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Biomedical subjects

A Benetos

Publications and source records attributed to A Benetos.

At least 127 records · Page 7Linked to original sources
PubMed1988

Vascular and sympathoadrenal responses to bradykinin and a bradykinin analogue.

These experiments were designed to assess the interaction of bradykinin and its antagonist (Arg-Pro-Hyp-Gly-Phe-Ser-DPhe-Phe-Arg-trifluoroacetic acid) with the sympathoadrenal system. Three groups of male Wistar rats received 5-minute intra-arterial infusions of either dextrose (Group 1, n = 6), bradykinin, 250 micrograms/min (Group 2, n = 5), or bradykinin, 25 micrograms/min (Group 3, n = 4). Six other groups received a similar infusion of the bradykinin antagonist at 250 micrograms/min. They were either intact rats (Group 4, n = 10) or rats previously submitted to chemical sympathectomy (Group 5, n = 17), to adrenal enucleation (Group 6, n = 8), to combined alpha-adrenergic and beta-adrenergic blockade (Group 7, n = 7), to alpha 1-adrenergic receptor blockade (Group 8, n = 8), or to alpha 2-adrenergic receptor blockade (Group 9, n = 8). Bradykinin infusion produced a sustained fall in mean arterial pressure (MAP) in Groups 2 and 3 (by -48 +/- 3 and -36 +/- 7 mm Hg, respectively) associated with similar increases in plasma epinephrine levels (100-fold), and norepinephrine (sevenfold) as compared with Group 1. The bradykinin antagonist infusion in intact rats produced a 23 +/- 4 mm Hg rise in MAP associated with a sixfold increase in epinephrine and a twofold increase in norepinephrine. Group 5 rats with lower baseline catecholamine levels had an even larger MAP rise (30 +/- 6 mm Hg) accompanied by a rise in epinephrine and norepinephrine proportionally similar to that of intact animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1987

Stimulation of vasopressin by calcium microinjections in the area of the paraventricular nucleus of the hypothalamus.

The present experiments were designed to investigate the effect of local calcium application on the paraventricular nucleus (PVN) on arginine-vasopressin (AVP) release and blood pressure. A microinjection of 2 microliter of calcium gluconate 10% in the PVN elevated AVP levels to 71.6 +/- 8.7 pg/ml compared to 3.3 +/- 0.6 pg/ml in control rats receiving iso-osmolar solution of dextrose 11% (P less than 0.001), whereas peripheral plasma epinephrine and norepinephrine were normal. Despite the increase of plasma AVP levels, blood pressure and heart rate remained unchanged indicating that other unknown mechanisms counteract AVP's pressor effect. These data suggest that locally applied Ca2+ in the vasopressinergic neurons of the hypothalamus strongly stimulates the release of AVP.

Animals↗
PubMed1987

Central catecholamines and alpha-adrenoceptors in acute hypertension induced by intracerebroventricular hypertonic saline.

We measured the tissue content of catecholamines and the numbers and affinities of alpha 1- and alpha 2-adrenergic receptors in specific areas of the hypothalamus and medulla oblongata of rats treated with intracerebroventricular microinjection of hypertonic saline, in comparison to controls treated with an equal volume of iso-osmolar dextrose solution. Rats given 20 microliter of 4% NaCl into the lateral ventricle showed an average rise in blood pressure of 14 +/- 2 mmHg and a decrease in heart rate of 63 +/- 11 beats/min (P less than 0.001 for both), associated with dopamine suppression in the anteroventral area of the third ventricle (AV3V) and increased concentrations of dopamine in the C2 region of the medulla and of epinephrine in the area postrema. Affinities of medullary alpha 2-adrenoceptors were decreased in the saline-treated rats, whereas the number of receptors tended to be higher. It is suggested that sodium may produce its pressor effect by diminishing the affinity of central alpha 2-adrenoceptors for neurotransmitters, resulting in disinhibition of certain sympathoinhibitory neurons and increased sympathetic outflow.

Animals↗
PubMed1987

Contribution of bradykinin to maintenance of normal blood pressure.

The purpose of these experiments was to investigate whether the vasodilator tissue hormone bradykinin contributes to the maintenance of normal blood pressure. A newly synthesized peptide competitive antagonist of bradykinin, the compound Arg-Pro-Hyp-Gly-Phe-Ser-DPhe-Phe-Arg-trifluoracetic acid (B3852), capable of inhibiting the depressor effect of exogenous bradykinin by over 50%, was infused into 10 normotensive rats at a rate of 500 micrograms/0.1 ml/min. Blood pressure rose immediately, from a baseline of 104 +/- 5 to 131 +/- 7 mm Hg at the end of a 5-minute infusion, and returned to baseline within 2 to 3 minutes after discontinuation of the infusion. When similar doses were administered by continuous infusion to previously nephrectomized rats (n = 5) or as an acute bolus to adrenalectomized rats (n = 5), blood pressure rose from 111 +/- 3 to 125 +/- 5 mm Hg and from 112 +/- 4 to 128 +/- 5 mm Hg, respectively. The data suggest that a vasodepressor action of endogenous bradykinin contributes to maintenance of normal peripheral vascular tone, and that this action is not mediated through adrenal catecholamines or renomedullary prostaglandins.

Animals↗
PubMed1987

The antihypertensive contribution of bradykinin as assessed by a specific bradykinin antagonist.

A new specific antagonist of bradykinin was used to examine the contribution of bradykinin to the depressor effect of different antihypertensive drugs in two-kidney renovascular rats. First we tested the inhibitory capacity of this peptide for exogenously injected bradykinin (75-200 ng). An inhibition of the vasodepressor action of bradykinin by over 50% was found when the bradykinin inhibitor was infused at a rate of 40 micrograms/min, with little difference at higher rates of infusion. We then infused this inhibitor in four groups of renovascular hypertensive rats. In three groups the blood pressure had been decreased by pretreatment either with the converting enzyme inhibitor MK 421, saralasin or sodium nitroprusside, respectively. The fourth group received no pretreatment. Infusion of the inhibitor produced an immediate increase in blood pressure by 30% only in the MK 421 group, but no change in the three other groups. These results indicate that bradykinin is involved in the decrease of blood pressure produced by converting enzyme inhibition in experimental renovascular hypertension.

Animals↗
PubMed1986

Norepinephrine applied in the paraventricular hypothalamic nucleus stimulates vasopressin release.

The present experiments were designed to investigate the effect of norepinephrine (NE) applied directly in the area of the paraventricular nucleus (PVN) of the hypothalamus on arginine-vasopressin (AVP) release and blood pressure. A microinjection of 0.4 micrograms NE in the PNV produced a plasma AVP level of 26.3 +/- 5.3 pg/ml compared to 5.3 +/- 0.6 pg/ml in controls receiving dextrose (P less than 0.001). This rise was associated with blood pressure elevations varying between 10 and 13 mm Hg, lasting for about 5 min. Systemic injection of an antivasopressor AVP antagonist reversed or prevented the blood pressure rise induced by NE microinjection. The data suggest that locally applied NE in vasopressinergic neurons of the hypothalamus stimulates the release of AVP and induces an AVP-dependent rise in blood pressure.

Animals↗
PubMed1986

Isosorbide dinitrate and pulsatile arterial haemodynamic variables in hypertension.

The effect of a sustained-release oral isosorbide dinitrate (ISDN) preparation on cerebral and forearm circulation was determined in 16 patients with mild to moderate essential hypertension. Measurements were made by pulsed Doppler velocimetry in the common carotid and the brachial arteries. Pulse wave velocity of the forearm was simultaneously recorded by means of strain gauge arterial mechanography allowing non-invasive evaluation of compliance and characteristic impedance of the brachial artery. Four hours after ISDN ingestion, the patients exhibited a significant decrease in blood pressure without a change in heart rate. An increase in carotid and brachial artery diameter was shown whereas blood flow increased only in the forearm. Resistance decreased significantly in both carotid and brachial vascular beds but only in the brachial vascular bed was the baseline resistance directly correlated with the change in brachial bed resistance. Concerning pulsatile large artery parameters, pulse wave velocity and characteristic impedance diminished, and brachial artery compliance increased significantly. The tangential tension of carotid and brachial arteries did not change. An increase in plasma renin activity was observed and related to the vasodilating effect on small arteries of the brachial vascular bed. This study showed that the antihypertensive effects of ISDN were accompanied by a strong vasodilatory action on small and large arteries and by an improvement in the pulsatile behaviour of large arteries.

Adult↗
PubMed1986

Calcium stimulates vasopressin release.

The association of acute hypercalcaemia with hypertension has long been known. Its mechanism has remained unexplained, however, since no significant pressor contribution from the renin-angiotensin system or the sympathetic nervous system has been detected. To assess the possible contribution of arginine vasopressin (AVP), we investigated the effect of a 2 h infusion of 2 ml isotonic calcium gluconate (0.46 mmol/ml Ca2+) on the mean blood pressure of anephric (n = 8) or intact (n = 7) rats and the blood pressure response to a specific vasopressin inhibitor (V1). In anephric rats, blood pressure rose by 30 +/- 3 mmHg (mean +/- s.e.m.) and plasma AVP levels rose to 34 +/- 9 pg/ml. In response to injection of the AVP inhibitor, blood pressure fell by 26 +/- 3 mmHg. In intact rats, blood pressure rose by 12 +/- 4 mmHg with plasma AVP levels 14.5 +/- 3.2 pg/ml (normal range 2.2 +/- 1.1 pg/ml), but did not respond consistently to AVP inhibition. Serum calcium levels at the end of the infusion were 25.0 +/- 4.3 mg/dl in anephric and 24.9 +/- 1.2 mg/dl in intact rats. In order to confirm that the calcium ion was indeed responsible for the AVP-dependent changes in blood pressure, another group of anephric rats (n = 8) received a 2 h infusion of CaCl2 (0.46 mmol/ml Ca2+) and exhibited a blood pressure rise of 35 +/- 3 mmHg, which responded to the AVP inhibitor with a blood pressure fall of 22 +/- 3 mmHg. Moreover, prior treatment with indomethacin greatly attenuated the pressor effect of calcium infusion and prevented the rise of AVP.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Haemodynamic effects of vasodilating drugs on the common carotid and brachial circulations of patients with essential hypertension.

The haemodynamic pattern of the common carotid artery was studied in men with sustained essential hypertension using pulsed Doppler methods before and after administration of vasodilating drugs. Captopril produced both a fall in vascular resistance and an increase in arterial diameter of the common carotid artery. Isosorbide dinitrate increased markedly the arterial diameter but did not change vascular resistance. Nitrendipine decreased vascular resistance with no change in the arterial diameter. In the common carotid circulation of patients with essential hypertension, vasodilating drugs may either dilate small arteries (nitrendipine), large arteries (isosorbide dinitrate), or both (captopril).

Administration, Oral↗
PubMed1986

Hypertensive effect of a bradykinin antagonist in normotensive rats.

The purpose of these experiments was to study the possible contribution of bradykinin to normal blood pressure maintenance. The bradykinin analogue B4146, a competitive antagonist-partial agonist of bradykinin, was used in three groups of normotensive unanesthetized Wistar rats. Two intra-aortic injections of B4146 (1 mg in 0.2 ml of dextrose) were given 5 minutes apart (i.e., well after return of blood pressure to baseline, which occurred within 68 +/- 19 seconds). One group had been pretreated with the angiotensin converting enzyme inhibitor HOE 498, 1 mg/kg (Hoechst), and one received only dextrose as the first injection to serve as controls. The bradykinin antagonist produced an average increase in mean arterial pressure of approximately 13 mm Hg for all groups. In five animals, however, the first injection of B4146 produced a hypotensive effect, whereas the second one consistently produced a rise in blood pressure. Pretreatment with the angiotensin converting enzyme inhibitor did not affect the magnitude of the subsequent blood pressure increase in response to B4146. Since smaller doses of B4146, sufficient to block exogenous bradykinin, do not cause changes in normal blood pressure, we conclude that endogenous bradykinin does contribute to normal blood pressure maintenance, but its effect can be demonstrated only if very high doses of its antagonist are injected, maybe because a high concentration of the compound is necessary to displace not only circulating but possibly tissue receptor-bound bradykinin as well.

Animals↗
PubMed1986

Vasodepressor role of endogenous bradykinin assessed by a bradykinin antagonist.

This study was designed to examine the contribution of bradykinin to the depressor effect of different antihypertensive drugs in two-kidney renovascular hypertensive rats, using a new specific antagonist of bradykinin. First, the inhibitory capacity of this peptide for exogenously injected bradykinin (75-200 ng) was tested. An inhibition of the vasodepressor action of bradykinin by over 50% was found when the bradykinin inhibitor was infused at a rate of 40 micrograms/min, with little difference at higher rates of infusion. This inhibitor then was infused in three groups of renovascular hypertensive rats after their blood pressure had been decreased by pretreatment with the converting enzyme inhibitor enalapril (MK 421), saralasin, or sodium nitroprusside, respectively. Infusion of the inhibitor produced an immediate 30% increase in blood pressure only in the enalapril-treated group. These results indicate that bradykinin is involved in the decrease of blood pressure produced by converting enzyme inhibition in experimental renovascular hypertension.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1986

Common carotid blood flow in patients with hypertension and stenosis of the internal carotid artery.

Common carotid blood flow has been measured using pulsed Doppler techniques in hypertensive patients over 45 years of age, with and without stenosis of the internal carotid artery. In hypertensive patients without stenosis, arterial diameter remained within the normal range, whereas blood flow velocity and blood flow were significantly reduced. Vascular resistance was significantly increased but did not change markedly after administration of the vasodilating drug isosorbid dinitrate. Patients with hypertension and stenosis of the internal carotid artery were compared with two different populations used as controls: In comparison with hypertensive patients without stenosis of the internal carotid artery, both arterial diameter and blood flow velocity were reduced, leading to a more pronounced decrease in blood flow; and in comparison with normotensive patients with stenosis of the internal carotid artery, common carotid blood flow was more reduced at any degree of stenosis. In a subset of patients, blood flow returned toward normal ranges after endarterectomy. The study suggested that in patients with hypertension without stenosis of the internal carotid artery, the decrease in blood flow is due to a decrease in blood flow velocity with normal arterial diameter despite the elevated blood pressure, and in patients with hypertension and stenosis of the internal carotid artery, blood flow was more reduced than in the normotensive patients with stenosis of the internal carotid artery, suggesting that caution must be taken with indications of antihypertensive treatment.

Adult↗
PubMed1985

Pulsed Doppler evaluation of diameter, blood velocity and blood flow of common carotid artery in sustained essential hypertension.

Diameter, blood flow velocity, and volumic flow of the common carotid artery were measured in 38 patients with sustained essential hypertension and compared with those of 38 age-matched normal subjects. Both hypertensive and control subjects were classified according to age into those younger and those older than 45 years. For the determinations, a pulsed Doppler velocimeter with an adjustable range-gated time system and a double transducer probe was used. In the younger group, the diameter of the common carotid artery had a similar value in hypertensive patients (0.639 +/- 0.014 cm) and in controls (0.651 +/- 0.015). The same level of blood flow velocity in hypertensive patients (19.7 +/- 0.9 cm/s) and in controls (21.2 +/- 0.9 cm/s) was observed. Therefore, the volumic flow was equal in the common carotid artery of the hypertensive patients (385 +/- 20 ml/min) and of the normotensive subjects (410 +/- 23 ml/min). In the older group, blood flow velocity was reduced in the common carotid artery of the hypertensive patients (19.4 +/- 1.0 cm/s vs. 15.6 +/- 0.6 cm/s; p less than 0.01), but the diameter was unchanged (0.653 +/- 0.018 cm in hypertensive patients and 0.665 +/- 0.018 cm in controls). Thus, there was a significant reduction of volumic blood flow in common carotid artery of the hypertensive patients over 45 years (321 +/- 14 ml/min). A negative relationship was observed between common carotid artery blood flow and age in elderly hypertensive patients (r = -0.42; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Comparison of oral MK 421 and propranolol in mild to moderate essential hypertension and their effects on arterial and venous vessels of the forearm.

The efficacy of MK 421 and propranolol was compared in 48 patients with mild to moderate hypertension. Each patient was randomly assigned to receive 1 of the drugs for 12 weeks. Additionally, a subgroup of 28 patients underwent studies of forearm arterial and venous circulation by means of pulsed Doppler and mercury-in-silastic plethysmography. Both drugs reduced supine and standing blood pressure (BP) (p less than 0.001). Propranolol reduced heart rate (p less than 0.001), while MK 421 did not change it. Brachial artery diameter, blood velocity and flow increased after MK 421 (p less than 0.001), but were not changed after propranolol therapy. Forearm vascular resistance decreased after MK 421 (p less than 0.001) and after propranolol (p less than 0.05). Forearm venous tone was unaffected on MK 421, but increased after propranolol (p less than 0.01). Thus, in moderate hypertension, 3 months of treatment with MK 421 or propranolol similarly decrease BP, but affect the forearm circulation differently: MK 421 dilates both the brachial artery and the arterioles of the forearm, but does not affect the venous vessels, and propranolol causes little arterial change but increases the forearm venous tone.

Adult↗
PubMed1984

Post-synaptic alpha-blockade and brachial artery compliance in essential hypertension.

Central (six patients) and brachial (12 patients) haemodynamics were studied in men with sustained essential hypertension before and after intravenous administration of an alpha post-synaptic adrenergic blocking drug, urapidil. Brachial arterial compliance was evaluated non-invasively from the simultaneous measurement of pulse wave velocity and arterial diameter. In basal conditions, arterial compliance was reduced in hypertensives. Urapidil caused a significant drop in blood pressure, due to a significant decrease in total peripheral resistance with no change in cardiac output and heart rate. Brachial arterial diameter and compliance did not change significantly. The results show that the decreased arterial compliance in hypertensive patients was not due exclusively to the elevation of blood pressure or to a predominant activation of the autonomic nervous system, or both. Such observations suggest that, in men with sustained essential hypertension, the decreased compliance was probably related to structural alterations of large arteries.

Blood Flow Velocity↗
PubMed1983

[Systolic arterial hypertension in patients amputated for injury].

The blood pressure of 106 men who had undergone amputation of one limb on account of war injury was compared with that of 184 male controls of the same ages. All subjects with a diastolic pressure above 90 mmHg were excluded from the study. The diastolic pressure was statistically equivalent in both groups, but the amputees had a significantly higher systolic pressure. Changes in the visco-elastic properties of the arterial system related to amputation might be responsible for this rise in systolic pressure.

Adult↗
PubMed1982

[Systolic arterial hypertension: demonstration and mechanism in obliterating arteriopathy of the lower extremities].

Hemodynamic parameters were measured in 24 patients with arteriosclerosis obliterans of the lower limbs, in comparison with 16 normal subjects of same age. Systemic arterial compliance was estimated from a simple visco-elastic model. In patients with arteriosclerosis obliterans, systolic pressure was significantly increased (P less than 0.001) while diastolic pressure remained within normal ranges. Arterial compliance was reduced (P less than 0.01) and was negatively correlated with systolic pressure (r = -0.72). Intravenous administration of nitroglycerin significantly decreased systolic pressure (P less than 0.05) and increased arterial compliance (P less than 0.01) without any change in mean arterial pressure. This study provided evidence that, in patients with arteriosclerosis obliterans of the lower limbs, the reduced systemic arterial compliance contributes in the increase in systolic pressure.

Arterial Occlusive Diseases↗