) has been studied in 10 patients with various forms of hypertension under four different conditions: before and after salt depletion and with or without propranolol treatment. The fall in B.P. after P113 infusion significantly correlated with log P.R.A. (plasma-renin activity), irrespective of diagnosis or treatment. P113 infusion caused a consistent fall in B.P. only after sodium depletion. The changes in B.P. after P113 infusion and those induced by propranolol correlated only during sodium depletion, when P.R.A. values rose. It is concluded that sodium depletion induced "renin dependency" of B.P. in all patients. The decrease in B.P. renin dependency after propranolol therapy suggests that suppression of P.R.A. is one of the antihypertensive mechanisms underlying the action of this drug.
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PMID:Renin dependency of blood-pressure. Analysis by angiotensin II antagonist P113 in hypertensive patients treated with salt depletion and propranolol. 5 53

1. A P113 Saralasin infusion test was performed in 10 patients on long-term regular hemodialysis. Six patients were considered to have hypertension resistant to dialysis treatment and 4 had their arterial pressure controlled by dialysis. 2. Five out of 6 resistant and 3 out of 4 responsive patients had a positive response to Saralasin associated with a normalization of diastolic arterial pressure. 3. The value of the Saralasin infusion test to pre-select the patients for bilateral nephrectomy is discussed and it is felt that a negative test may be of more value in encouraging more aggressive ultrafiltration in hypertension apparently resistant to dialysis therapy.
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PMID:The hypertension of long-term hemodialysis patients: studies with an angiotensin II antagonist (P113). 95 96

1 Three normal subjects were infused with Sar1-ala8-angiotensin II (Saralasin, P113) whilst on a high sodium (200 mEq + normal diet) and a low sodium (10 mEq diet) intake. 2 On the high sodium intake when angiotensin II and plasma renin activity (PRA) were suppressed, P113 infusion (5-10 mug kg-1 min-1) caused a slight rise in BP and a marked drop in urine flow and sodium excretion, with a fall in glomerular filtration rate, and effective renal plasma flow. 3 On the low sodium intake, when angiotensin II and PRA were increased, P113 infusion (5-10 mugkg-1 min-1) caused no change in blood pressure, urine flow or sodium excretion. However, when P113 was infused at an incremental rate starting at 0.25 mug kg-1 min-1 there was a fall in standing BP, which was maximal at an infusion rate of 1 mug kg-1 min-1, and this fall in standing BP was largely abolished as the rate of infusion was increased to 10 mug kg-1 min -1. 4 These results show firstly that angiotension II is involved in maintaning standing blood pressure during dietary sodium depletion in normal man and secondly that P113 does have agonist as well as antagonist activity in normal man, the effect depending on the level of angiotension II and sodium intake. When looking for angiotensin II mediated hypertension it may ne important to use an incremental rate of infusion of P113 as the agonist activity of larger doses may mask its hypotensive action.
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PMID:Agonist and antagonist effects of Sar1-ala8--angiotensin II in salt-loaded and salt-depleted normal man. 97 74

1. Plasma renin activity (PRA) and renin dependency of the blood pressure was analysed in ten patients with various forms of hypertension before and during treatment with volume depletion and/or propranolol. Renin dependency was tested by infusion of the specific competitive angiotensin II antagonist Sar1-Ala8-angiotensin II (P113). 2. The P113-induced fall of the blood pressure did correlate with the log PRA (r=0-888, P less than 0-001). This correlation was found irrespective of different types of hypertension and treatment schedules. 3. During volume depletion, PRA was stimulated and renin dependency of the blood pressure increased. Propranolol therapy suppressed PRA during normovolaemia as well as during volume depletion, and this was accompanied by a decrease of the renin dependency. 4. No incication was found that a given PRA is of special importance for blood pressure elevation in different patients. 5. Suppression of PRA by propranolol is one of the anti-hypertensive mechanisms of this drug.
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PMID:Change in the renin dependency of blood pressure induced by volume depletion and/or propranolol therapy in hypertensive patients. 107 4

We have assessed the capacity of an analogue of angiotensin II (A II), 1-Sar, 8-Ala A II (P113) in normal man to stimulate and block responses to A II in four systems: blood pressure was monitored directly from an arterial catheter, and renal blood flow was measured with 133Xe and arterial renin and aldosterone concentrations by radioimmunoassay. The 31 normal subjects were in balance on a daily intake of 200 meg sodium and 100 meq potassium to suppress endogenous renin. P113 administered intravenously induced a dose-related renal blood flow reduction, with a threshold dose of 0.1 mug/kg/min. This dose also induced a small but significant increase in arterial blood pressure and plasma aldosterone as well as a reduction in plasma renin activity. In contrast to its effect on the renal vasculature, no tendency to a progressive response in the latter three parameters was noted as the P113 dose was increased 30-fold, to 3.0 mug/kg/min. P113 also reduced the clearance of para-aminohippurate, creatinine, sodium, and potassium, a pattern similar to that induced by A II. P113 at 0.1 mug/kg/min reduced significantly the blood pressure and renal vascular and aldosterone responses to graded doses of A II. Higher P113 doses totally obliterated all three responses to A II infused at 10 ng/kg/min, a dose that provides arterial A II concentrations in the range found in angiotensin-mediated hypertension. When A II was infused first, to induce a pressor, renal vascular, and aldosterone response, P113 induced a dose-related reversal of the response in each system. In conclusion, P113 is a partial agonist in normal man, inducing an angiotensin-like response in settings in which endogenous A II is not playing a tonic role, and displaying dominant antagonist activity in settings in which A II is active. Moreover, the studies suggest that the receptors mediating the responses to A II are different in the renal vasculature and other systemic vascular beds. The adrenal receptor must also differ. This agent should be useful in dissecting the role of A II in diseases characterized by hypertension or abnormalities of renal and adrenal function.
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PMID:Blockade and stimulation of renal, adrenal, and vascular angiotensin II receptors with 1-Sar, 8-Ala angiotensin II in normal man. 124 2