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Biomedical subjects

H Gavras

Publications and source records attributed to H Gavras.

At least 217 records · Page 12Linked to original sources
PubMed1981

Uncontrollable hypertension in patients on hemodialysis: long-term treatment with captopril and salt subtraction.

It has been suggested that an inappropriate relationship between renin and exchangeable sodium is responsible for the hypertension of patients with chronic renal failure. Long-term blockade of the renin system by captopril made it possible to test this hypothesis in 8 patients on maintenance hemodialysis. Captopril was administered orally in 2 daily doses of 25 to 200 mg. Previously, blood pressure averaged 179/105 +/- 6/3 (mean +/- SEM) pre- and 182/103 +/- 7/3 mm HG post-dialysis, despite intensive ultrafiltration and conventional antihypertensive therapy. The 4 patients with the highest plasma renin activity normalized their blood pressure with captopril alone, whereas in the 4 remaining patients, captopril therapy was complemented by salt subtraction which consisted in replacement of 1-2 liters of ultrafiltrate by an equal volume of 5% dextrose until blood pressure was controlled. After an average treatment period of 5 months, blood pressure of all 8 patients was reduced to 134/76 +/- 7/5 mm Hg (P less than 0.001) pre- and 144/81 +/- 9/5 mm Hg (P less than 0.001) post-dialysis without a significant change in body weight. The present data suggest that captopril alone or combined with salt subtraction normalizes blood pressure of patients on chronic hemodialysis with so called uncontrollable hypertension.

Adolescent↗
PubMed1980

Sodium-induced elevation of blood pressure in the anephric state.

Normotensive anephric rats infused with 2 milliliters of a hyperosmolar solution of either sodium chloride or mannitol showed an increase in arterial pressure that was very pronounced with the sodium chloride and that could be partly abolished by administration of an antagonist to the vasopressor action of antidiuretic hormone (ADH). Rats with congenital ADH deficiency subjected to the same treatment showed smaller increments in arterial pressure that remained unchanged after administration of the ADH antagonist. Expansion of intravascular fluid volume was similar in all four groups and bore no correlation to the change in arterial pressure. It is concluded that about half of the increase in blood pressure induced by saline was attributable to the vasopressor effect of stimulated ADH and the remainder to an additional sodium-related factor, since it was more pronounced in the saline-infused than in the mannitol-infused groups. Expansion of the intravascular volume per se could only account for a minimal part of the increment in pressure.

Animals↗
PubMed1980

Is the renin system necessary?

Numerous studies have been carried out to assess the role of the renin system in sustaining abnormally high blood pressure and in contributing to various other cardiovascular disorders such as congestive heart failure, ascites, and shock. The clinical use of potent and specific inhibitors of the renin-angiotensin system has produced important application in the treatment of high blood pressure, severe congestive cardiac failure and experimental hemorrhagic shock. Only in the state of considerable sodium depletion does blockade of the renin system produce any untoward effect, i.e. hypotension. These results are very similar to those obtained previously in patients with bilateral nephrectomy. They raise the question whether under conditions of our present salt-eating habits the renin system is really necessary.

Angiotensin II↗
PubMed1980

Converting enzyme inhibition during chronic angiotensin II infusion in rats: evidence against a non-angiotensin mechanism.

1. To investigate the non-angiotensin effects of converting enzyme inhibition, angiotensin II was infused intravenously at 30 ng/min for 9 days in conscious rats to produce moderate blood pressure elevation. One group was given captopril (SQ 14 225) by gavage (100 mg/kg twice daily) and the other glucose. 2. After 7 days of captopril administration, enzyme blockade was confirmed by a tenfold greater depressor sensitivity to exogenous bradykinin and a markedly decreased plasma angiotensin converting enzyme activity. 3. Mean arterial pressure, heart rate and plasma renin activity were not different between captopril and glucose-treated groups in the presence of angiotensin II. Metabolic studies also revealed no long-term differences in water and food intake, weight change or sodium and potassium metabolism. 4. These findings suggest that, in the presence of angiotensin II, there is no detectable haemodynamic or metabolic effect of converting enzyme inhibition in rats and, therefore, that bradykinin plays little or no role in its long-term antihypertensive action.

Angiotensin II↗
PubMed1980

Reninlike enzymatic activity in the cerebral microvessels of the rat.

Extrarenal renin has been a subject of considerable interest. Chiefly, studies have focused on brain and vascular renin activity in large arteries. A method now exists for the isolation from the cerebrum of microvascular tissues consisting of arterioles, capillaries and venules. The present study has demonstrated reninlike enzymatic activity within the cerebral microvasculature of the rat that is distinct from plasma renin activity. Maximal activity was observed at pH 4.5 with no measurable activity at pH 7.4. Activity with homologous renin substrate was only 13% of that measured with hog substrate whereas a 400-fold increase in reninlike specific activity was observed when microvessel homogenates were incubated with synthetic tetradecapeptide renin substrate. Bilateral nephrectomy did not affect microvascular reninlike activity. Pepstatin 15 nM, abolished reninlike activity in microvessel homogenates. Mean specific microvessel reninlike activity was 1.15 +/- 0.20 pg angiotensin I . microgram protein-1 . h-1 in control animals. Neither sodium depletion nor DOC-saline administrations caused a significant change in microvascular reninlike activity. It is suggested that the reninlike activity observed in microvessels is an acid protease, perhaps cathepsin D derived from lysosomes.

Angiotensin I↗
PubMed1980

Effects of tyrosine infusion in normotensive and hypertensive rats.

To clarify further the action of acute administration of L-tyrosine in lowering blood pressure, L-tyrosine ethylester was infused intravenously into awake [deoxycorticosterone acetate (DOCA)-salt] hypertensive rats, two-kidney Goldblatt hypertensive rats, and normotensive rats. The effects of tyrosine were measured on arterial pressure, heart rate, plasma catecholamine levels, and plasma renin activity. Blood pressure and heart rate were lowered in all groups despite significant elevation of plasma dopamine in all groups and epinephrine in the hypertensive groups, norepinephrine did not rise significantly, and plasma renin activity was always found to be within the ranges expected for each model. It was concluded that tyrosine produced the progressive decline in blood pressure and heart rate by bringing about a sustained state of parasympathetic dominance, as effective sympathetic compensation did not occcur. This could be attributed to increased alpha-adrenergic activity in certain sites in brain secondary to increased catecholaminergic activity in these areas.

Animals↗
PubMed1980

Acute renovascular hypertension in conscious dogs. Interaction of the renin-angiotensin system and sympathetic nervous system in systemic hemodynamics and regional blood flow responses.

The effects of acute renovascular hypertension on the sympathetic nervous system, regional blood flow and cardiac function were studied in conscious dogs submitted to renal artery occlusion by inflation of a cuff implanted previously around one renal artery. We then compared the alterations in plasma renin and catecholamine levels and in the various hemodynamic parameters induced by those maneuvers in intact dogs, to those in dogs pretreated with alpha- and beta-adrenergic receptor blockers. Subsequently, the converting enzyme inhibitor teprotide was administered to inhibit angiotensin formation in both experiments. Our results suggest that both the renin-angiotensin system and the sympathetic system contribute to the rise in blood pressure. The hemodynamic changes and alterations in regional blood flows accompanying this acute hypertension appear to be due mostly to the increase in plasma angiotensin, since prior adrenoceptor blockade only attenuated their magnitude but did not alter their direction. However, angiotensin-induced coronary vasoconstriction was observed only in adrenergically blocked but not intact animals, probably because of the protective effect of baroreceptor-mediated reflex sympathetic coronary vasodilation.

Acute Disease↗
PubMed1980

Enhancement by diuretics of the antihypertensive action of long-term angiotensin converting enzyme blockade.

Thirty-nine patients with various types of hypertension were treated by chronic blockage of the angiotensin converting enzyme, i.e. by twice daily administration of captopril, 50 to 200 mg p.o. The blood pressure reduction observed 1 hour following administration of the inhibitor was directly related to the baseline plasma renin activity (r=- 0.67, p < 0.001). Whenever blockade of the renin system alone did not lower blood pressure to normal levels additional sodium subtraction brought it under control. With the renin system neutralized, blood pressure becomes exquisitely sensitive to changes in sodium balance. Diuretics seem to preserve optimal natriuretic efficacy despite blood pressure reduction, probably because aldosterone levels are reduced and renal blood flow increases. Blockade of the renin system together with individually tailored salt subtraction provides an attractive new approach to long-term treatment of clinical hypertension.

Adolescent↗
PubMed1980

Angiotensin inhibitors for hypertension.

Inhibition of the angiotensin-converting enzyme emerges as a new promising approach to the treatment of hypertension. The intravenously administered teprotide appears to be suitable as a diagnostic test and for initial treatment of certain hypertensive emergencies. The oral inhibitor captopril is effective for chronic maintenance of blood pressure control in various types of hypertension but has been associated with a number of adverse reactions.

Administration, Oral↗
PubMed1979

Mineralocorticoid-induced hypertension in patients with orthostatic hypotension.

The mechanism of recumbent hypertension induced by fludrocortisone was studied in seven patients with orthostatic hypotension. All showed increases in blood pressure in the recumbent and standing positions, and hypertensive levels were achieved on recumbency in four of them. Hypertensive retinopathy developed in two patients and cardiomegaly in one. Initial blood-pressure elevations were associated with sodium retention and plasma-volume expansion. However, with long-term treatment, plasma volume decreased to control levels despite further blood-pressure increases. Treatment did not affect plasma levels of catecholamines but did enhance pressor responsiveness to infused norepinephrine in some subjects. Hemodynamic studies indicated that hypertension in the recumbent position was related to increases in total peripheral-vascular resistance and not to changes in cardiac output. Clinically, hypertension in the recumbent position is an important risk of fludrocortisone treatment in patients with orthostatic hypotension. This unusual model of chronic mineralocorticoid-induced hypertension is not volume dependent but is related to increased peripheral-vascular resistance.

Adult↗
PubMed1979

Improvement of chronic congestive heart-failure by oral captopril.

Catopril, an inhibitor of angiotensin converting enzyme, was given orally during cardiac catheterisation to 6 normotensive patients with refractory congestive heart-failure. 60--180 minutes after administration of 25 mg captopril, arterial pressure fell by 25%, cardiac index rose by 38%, and left-ventricular pressure and right-atrial pressure fell by 25% and 40% respectively. Plasma-renin activity rose while plasma noradrenaline and aldosterone fell. These data suggest that, in the short term, captopril can reduce both preload and afterload, and improve cardiac function, in refractory congestive heart-failure.

Administration, Oral↗