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Biomedical subjects

I Gavras

Publications and source records attributed to I Gavras.

At least 145 records · Page 8Linked to original sources
PubMed1979

Oral angiotensin-converting enzyme inhibitor in long-term treatment of hypertensive patients.

The antihypertensive effect of the orally active angiotensin-converting enzyme inhibitor captopril (SQ 14225) was assessed in 22 hypertensive patients of whom 17 were followed for periods ranging from 1 to 7 months. Of these, eight had essential hypertension, eight had renovascular hypertension, and six had hypertension associated with chronic renal failure. Blood pressure decreased markedly in all patients, including those with low renin levels. Nevertheless, the magnitude of blood pressure reduction correlated with the base-line plasma renin activity (r = 0.58, P less than 0.01). Increasing the dose of captopril from 25 to 200 mg did not enhance the amplitude of the antihypertensive effect but did increase its duration. Patients' blood pressure remained well controlled and free of side-effects with a maximal daily dose of up to 200 mg by mouth twice daily. Despite the blood pressure reduction, sodium excretion tended to increase, probably because of reduced aldosterone secretion. There was no evidence of orthostatic hypotension, and no escape from the antihypertensive effect was observed. These results indicate that chronic inhibition of the angiotensin-converting enzyme with an orally active compound offers a new, efficient, and well-tolerated approach to the treatment of hypertension.

Adult↗
PubMed1979

Converting enzyme inhibition in hypertensive emergencies.

The diagnostic and therapeutic value of the angiotensin converting enzyme inhibitor teprotide (SQ 20881) was assessed in 18 patients with hypertensive emergencies. Mean blood pressure fell 31 +/- 18 mm Hg in the 10 subjects who responded to 1 mg/kg body weight administered intravenously, whereas it fell 5 +/- 3 mm Hg in the eight nonresponders. In patients who had received no previous drug treatment, log baseline plasma renin activity and change in mean blood pressure after SQ 20881 correlated significantly (r = 0.651, P less than 0.05). After acute therapy with SQ 20881, the patients who had a satisfactory response to the drug were treated with propranolol and a relatively normal sodium intake (88 meq/day). Nonresponders were treated with diuretics and sodium restriction (10 meq/day), and intermediate responders were given combination therapy. Mean blood pressure responded favorably within 24 h to the chosen regimen for each group from 152 +/- 47 to 102 +/- 31 mm Hg. SQ 20881 allows prompt evaluation of the role of renin in hypertensive emergencies and permits early choice of appropriate therapy based on the prevailing mechanism.

Adult↗
PubMed1979

Antihypertensive action of beta-adrenoceptor blockade and the renin-angiotensin system.

1 The regulation of renin secretion is mediated by way of adrenoceptors. The role of alpha-adrenoceptors remains controversial, whereas it is generally accepted that activation of beta-adrenoceptors stimulates renin and their blockade suppresses renin. 2 Although experimental renin regulation appears to be a beta 2-receptor function, clinical studies suggest that in man it is a beta 1 effect. 3 beta-Adrenoceptor-blocking agents are effective antihypertensive agents, but have variable effects on renin secretion; this variability may be attributable to different degrees of instrinsic partial beta-agonistic activity and/or different receptor or organ selectivity of various compounds. 4 Antihypertensive effectiveness seems unrelated in magnitude or timing to the baseline levels or the changes of plasma renin activity for the majority of beta-adrenoceptor-blocking drugs.

Adrenergic beta-Antagonists↗
PubMed1978

Antihypertensive effect of the oral angiotensin converting-enzyme inhibitor SQ 14225 in man.

We investigated the antihypertensive effect of the angiotensin converting-enzyme inhibitor SQ 14225 in 12 hypertensive patients for periods of three to 24 weeks. Blood pressure decreased in all patients (from 177 +/- 8/110 +/- 2 to 136 +/- 6/88 +/- 2 mm Hg--mean +/- S.E.); oral doses ranged from 400 to 1000 mg daily. Concomitant effects noted were small increases in plasma potassium concentration and pulse rate. One patient experienced a transient febrile reaction. Plasma renin activity rose during treatment, plasma aldosterone decreased, and angiotensin-converting-enzyme activity was virtually eliminated. There was no significant correlation between pretreatment plasma renin activity and degree of blood-pressure fall with SQ 14225. The exact mechanisms contributing to the blood-pressure-lowering effect of this agent remain unclear. SQ 14225 is a promising new antihypertensive agent, effective in patients refractory to traditional medical therapy.

Administration, Oral↗
PubMed1978

Relationship of basal plasma noradrenaline to blood pressure, age, sex, plasma renin activity and plasma volume in essential hypertension.

1. The relationship of basal plasma noradrenaline to blood pressure, age, sex, urinary sodium excretion, and plasma volume has been examined in 117 untreated ambulatory patients with essential hypertension. 2. No significant correlations between basal plasma noradrenaline and either age or sex were apparent in the total group of essential hypertensive patients. In addition, no significant correlations were observed between plasma noradrenaline and 24 h urinary sodium excretion. 3. Basal plasma noradrenaline concentration was significantly higher in high renin essential hypertensive subjects compared with those with normal or low plasma renin activity. 4. Plasma noradrenaline was reduced significantly in relatively young patients with low renin essential hypertension, but appeared to be normal in other low renin subjects. 5. Basal plasma noradrenaline correlated significantly with blood pressure in patients with normal or low renin essential hypertension but the relationships were only significant in male patients. 6. No significant relationship between basal plasma noradrenaline and either blood pressure or plasma volume could be demonstrated in this population of essential hypertensive patients.

Age Factors↗
PubMed1978

Studies on the activity of the sympathetic nervous system in essential hypertension.

Plasma catecholamine and norepinephrine concentrations have been measured in carefully characterized ambulatory patients with essential hypertension under basal conditions and following experimental procedures known to enhance sympathetic activity. The studies have demonstrated increased levels of plasma catecholamines in patients with mild hypertension as compared with matched controls following 70 degree upright tilt or cold pressor testing. Considerable heterogeneity was apparent in the population of patients with essential hypertension with respect to their plasma norepinephrine concentrations. Significantly greater levels of plasma norepinephrine were present in patients with high plasma renin activity and lesser levels in patients with low renin activity than in normal renin or labile hypertensives. Blood pressure correlated significantly with plasma norepinephrine in male patients with normal renin essential hypertension but not in females. Administration of the diuretic furosemide produced an increase in plasma norepinephrine in almost all hypertensive subjects studied. These studies suggest that peripheral sympathetic activity is abnormal in certain patients with essential hypertension. The results underscore the need to differentiate between subgroups of essential hypertension in studies relating to the role of the adrenergic system in the hypertension. The findings also suggest that the recently developed sensitive techniques for measuring plasma catecholamines of plasma norepinephrine are of value in assessing changes in peripheral sympathetic activity but that enzymatic assays of serum dopamine-beta-hydroxylase activity are probably not useful for this purpose.

Adult↗
PubMed1978

Relationship of basal plasma norepinephrine to blood pressure, plasma renin activity, mineralocorticoids, and plasma volume in essential hypertension.

The basal levels of plasma norepinephrine have been measured in 113 carefully characterized patients with essential hypertension, and the results have been correlated with the PRA sub-grouping and the levels of blood pressure, plasma aldosterone, plasma 18-hydroxy-deoxycorticosterone, and plasma volume. In addition, the influence of furosemide on plasma norepinephrine concentration has been assessed. Essential hypertensives, when considered as a whole, did not exhibit any significant abnormality in basal plasma norepinephrine concentration, but interesting alterations were observed in certain specific sub-groups. High renin patients had significantly elevated levels of basal plasma norepinephrine. In addition, a sub-group of the low renin population who were relatively young had reduced plasma norepinephrine conentration. In these individuals with both reduced PRA and plasma norepinephrine, the levels of both increased concomitantly to the normal range with marked salt depletion. Furosemide administration induced increases in plasma norepinephrine in all PRA sub-groups. Plasma norepinephrine correlated significantly with blood pressure in normal and low renin hypertensives, but the relationships were confined only to male subjects. Significant correlations were also observed between plasma norepinephrine and plasma aldosterine in males with normal PRA but not in the other sub-categories. No significant relationships between plasma volume and either plasma norepinephrine or blood pressure could be detected. Plasma 18-hydroxy-deoxycorticosterone was greater in males as compared with females and appeared elevated above control levels in normal and high renin essential hypertensives. Significant positive correlations between plasma aldosterone and plasma 18-hydroxy-deoxycorticosterone were observed in both males and females with normal renin hypertension. These studies have demonstrated abnormalities in basal plasma norepinephrine concentration in certain patients with essential hypertension. They also suggest that the levels of blood pressure and plasma aldosterone may be related to peripheral sympathetic activity in essential hypertension.

18-Hydroxydesoxycorticosterone↗
PubMed1977

Angiotensin II inhibition. Treatment of congestive cardiac failure in a high-renin hypertension.

A patient with intractable congestive cardiac failure secondary to renovascular hypertension and severe coronary artery disease was infused with the competitive antagonist of angiotensin II, saralasin acetate. The infusion produced an impressive increase in cardiac output and left ventricular stroke work index in parallel with a striking decrease in the systemic and pulmonary vascular resistance, the coronary resistance, and the myocardial oxygen consumption. It is suggested that angiotensin inhibition may present advantages over other forms of treatment of congestive cardiac failure in selected cases.

Angiotensin II↗
PubMed1977

Is elevated plasma renin activity of prognostic importance in progressive systemic sclerosis?

The pathologic lesions of the kidney in scleroderma in many respects resemble those of malignant hypertension, perhaps even in the absence of comparable blood pressure elevation. Because the malignant vascular changes have been related to hyperreninemia, we measured plasma renin activity in 23 patients with scleroderma with or without hypertension and/or renal failure. We found that high renin levels in most cases shortly preceded or coincided with a phase of sudden deterioration of the disease, characterized by a rapidly progressive renal failure. The outcome of this phase was invariably fatal, except for two patients in whom bilateral nephrectomy successfully arrested the rapid downhill course. These findings suggest that an unexplained increase in circulating renin levels in an otherwise stable patient with scleroderma may be taken as a possible marker of imminent deterioration requiring close monitoring and immediate therapeutic intervention.

Adult↗
PubMed1976

Reciprocal relation between renin dependency and sodium dependency in essential hypertension.

To investigate the roles of angiotensin II and sodium in essential high-renin, normal-renin and low-renin hypertension, 14 patients received the competitive antagonist of angiotensin II, saralasin, during periods of sodium depletion and repletion. Blood-pressure response to saralasin was determined by the state of sodium balance. Patients from all three renin subgroups exhibited a fall in blood pressure when sufficiently sodium depleted, and an elevation in blood pressure when sodium replete or insufficiently depleted. However, those with low renin required loss of substantially more sodium (sufficient to elicit compensatory stimulation of renin) before depletion could be achieved. In patients with essential hypertension of all three renin subgroups, sodium balance determines the degree of participation of the renin-angiotensin system in sustaining high blood pressure. Even the low-renin type can become renin dependent with sufficient sodium depletion.

Adult↗
PubMed1976

Determination of renin-dependency and sodium-dependency in the three renin sub-groups of essential hypertension.

1. In all three renin sub-groups of essential hypertension, the state of sodium balance determines the degree of participation of the renin-angiotensin system in sustaining high blood pressure. 2. Even the low-renin type can become renin-dependent when sufficient sodium depletion has bee achieved. 3. The main difference between patients of these sub-groups appears to be their variable capacity to become depleted of sodium under standard dietary regimens.

Aldosterone↗
PubMed1975

Blood viscosity, plasma proteins, and Raynaud syndrome.

The rheology of the blood was studied in 20 patients with Raynaud syndrome. Sixteen patients had scleroderma, two had nonspecific angiitis, one had systemic lupus erythematosus, and one had Raynaud disease. Viscosity measurements were performed on whole blood, plasma, and suspensions of 45% red blood cells (RBCs). In autologous plasma, over a wide range of shear rates. The relative viscosity, an index of RBC aggregation, was obtained by dividing the RBC viscosity in autologous plasma (at a hematocrit value of 45%) by the plasma viscosity. Concentrations of the plasma globulins and fibrinogen were also measured. The mean plasma viscosity was significantly (P less than .01) elevated over established normal controls. The mean RBC viscosity and the relative viscosity were significantly (P less than .01) elevated over normal controls, as were fibrinogen and the globulins. These studies demonstrate increased blood viscosity and red blood cell aggregation, which may constitute an important hindrance to flow.

Adolescent↗
PubMed1975

The use of angiotensin-converting enzyme inhibitor in the diagnosis and treatment of hypertension.

1. The anti-hypertensive effect of converting enzyme inhibition was evaluated in twenty-three hypertensive patients (seven renovascular, four essential, four malignant, one scleroderma, three chronic renal failure, four primary or idiopathic aldosteronism). 2. In sixteen patients a single injection (1--4 mg/kg) of the inhibitor produced an immediate anti-hypertensive effect, which lasted up to 16 h. In six patients the anti-hypertensive effect of the inhibitor was significantly improved after sodium depletion. 3. Plasma renin activities increased and plasma aldosterone concentrations decreased consistently except in idiopathic aldosteronism. 4. Converting enzyme inhibition provides a direct way of defining the degree of renin-dependency of the hypertension. Accordingly, it can be used diagnostically and for planning appropriate therapy. Therapeutically, it could be advantageous in hypertensive emergencies because of its safety, specificity and capacity to reduce aldosterone secretion.

Adolescent↗
PubMed1975

Malignant hypertension resulting from deoxycorticosterone acetate and salt excess: role of renin and sodium in vascular changes.

The evolution of malignant hypertension was studied under metabolic balance conditions in 11 uninephrectomized rats given deoxycorticosterone acetate and 1% NaCl as drinking water. Changes in sodium and potassium balance were related to changes in blood pressure, plasma renin activity, hematocrit, and kidney histology. After 3-4 weeks of steadily positive sodium balance accompanied by continuously increasing blood pressure up to 185 plus or minus 19 (SE) mm Hg, periods of sodium loss accompanied by evidence of hemoconcentration were observed marking the onset of the malignant phase as defined by the development of fibrinoid necrosis in the kidney. Plasma renin activity remained markedly suppressed both at the fourth week (0.33 plus or minus 0.02 ng/ml hour-1) when the sodium balance was positive and the kidney biopsy negative and at the end of the experiment (0.35 plus or minus 0.36 ng/ml hour-1) when the sodium balance was negative and the kidney histology revealed malignant vasculitis. Infusion of the angiotensin II inhibitor 1-Sar-8-Ala-angiotensin II consistently failed to affect blood pressure, and the kidney tissue norepinephrine level was reduced (0.054 plus or minus 0.01 mug/g) compared with the control level (0.132 plus or minus 0.02 mug/g). We conclude that malignant vasculitis in this model is preceded by hypertension associated with sodium and water retention and is accompanied by negative sodium balance, decreases in body weight, falling blood pressure, and hemoconcentration without demonstrable participation of the renin-angiotensin system or the renal catecholamines.

Alanine↗