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Biomedical subjects

M Tree

Publications and source records attributed to M Tree.

At least 37 records · Page 2Linked to original sources
PubMed1981

Circulating dopamine: its effect on the plasma concentrations of catecholamines, renin, angiotensin, aldosterone and vasopressin in the conscious dog.

1. Six male beagle dogs with carotid loops were infused with sodium chloride solution (150 mmol/l; saline) during control observations followed by dopamine infusion at various rates. Arterial blood samples were drawn during the control period and at the end of each period of dopamine infusion for the measurement of plasma dopamine, noradrenaline, adrenaline, renin, angiotensin II, aldosterone, vasopressin, electrolytes and packed cell volume. Blood pressure and pulse were recorded throughout. 2. The rate of infusion and plasma dopamine levels were closely correlated (r = 0.99, P less than 0.001). Plasma dopamine levels two to 20 times basal values produced no significant change in any of the other variables measured; levels 200 times basal values caused a significant increase (P less than 0.05) in plasma renin concentration; levels 2000 times basal values were associated with significant increases (P less than 0.05) in plasma renin and angiotensin II, packed cell volume and blood pressure, without significant changes in other measurements. 3. Circulating dopamine is unlikely to be important in the control of sodium and water metabolism.

Aldosterone↗
PubMed1980

A microassay for active and total renin concentration in human plasma based on antibody trapping.

We have developed and validated a new enzyme-kinetic method for measurement of renin concentration (PRC) in human plasma, based on radioimmunoassay of angiotensin I generated during incubation of plasma and excess sheep or ox renin substrate. Angiotensin I breakdown during incubation is prevented by the presence of anti-angiotensin I serum. The assya does not require prior extraction of renin, is technically simple, and is sufficiently sensitive to measure subnormal renin levels. With minor modifications both "active and "total" renin may be measured. Assay results have been calibrated with the International Standard Renin. PRC measured by this technique correlates significantly with angiotensin I and II, plasma renin activity, and with the PRC method previously used by us.

Angiotensin I↗
PubMed1980

The effect of captopril on blood pressure and angiotensins I, II and III in sodium-depleted dogs: problems associated with the measurement of angiotensin II after inhibition of converting enzyme.

1. Changes in arterial blood pressure, blood angiotensin I, plasma angiotensin II and plasma angiotensin III were measured in conscious sodium-depleted dogs after infusion of captopril, an orally active inhibitor of converting enzyme. 2. Angiotensins II and III were measured after chromatography to remove angiotensin I, which increased in concentration after inhibition of converting enzyme and which interfered in the direct assay for angiotensin II. 3. Infusion of captopril at 20, 200, 2000 and 6000 microgram h-1 kg-1, each for 3 h, produced a rapid fall in blood pressure and in concentration of angiotensin II. Angiotensin II was undetectable at 6000 microgram h-1 kg-1 (mean pre-infusion value for all samples was 39 +/- SD 15 pmol/1, n = 14). 4. The percentage fall in blood pressure correlated with the percentage fall in plasma angiotensin II (r = 0.65, P < 0.001). 5. These results suggest that the initial fall in blood pressure may be mediated in part by the suppression of angiotensin II. 6. Blood angiotensin I concentration rose with each rate of infusion of drug to a maximum 16-fold increase at 6000 microgram h-1 kg-1 (26-416 pmol/l). The rise in angiotensin I was inversely related to the fall in angiotensin II (r = 0.68, P < 0.001).

Angiotensin I↗
PubMed1980

Evidence that the acute hypotensive effect of captopril in dogs is not wholly explained by a reduction of plasma angiotensin II and its direct vasoconstrictor effect.

1. Captopril infused into sodium-loaded dogs produced a fall in both blood pressure [117 +/- 9.7 to 96.6 +/- 11.4 (SD) mmHg] and plasma angiotensin II [11.0 +/- 3.0 to 1.6 +/- 1.3 (SD) pmol/l]. Plasma aldosterone fell while both blood angiotensin I and renin concentration rose. 2. Angiotensin II was infused at 2, 6, 18 and 54 ng min-1 kg-1 into sodium-depleted dogs. Plasma angiotensin II and arterial pressure both rose and were related in a dose-response curve. 3. On a separate occasion the same dogs were given an intravenous infusion of captopril (6 mg h-1 kg-1) and the angiotensin II infusion was repeated. Again plasma angiotensin II and arterial pressure rose but the dose-response curve was displaced downwards; a higher concentration of angiotensin II being required to produce the same blood pressure as in the dogs not given captopril. 4. These finding suggest that the acute hypotensive effect of captopril is not wholly explained by a decrease in plasma angiotensin II concentration and the consequent reduction of its acute vasoconstrictor effect.

Aldosterone↗
PubMed1980

Influence of sodium balance on ACTH/adrenal corticosteroid dose-response curves in the dog.

In order to define short-term ACTH/corticosteroid dose-respone characteristics, we infused ACTH for 1 h at each of five incremental rates into pedigreed male beagle dogs in four different states of sodium balance. Progressive sodium depletion was associated with progressive increased in basal (pre-ACTH) plasma levels of renin, angiotensin II, aldosterone, 18-hydroxycorticosterone (18-OH-B), and 18-hydroxy-11-deoxycorticosterone (18-OH-DOC). Administration of dexamethasone significantly reduced the preinfusion levels of cortisol, aldosterone, 18-OH-B, and 18-OH-DOC. The threshold dose of ACTH required to elicit an aldosterone response during low-sodium intake was similar to that for cortisol, but was higher during normal or high-sodium intake. Steepest portions of the dose-response curves were at lower rates of ACTH infusion for cortisol than for aldosterone, and maximum increment was much greater for cortisol (60-fold) than for aldosterone (12-fold). Whereas the slopes of ACTH/aldosterone and ACTH/18-OH-B dose-response curves were steepened by lower sodium diets, the ACTH/cortisol response was significantly flattened by severe sodium depletion. We conclude that ACTH is a potent and direct-acting short-term regulator of aldosterone secretion, subject to modification by altered sodium balance.

Adrenal Cortex Hormones↗
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↗