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Biomedical subjects

M Tree

Publications and source records attributed to M Tree.

At least 19 recordsLinked to original sources
PubMed1992

Effects of the angiotensin II receptor antagonist Losartan (DuP 753/MK 954) on arterial blood pressure, heart rate, plasma concentrations of angiotensin II and renin and the pressor response to infused angiotensin II in the salt-deplete dog.

1. The blood pressure, heart rate, hormonal and pressor responses to constant rate infusion of various doses of the angiotensin (type 1) receptor antagonist Losartan (DuP 753/MK 954) were studied in the conscious salt-deplete dog. 2. Doses in the range 0.1-3 micrograms min-1 kg-1 caused no change in blood pressure, heart rate or pressor response to angiotensin II (54 ng min-1 kg-1), and a dose of 10 micrograms min-1 kg-1 had no effect on blood pressure, but caused a small fall in the pressor response to angiotensin II. Infusion of Losartan at 30 micrograms min-1 kg-1 for 3 h caused a fall in mean blood arterial pressure from baseline (110.9 +/- 11.2 to 95.0 +/- 12.8 mmHg) and a rise in heart rate (from 84.6 +/- 15.1 to 103 +/- 15.2 beats/min). Baseline plasma angiotensin II (42.5 +/- 11.8 pg/ml) and renin (64.5 +/- 92.7 mu-units/ml) concentrations were already elevated in response to salt depletion and rose significantly after Losartan infusion to reach a plateau by 70 min. The rise in mean arterial blood pressure after a test infusion of angiotensin II (35.3 +/- 11.6 mmHg) was reduced at 15 min (11.8 +/- 6.8 mmHg) by Losartan and fell progressively with continued infusion (3 h, 4.3 +/- 3.3 mmHg). The peak plasma angiotensin II concentration during infusion of angiotensin II was unaffected by Losartan, but the rise in plasma angiotensin II concentration during infusion was reduced because of the elevated background concentration. Noradrenaline infusion caused a dose-related rise in mean blood arterial pressure (1000 ng min-1 kg-1, +19.9 +/- 8 mmHg; 2000 ng min-1 kg-1, +52.8 +/- 13.9 mmHg) with a fall in heart rate (1000 ng min-1 kg-1, -27.9 +/- 11.5 beats/min; 2000 ng min-1 kg-1, -31.2 +/- 17.3 beats/min).(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1979

Inhibitors of the renin-angiotensin system in experimental hypertension, with a note on the measurement of angiotensin I, II and III during infusion of converting-enzyme inhibitor.

1 Prolonged infusion (11 h) of both saralasin and angiotensin-converting enzyme inhibitor (SQ20881) gradually lowered BP in two-kidney hypertensive rats to levels similar to that in normotensive rats infused with dextrose. 2 Saralasin did not lower BP in DOCA-salt hypertensive rats. 3 These observations support the notion that in chronic renal hypertension, angiotensin II may maintain hypertension by a slowly developing action. 4 Plasma angiotensin II in rats infused with SQ20881 was suppressed relative to renin, but was not eliminated. 5 Chromatography of angiotensin II extracts from dogs infused with converting enzyme inhibitor (SQ14,225) showed that the very high levels of angiotensin I achieved after treatment with SQ14,225 can lead to falsely high estimated angiotensin II levels as a result of angiotensin I cross-reacting with the angiotensin II assay.

Angiotensin I↗
PubMed1978

An altered relation between arterial pressure and plasma angiotensin II concentration resulting from prolonged infusion of angiotensin II.

1. Infusion of angiotensin II into dogs at constant dose over 2 weeks caused a progressive rise in arterial pressure. 2. When the infusion was stopped the pressure dropped slowly from hypertensive levels over 48 h. 3. Dose-response studies at weekly intervals showed progressive elevation, without steepening, of the plasma angiotensin II-blood pressure curve. 4. Thus, during prolonged administration of angiotensin II, a given plasma concentration of the peptide can sustain a higher arterial pressure than it can during acute infusions.

Aldosterone↗
PubMed1978

Angiotensin II/aldosterone dose-response curves in the dog: effect of changes in sodium balance.

The possibility that the responsiveness of plasma aldosterone concentration to angiotensin II alters with changes in sodium balance was investigated in male beagle dogs under conditions of controlled sodium and potassium intake. Angiotensin II was infused at four different rates (usually 3, 6, 12, and 24 ng/kg/min), each for 1 h, 1) after periods of normal sodium diet (32 mEq/day), 2) after moderate sodium depletion (negative cumulative sodium balance 25-58 mEq), 3) after severe sodium depletion (65-116 mEq negative cumulative sodium balance), and 4) after sodium loading (150-212 mEq positive sodium balance), daily potassium intake remaining constant (26 mEq/day) throughout. Angiotensin II/aldosterone dose-response curves after moderate sodium depletion were both elevated and steepened in comparison with those found during normal sodium intake. Severe sodium depletion was associated with even greater elevation of dose-response curves, but individual aldosterone responses to angiotensin II were irregular and unpredictable. Sodium loading significantly diminished aldosterone responsiveness to angiotensin II. Blood pressure increments during angiotensin II infusion were attenuated by sodium depletion.

Aldosterone↗
PubMed1978

[des-Asp1]angiotensin II in the dog: blood levels and effect on aldosterone.

Circulating levels of [des-Asp1]angiotensin II ([des-Asp1]-AII), angiotensin II (AII), and aldosterone were measured in five conscious beagle dogs before and during iv infusion of [des-Asp1]AII at rates of 3, 6, 12, and 24 ng/kg/min. The animals were studied after 4 days on a normal sodium and potassium diet and again after a period of sodium depletion accomplished by iv furosemide (2-5 mg/kg) and 4 days of low sodium diet (2-5 mmol/day). Compared to the normal sodium diet, sodium depletion resulted in increases in the plasma levels of aldosterone from 10 +/- 2 (SE) to 66 (16-116) ng/100 ml of AII from 16 +/- 4 to 52 +/- 13 pmol/liter and of [des-Asp1]AII from 2 +/- 0.7 to 12 +/- 4 nmol/liter. Incremental infusions of [des-Asp1]AII in the sodium replete state resulted in progressive increases in the plasma levels of aldosterone in all dogs. In comparison with a previous study in which dogs were infused with AII, it was apparent that [des-Asp1]AII was equally or slightly more potent in stimulating aldosterone and had a higher metabolic clearance rate than AII. [des-Asp1]AII stimulated aldosterone in four of the five sodium-depleted dogs but no steepening of the [des-Asp1]AII/aldosterone dose-response curves was apparent. These results do not support the hypothesis that circulating [des-Asp1]AII mediates the effect of AII on aldosterone in the dog.

Aldosterone↗
PubMed1977

Angiotensin II in essential hypertension.

Plasma concentrations of angiotensin II (PAC) were measured in a group of 146 hypertensive patients (diastolic pressure greater than 105 mm Hg) who had no apparent underlying cause for their condition and 113 randomly selected normotensive controls (diastolic pressure less than 90 mm Hg). There was no evidence of bimodality in the frequency distribution curves for plasma angiotensin II concentrations among the hypertensive patients. It was concluded that hypertension associated with low angiotensin II concentration and by implication "low-renin" hypertension is not a condition separate from essential hypertension.

Angiotensin II↗
PubMed1977

An inactive renin in human plasma.

Normal human plasma contains an active form of renin that is activated by acidification to pH 3.0 and comprises 56% of the total renin. In our study, inactive renin was also present in plasma from five anephric persons, and the proportion of active to inactive renin in these subjects was similar to normal. Plasma from normal pregnant women contained increased concentrations of inactive renin and the proportion of inactive renin was raised to around 66%. Plasma from persons with renal hypertension contained varying amounts of inactive renin but the mean percentage (35%) was lower than normal. An infusion of saralasin sufficient to lower the blood pressure in five subjects with renal hypertension resulted in a rise in active renin concentration but no change in the concentration of inactive renin. Plasma angiotensin II correlated with active renin but not with inactive renin, suggesting that the inactive renin does not produce angiotensin II in vivo.

Angiotensin II↗
PubMed1976

Measurement of plasma renin concentration and angiotensin II in peripheral and renal venous plasma in the management of renovascular hypertension.

Athough in general, measurement of renal vein renin appears to give a good prediction as to the subsequent response to surgery, its main value lies in its ability to reflect changes in renal plasma flow; true changes in renin secretion rate being much more difficult to detect. Although it is a little early to say how much information can be derived from saralasin infusions, caution must be exercised in necessarily assuming that the test accurately reflects subsequent surgical response.

Adult↗
PubMed1976

Response of aldosterone and blood pressure to angiotensin II infusion in anephric man. Effect of sodium deprivation.

Angiotensin II, infused intravenously, increased plasma aldosterone concentration in two of six anephric subjects taking their usual dietary quantities of sodium. After 3 days of dietary sodium restriction and weight-reducing hemodialysis, the aldosterone response to infused angiotensin II in the two previously reactive subjects was enhanced, while the four previously unreactive subjects also showed a rise in plasma aldosterone. Before and after sodium depletion the anephric subjects were less responsive than normal subjects. Even when sodium-depleted, the anephrics showed no further rise in plasma aldosterone when arterial plasma angiotensin II was increased by infusion to concentrations greater than 50-199pg/ml, in contrast to sodium-depleted normals who show progressive aldosterone responses with plasma angiotensin II concentrations up to at least 370pg/ml. Before the infusion of angiotensin II, arterial plasma renin, angiotensin II, and aldosterone were detectable in the anephrics, but were unchanged by dietary sodium restriction or weight-reducting hemodialysis. Sodium depletion caused significant falls in weight, plasma sodium, and blood pressure, but no changes in plasma potassium or cortisol. Increases in blood pressure in relation to increments of arterial plasma angiotensin II were unaffected by sodium depletion, as might be expected in the absence of a rise in endogenous angiotensin II.

Adult↗