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Biomedical subjects

M Condorelli

Publications and source records attributed to M Condorelli.

At least 73 records · Page 4Linked to original sources
PubMed1988

Contribution of the renin-angiotensin system and of the sympathetic nervous system to blood pressure homeostasis during chronic restriction of sodium intake.

In a previous paper, we showed that during a long-term, moderate restriction in sodium intake, sympathetic nervous system activity was only transiently stimulated, whereas a sustained rise of plasma renin activity occurred. However, the contribution from stimulation of the renin-angiotensin system in the maintenance of blood pressure homeostasis during a low-salt diet is still unclear. To investigate this issue, in eight normal subjects blood pressure, heart rate, plasma catecholamines, renin activity, and aldosterone were measured during normal sodium intake (150 mEq/d), after converting-enzyme inhibition (enalapril 20 mg/d po), and during one month of sodium intake restriction (50 mEq/d) associated with chronic inhibition of converting-enzyme (CEI). During a low-salt diet with CEI, plasma renin activity rose significantly as a result of CEI. In addition, even in the presence of a marked and sustained increase in plasma norepinephrine and in upright heart rate, a decrease in blood pressure was observed in all the measurements performed during the course of the study as compared to the control values. Our findings support the hypothesis that renin-angiotensin system activation plays an important role in the maintenance of blood pressure homeostasis during a low-salt diet. In fact, in the presence of an effective blockade of angiotensin II formation, blood pressure is decreased, despite the concurrent, sustained stimulation of the sympathetic nervous system.

Adolescent↗
PubMed1988

Atrial natriuretic factor potentiates forearm reflex vasoconstriction induced by cardiopulmonary receptor deactivation in man.

Previous evidence suggests that atrial natriuretic factor (ANF) interferes with the autonomic control of circulation. In the present study we investigated whether ANF modulates forearm vasoconstriction reflexly induced by cardiopulmonary receptor unloading in man. For this purpose, the hemodynamic response to -20 mm Hg lower body negative pressure (LBNP) was assessed under control conditions and during the constant infusion of alpha-human ANF (0.5 micrograms/kg bolus followed by 0.05 micrograms/kg/min) in seven normal subjects. ANF infusion resulted in a slight reduction in blood pressure and right atrial pressure, did not modify heart rate or forearm vascular resistance, but significantly potentiated the reflex increase in forearm vascular resistance during LBNP (+25 +/- 9% under control conditions vs +40 +/- 12% during ANF, p less than .05). In an attempt to clarify the mechanisms underlying the enhanced reflex vasoconstriction during infusion of ANF, in five additional subjects we demonstrated that there was a comparable vascular reflex response to LBNP under control conditions and during nitroglycerin infusion at a dose that induced a reduction in atrial pressure comparable to that observed during ANF. Finally, in seven additional subjects we found that ANF infusion did not alter the reflex hemodynamic responses elicited by carotid baroreceptor unloading induced by a +60 mm Hg increase in external neck pressure. We conclude that during the infusion of a pharmacologic dose of ANF the reflex forearm vasoconstriction in response to selective cardiopulmonary receptor unloading is potentiated. This effect does not seem to be related to the hemodynamic actions of the peptide or to interference with the sympathetic control of peripheral circulation.

Adult↗
PubMed1988

Reduction of atrial natriuretic factor circulating levels by endogenous sympathetic activation in hypertensive patients.

The effects of endogenous activation of sympathetic nervous system on systemic and regional hemodynamics and on plasma levels of atrial natriuretic factor (ANF) were studied in subjects with essential hypertension. Stimulation of sympathetic nervous system was reflex-induced by a selective deactivation of carotid baroreceptors obtained by increasing external neck-tissue pressure (NTP) by means of a neck chamber. The effects of graded levels (+30, +45, and +60 mm Hg) and one single and sustained level (+45 mm Hg for 15 min) of NTP were studied. As expected, NTP caused reflex increases in blood pressure, heart rate, and forearm vascular resistance, whereas atrial pressures did not change significantly and cardiac output tended to increase. In the studies based on graded levels of NTP, immunoreactive ANF (irANF) progressively fell (from 31.7 +/- 10 to 13.3 +/- 4 fmol/ml; p less than .05) and the changes in irANF were significantly correlated with those observed in FVR (r = -.671, p less than .001). Both hemodynamic and irANF changes were prevented by adrenergic blockade (phentolamine + propranolol). During +45 mm Hg NTP for 15 min, the levels of irANF fell both in the pulmonary artery and in the inferior vena cava. The irANF arteriovenous difference also fell during this maneuver. These data show that, in hypertensive patients, factors other than atrial wall tension may influence ANF release. They also show that endogenous sympathetic activation may reduce ANF release.

Atrial Natriuretic Factor↗
PubMed1988

Hemodynamic responses to atrial natriuretic factor in nephrectomized rabbits: attenuation of the circulatory consequences of acute volume expansion.

We investigated the hemodynamic responses to three doses of atrial natriuretic factor [human atrial natriuretic factor-(99-126)] (ANF) in nephrectomized rabbits anesthetized with ketamine and acepromazine. The influence of the different doses of the peptide on the hemodynamic consequences produced by acute volume expansion (0.9% NaCl, 1.4 ml/kg/min for 60 minutes) was also studied. All three dosages of ANF (0.001, 0.01, and 0.2 micrograms/kg/min for 20 minutes) significantly reduced blood pressure. With the lowest dose, the hypotensive effect was associated with reduction in systemic vascular resistance and no significant change in heart rate, stroke volume, central venous pressure, and hematocrit. In contrast, the intermediate and high doses, which resulted in markedly higher plasma levels, caused a significant decrease in heart rate, central venous pressure, and stroke volume; a slight rise in hematocrit; and no change in systemic vascular resistance. Volume expansion produced by saline infusion in an additional group of nephrectomized rabbits increased central venous pressure and decreased hematocrit. When ANF infusion was associated to volume expansion, each dosage of ANF was able to reduce the rise in central venous pressure, while only the higher dosage attenuated the progressive fall in hematocrit caused by volume expansion. Plasma volume, measured at the end of volume expansion was lower in the group treated with the highest dose of ANF than in the control animals (28.2 +/- 9 vs. 35.1 +/- 3 ml/kg, p less than 0.05). We conclude that 1) ANF induces significant hemodynamic effects independently from its renal action.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Long-term reduction of peripheral resistance with celiprolol and effects on left ventricular mass.

The antihypertensive efficacy of a new beta-blocker, celiprolol, was compared with that of a well established antihypertensive drug, metoprolol. Systemic and forearm haemodynamic effects were investigated using echocardiography and two-dimensional pulsed Doppler flowmetry, respectively. Twenty hypertensive patients completed the double-blind crossover randomized study. Each 6-week active treatment period was both preceded and followed by 2 weeks of placebo treatment such that the total duration of the study was 18 weeks. Despite comparable efficacy in reducing systolic and diastolic blood pressures by approximately 10% of the basal value, the two drugs differed in their systemic and haemodynamic effects. Celiprolol significantly decreased forearm peripheral resistance and total peripheral resistance. Cardiac output remained unchanged and forearm blood flow was increased. Metoprolol reduced cardiac output through a reduction in heart rate, but stroke volume was unaltered. Neither drug significantly modified cardiac performance, as evaluated by left ventricular circumferential fibre shortening and left ventricular ejection fraction. Differences in the systemic and regional haemodynamic effects of the two drugs could account for the different blood pressure response seen in some patients. There was no observable change in left ventricular wall thickness or left ventricular mass. These results confirm previous reports which demonstrate that antihypertensive treatment with beta-blockers does not reduce left ventricular mass in patients with a left ventricle of normal size. It is generally accepted, however, that the ability of beta-blockers to reverse left ventricular hypertrophy is unrelated to the individual pharmacological characteristics of each agent.

Adrenergic beta-Antagonists↗
PubMed1988

Effects of moderate low sodium/high potassium diet on essential hypertension: results of a comparative study.

It is generally accepted that a significant restriction in sodium intake can lower blood pressure in hypertensive patients and more recently it has also been suggested that a high potassium intake can exert an antihypertensive effect. We have therefore, conducted a double-blind, randomized, cross-over study to evaluate the antihypertensive efficacy of the combination of a modest dietary sodium restriction and a high potassium intake in hypertensive patients of mild and moderate degrees. During the modest sodium (100 mmol/day)/high potassium (130 mmol/day) diet the blood pressure was significantly reduced (-17/-6 mmHg) when compared to the normal diet (160 mmol Na/day and 80 mmol K/day). The blood pressure reduction did not interfere with hemodynamic and humoral responses to dynamic exercise. The modest reduction in sodium intake and increase in potassium content in the diet was well tolerated by the patients.

Adult↗
PubMed1988

Bioethics.

Explore the source record for details and available documents.

Bioethics↗
PubMed1988

Atenolol and/or nifedipine in effort angina: which is the treatment of choice for exercise coronary protection?

The authors performed a long-term, double-blind, crossover, randomized study on the effects of two drugs (atenolol, 100 mg/day, or nifedipine, 10 mg t.i.d.) when administered alone or in combination on the exercise tolerance in 10 patients with stable angina on effort (mean age 52 +/- 4 years, 8 males and 2 females) and documented significant (greater than or equal to 70%) obstructive coronary lesions at angiography. None of the drug treatments improved exercise duration or maximal sustained work load. Atenolol decreased significantly ST segment depression to -1 +/- 0.8 from -1.91 +/- 0.7, baseline and -2.05 +/- 0.5, placebo. Nifedipine was not better than placebo. The atenolol plus nifedipine treatment was better than placebo (p less than 0.001) or nifedipine alone (p less than 0.05) but was not more significantly efficacious than atenolol alone. Long-term management of exertional angina can be usefully performed using atenolol. The use of nifedipine at the present dose of 10 mg, although well tolerated, did not improve the ST signs of ischemia.

Adult↗
PubMed1987

[Mechanisms of regulation of arterial blood pressure: role of the sympathetic nervous system and of the renin-angiotensin system in patients on a low-sodium diet].

In order to discover more about the role of the sympathetic nervous and renin-angiotensin systems in the preservation of homeostasis during chronic reductions of salt intake, blood pressure, blood catecholamines and renin activity were measured in a group of healthy subjects in normal conditions and on a salt-free diet combined with blockade of the conversion enzyme by enalapril. The results confirmed the hypothesis advanced on an earlier occasion i.e. that both hormone systems contribute to pressure during salt depletion in the initial phase, while over the long term only the renin-angiotensin system is activated though when this is inhibited, the sympathetic nervous system will take over its function.

Adolescent↗
PubMed1987

[Regulation of coronary circulation in patients with hypertensive cardiopathy: role of ventricular mechanoreceptors].

In order to assess the involvement of the cardiopulmonary receptors in the regulation of the coronary circulation, changes in coronary resistance produced by the application of a -10 mmHg pressure to the lower body were studied in 6 healthy subjects and 6 patients with arterial hypertension and left ventricular hypertrophy. The results show that the inhibition of the ventricular receptors significantly increases coronary resistance and that this reflex response is eliminated in hypertensive patients with ventricular hypertrophy. The results show that the inhibition of the ventricular receptors significantly increases coronary resistance and that this reflex response is eliminated in hypertensive patients with ventricular hypertrophy.

Adult↗
PubMed1987

Effects of intravenous verapamil administration on left ventricular diastolic function in systemic hypertension.

The effects of intravenous verapamil administration (0.1 mg/kg as a bolus followed by an infusion of 0.007 mg/kg/min) were studied using high-temporal-resolution radionuclide angiography in 27 patients with hypertension. Verapamil administration increased heart rate from 69 +/- 11 to 75 +/- 12 beats/min (p less than 0.001) and decreased systolic, diastolic and mean blood pressures (BPs) from 155 +/- 21/102 +/- 12 mm Hg (mean 119 +/- 14) to 142 +/- 19/95 +/- 12 mm Hg (mean 109 +/- 13) (p less than 0.001 for all). Ejection fraction decreased significantly (from 65 +/- 10% to 60 +/- 11%, p less than 0.005); peak filling rate, however, increased significantly only in patients in whom it was subnormal in the basal study (from 2.2 +/- 0.4 to 3.0 +/- 0.6 end-diastolic counts/s, p less than 0.001). These latter patients had significantly higher values of left ventricular (LV) mass index than patients with normal or increased peak filling rate (129 +/- 22 vs 112 +/- 22 g/m2, respectively, p less than 0.05). The isovolumic relaxation period changes were inversely related to the baseline values (r = 0.83, p less than 0.001). In the subgroup of patients in whom isovolumic relaxation period lengthened, time to end systole decreased (from 360 +/- 31 to 329 +/- 30 ms, p less than 0.025) and time to onset of rapid filling increased (from 420 +/- 31 to 451 +/- 34 ms, p less than 0.025), whereas these 2 intervals had opposite patterns in patients in whom isovolumic relaxation period decreased or did not change.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1987

Ventricular parasystole and ventricular couplets: a re-entry within the parasystolic focus?

We report a 62-year-old man with a persistent ventricular rhythm originating in a parasystolic focus associated with frequent ventricular couplets with fixed coupling. Both intravenous (IV) procainamide (1 g) and propafenone (70 mg IV) promptly suppressed only the second component of ventricular couplets, suggesting that re-entry rather than enhanced automaticity was the mechanism of ventricular couplets. On the contrary, the nonresponse of ventricular rhythm and ventricular couplets to verapamil (10 mg IV) suggested that triggered activity should not play a role in the genesis of this ventricular rhythm. The mechanisms of the ventricular couplets (rapidly discharging parasystolic focus vs. re-entry) are discussed.

Arrhythmias, Cardiac↗
PubMed1987

Early diastolic time intervals during hypertensive pregnancy.

Early diastolic time intervals have been assessed by means of the echopolycardiographic method in 17 pregnant women who developed hypertension during pregnancy (HP) and in 14 normal pregnant women (N). Systolic time intervals (STI), stroke volume (SV), ejection fraction (EF), and mean velocity of myocardial fiber shortening (VCF) were also evaluated. Recordings were performed in the left lateral decubitus (LLD) and then in the supine decubitus (SD). In LLD, isovolumic relaxation period (IRP) was prolonged in the hypertensive pregnant women compared with normal pregnant women (HP 51 +/- 12.5 ms, N 32.4 +/- 15 ms p less than 0.05), whereas time of the mitral valve maximum opening (DE) was not different in the groups. There was no difference in SV, EF, and mean VCF, whereas STI showed only a significant (p less than 0.05) lengthening of pre-ejection period (PEP) in HP. When the subjects shifted from the left lateral to the supine decubitus position, left ventricular ejection time index (LVETi) and SV decreased significantly (p less than 0.05) in both normotensive hypertensive pregnant women. IRP and PEP lengthened significantly (p less than 0.05) only in normals, whereas they were unchanged in HP. DE time did not vary in either group. In conclusion, hypertension superimposed on pregnancy induces lengthening of IRP, as well as of PEP, and minimizes the effects of the postural changes in preload on the above-mentioned time intervals.

Adolescent↗
PubMed1987

Effects of celiprolol on systemic and forearm circulation in hypertensive patients: a double-blind cross-over study versus metoprolol.

The antihypertensive efficacy of a new beta-receptor blocking agent, celiprolol, was compared with that of a well-established antihypertensive drug, metoprolol. Their systemic and forearm hemodynamic effects were investigated using echocardiography and two-dimensional pulsed Doppler flowmetry, respectively. Twenty hypertensive patients completed a double-blind, cross-over, randomized study using celiprolol and metoprolol. Two six-week courses with celiprolol or metoprolol were preceded and followed by a two-week placebo period; the total duration of the study was 18 weeks. In spite of a comparable efficacy in reducing systolic and diastolic blood pressure (about 10% of the basal value), the two drugs showed quite different systemic and regional hemodynamic effects. Celiprolol induced a significant decrease in forearm vascular resistance (from 157 +/- 17 to 113 +/- 13 mm Hg/mL/s, P less than .01) and total peripheral resistance (from 1596 +/- 90 to 1398 +/- 91 dyne.s.cm-5, P less than .05) whereas cardiac output remained unchanged and forearm blood flow increased. Metoprolol reduced cardiac output (from 6.5 +/- 3 to 5.7 +/- 3 L/min, P less than .05), through a reduction in heart rate, since stroke volume was unchanged. Both drugs did not significantly modify cardiac performance, as evaluated by left ventricle fractional shortening and ejection fraction. Thus, the two drugs seem to reduce blood pressure through different hemodynamic mechanisms.

Adrenergic beta-Antagonists↗