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Biomedical subjects

L Gregorini

Publications and source records attributed to L Gregorini.

At least 37 records · Page 2Linked to original sources
PubMed1990

Haemodynamic effects of ACE inhibitors.

This paper reviews the haemodynamic effects of angiotensin-converting enzyme (ACE) inhibitors in hypertension, focusing on their ability to cause a fall in systemic vascular resistance, with no change in cardiac output and no reduction and even an increase in blood flow to vital organs such as the brain, the kidney and the heart. The haemodynamic effects of ACE inhibitors are qualitatively similar in congestive heart failure, except that, in the presence of impaired cardiac function, the fall in resistance is accompanied by a pronounced increase in cardiac output and tissue perfusion. In both conditions ACE inhibition opposes sympathetic influences and enhances vagal influences and, in hypertension, this intervention is followed by a regression of left ventricular hypertrophy providing a multifold background for a cardioprotective action. The new ACE inhibitor quinapril appears to share the haemodynamic effects of other ACE inhibitors with an improvement of cardiovascular function in congestive heart failure.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1987

Effects of altering the interval between the stimulus and the reflex response in the analysis of the baroreceptor control of the sinus and atrioventricular nodes in man.

Baroreceptor control of the sinus node may be determined by raising or lowering blood pressure with intravenous bolus injections of phenylephrine or glyceryl trinitrate and calculating the slope of the linear regression between the drug induced changes in systolic blood pressure and RR interval using shift 1 coupling--namely, coupling of each systolic blood pressure value with the interval of the following cardiac cycle. To assess whether shift 1 coupling provides the best linear fit and the highest regression slope nine subjects received phenylephrine and glyceryl trinitrate injections both during spontaneous sinus rhythm and during atrial pacing to evaluate baroreflex control of the sinus and of the atrioventricular node respectively. In regression analysis of the data, for each drug injection nine different shifts (from 0 to 8) were used to couple systolic blood pressure with RR or StQ intervals. When the mean results from all subjects were compared the use of shift 1 was equal or superior to the use of any other shift for both the RR and the StQ interval responses evoked by either phenylephrine or glyceryl trinitrate. In many instances, however, the shift that provided the highest correlation and regression coefficient was different from shift 1, and the use of these best individual shifts provided results considerably different from those obtained with the standard shift 1. It is concluded that in the regression analysis of baroreflex cardiac responses to vasoactive drugs the regular use of shift 1 does not invariably provide the best estimation of baroreflex sensitivity. This is better achieved by calculating the best shift in individual responses.

Atrioventricular Node↗
PubMed1987

Calcium antagonists and neural control of circulation in essential hypertension.

Data from animals and from man suggest that calcium antagonists interfere with alpha-adrenergic receptors and that this mechanism may be responsible for some of the vasodilation induced by these drugs. However, alpha-adrenergic receptors play a primary role in baroreceptor regulation of the cardiovascular system and blood pressure homeostasis, which might therefore be adversely affected by calcium antagonist treatment. We addressed this question in 14 essential hypertensives studied before treatment, 1 h after 20 mg oral nitrendipine and 5-7 days after daily administration of 20 mg oral nitrendipine. Blood pressure was measured by an intra-arterial catheter, heart rate by an electrocardiogram, cardiac output by thermodilution and forearm blood flow by venous occlusion plethysmography. Total peripheral and forearm vascular resistances were calculated by dividing mean blood pressure by blood flow values. Plasma norepinephrine was also measured (high performance liquid chromatography) in blood taken from the right atrium. Compared with the pretreatment values, acute nitrendipine administration caused a fall in resting blood pressure, an increase in the resting heart rate and cardiac output, and a fall in resting peripheral and forearm vascular resistance. The resting hypotension and vasodilation were also evident during the prolonged nitrendipine administration, which was, however, accompanied by much less resting cardiac stimulation than that observed in the acute condition. Baroreceptor control of the heart rate (vasoactive drug method) was similar before and after acute and prolonged nitrendipine treatment. This was also the case for carotid baroreceptor control of blood pressure (neck chamber technique) and for control of forearm vascular resistance as exerted by receptors in the cardiopulmonary region (lower-body negative-pressure and passive leg-raising techniques).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Hemodynamic effects of acute and prolonged administration of nitrendipine in essential hypertension.

In six hospitalized subjects with mild or moderate and untreated essential hypertension, we measured mean blood pressure (MBP, brachial artery catheter), heart rate (HR, electrocardiogram), cardiac output (CO, thermodilution), and total peripheral resistance (TPR, MBP divided by CO) at rest and during a cold pressor test (CPT, 60 s), a hand-grip exercise (HG, 40% maximum strength for 90 s), and a cyclette exercise (CE, 50 W for 5 min). The study was performed in a no-drug condition, 1 h after 20 mg oral nitrendipine (aN) and 1 week after daily administration of 20 mg oral nitrendipine (pN). Compared with the no-drug condition, aN reduced resting MBP from 137.3 +/- 7.3 (mean +/- SEM) to 112.3 +/- 9 mm Hg (p less than 0.05), increased resting HR from 72.3 +/- 6.9 to 85.3 +/- 8.8 beats/min) (p less than 0.05), increased resting CO from 6,191 +/- 508, to 8,700 +/- 1,050 ml/min (p less than 0.05), and reduced resting TPR from 1,807 +/- 119 to 1,140 +/- 228 dynes/s/cm5 (p less than 0.05). The reduction in resting MBP and TPR were unchanged by pN, whereas the increase in HR and CO were attenuated by 47 and 42%, respectively (p less than 0.05). Neither aN nor pN altered the hemodynamic responses to CPT, HG, and CE. As a result, the peak MBP and TPR values that were measured during these maneuvers were always lower (p less than 0.05) during aN and pN than in the no-drug condition. Thus, nitrendipine exerts marked antihypertensive and vasodilatatory effects that are evident at rest and during conditions elevating BP.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Control of circulation by arterial baroreceptors and cardiopulmonary receptors in hypertension.

This article reviews observations made on reflex control of circulation in essential hypertension and in a few models of experimental hypertension. It is emphasized that a wide consensus exists on the fact that baroreceptor control of heart rate is impaired in essential hypertension and that this occurs not only in severe but also in mild and borderline hypertensive conditions. On the other hand, baroreceptor control of blood pressure is much less affected by chronic elevations in arterial blood pressure due to central or peripheral factors that differentially affect cardiac and vascular responses to the vagus and the sympathetic drive, respectively. Cardiopulmonary receptor control of peripheral circulation and renin release is also little affected by hypertension, and the suggestion has been made that its sensitivity may even be enhanced in early hypertensive stages and then undergoes a subsequent reduction as cardiac hypertrophy develops. Finally, the possible consequences of preservation of reflex control of circulation in hypertension are discussed. It is speculated that this phenomenon may be in part responsible for the similar percentage of blood pressure oscillations that can be observed in normotensive and borderline, moderate, and severe hypertensive subjects.

Animals↗
PubMed1985

Evaluation of an index of peripheral vascular resistance in human subjects.

Based on evidence in animal studies, an index of resistance in man has been evaluated. In 10 human subjects, ranging in age from 31 to 60 years, direct brachial arterial pressure was measured, and a computer program using linear regression calculated the index of resistance from the slope of the logarithm of the pressure versus time during the second half of diastole. Resistance was independently calculated from 20-s averages of pressure and cardiac output obtained by thermodilution. Resistance was varied by infusion of phenylephrine and nitroprusside. The values of the index of resistance were compared with independently calculated resistance by linear regression and correlation. The index of resistance was variably correlated with independently calculated resistance. However, when the comparison was limited to points with a model correlation coefficient greater than or equal to 0.98 (i.e. a good fit of a straight line to the logarithm of pressure versus time), the correlation of the index of resistance with calculated resistance approached or exceeded 0.9 in eight of 10 subjects. In the two subjects showing poor correlation of the index with calculated resistance, estimated compliance from the same model was much lower than in the other subjects. In the same two subjects pressure dependence of estimated compliance was much higher than in the other subjects, suggesting the presence of significant atherosclerosis. We concluded that the diastolic decay of pressure may be used to calculate a useful index of resistance, provided that a single exponential decay fits the observed diastolic waveform well, and arterial compliance is not significantly reduced by atherosclerosis.

Adult↗
PubMed1984

Twenty-four-hour blood pressure profile and blood pressure variability in untreated hypertension and during antihypertensive treatment by once-a-day nadolol.

First, blood pressure and heart rate variability was studied in 89 normotensive and hypertensive ambulatory subjects with the use of an intra-arterial monitoring device. Short- and long-term variabilities were analyzed by computer. Absolute variabilities (standard deviations) were greatest in patients with hypertension, but relative variabilities (variation coefficients, i.e., standard deviations as percent of means) were slightly lower in the subjects with more severe hypertension. Second, the effect of nadolol on 24-hour blood pressure and heart rate values and on their variability was assessed in seven ambulatory patients with essential hypertension by means of the same intra-arterial device and computer analysis. Two recording sessions were performed (1) without treatment and (2) after 10 days' administration of nadolol once a day (dose range, 80 to 320 mg). Nadolol, given once a day, was shown to reduce blood pressure uniformly throughout the 24-hour period without loss of activity in the hours farthest from administration. The lack of alteration in relative blood pressure variability suggests that nadolol lowers blood pressure without interfering with the mechanisms involved in cardiovascular homeostasis. Reduction in heart rate variability after nadolol suggests less chance of tachycardia episodes in patients with angina and/or arrhythmias receiving nadolol.

Adrenergic beta-Antagonists↗
PubMed1983

Effects of blood-pressure measurement by the doctor on patient's blood pressure and heart rate.

Changes in blood pressure in 10 or 15 min periods during which a doctor repeatedly measured blood pressure by the cuff method were monitored by a continuous intra-arterial recorder. In almost all the 48 normotensive and hypertensive subjects tested the doctor's arrival at the bedside induced immediate rises in systolic and diastolic blood pressures peaking within 1 to 4 min (mean 26.7 +/- 2.3 mm Hg and 14.9 +/- 1.6 mm Hg above pre-visit values). There were large differences between individuals in the peak response (range, 4--75 mm Hg systolic and 1--36 mm Hg diastolic) unrelated to age, sex, baseline blood pressure, or blood-pressure variability. There was concomitant tachycardia (average peak response 15.9 +/- 1.5 beats/min, range 4--45 beats/min) which was only slightly correlated with the blood-pressure rise. After the peak response blood pressure declined and at the end of the visit was only slightly above the pre-visit level. A second visit by the same doctor did not change the average size of the early pressor response or the slope of its subsequent decline.

Adolescent↗
PubMed1983

Plasma catecholamines do not invariably reflect sympathetically induced changes in blood pressure in man.

Plasma concentrations of noradrenaline and adrenaline were measured radioenzymatically in nine subjects during 4 min pressor and depressor responses (intra-arterial measurements) induced by increasing and reducing sympathetic vasoconstrictor tone via carotid baroreceptor deactivation and stimulation (neck chamber technique). During the pressor response (15 +/- 3 mmHg, mean +/- SE) plasma noradrenaline and adrenaline showed various changes in the different subjects and on average were not significantly increased above control. During the depressor response (-9 +/- 2 mmHg) plasma noradrenaline and adrenaline also showed various changes in the subjects and were on average not significantly reduced below control. In contrast the same subjects all showed an increase in noradrenaline and adrenaline (average 76 and 117%) at the fourth minute of a tilting manoeuvre with a return to pretilting values no more than 4 min after resumption of the supine position. These results suggest that the moderate and/or restricted alterations in sympathetic tone produced by manipulating a single baroreflex, though capable of affecting blood pressure, are not reflected by alterations in plasma catecholamines. To modify these humoral indices significantly, the more drastic or more diffuse alterations in sympathetic activity that may be produced by manipulating low as well as high pressure reflexogenic areas are needed.

Adult↗
PubMed1983

Modification of the baroreceptor control of atrio-ventricular conduction induced by digitalis in man.

Several studies in animals and in man have suggested that the inhibitory influence of baroreceptors on heart rate and peripheral circulation is enhanced by digitalis. Because the atrio-ventricular node represents a key site for the clinical action of digitalis we studied how baroreceptor control of atrio-ventricular conduction is modified by digitalis at therapeutical doses. In eight subjects heart rate was kept constant by atrial pacing to assess neural influences on atrio-ventricular conduction rate without the modifications caused by simultaneous changes in cardiac cycle length. Arterial baroreceptors were stimulated by increasing or reducing blood pressure (intra-arterial recording), via an iv bolus of phenylephrine or nitroglycerine. The baroreflex sensitivity was assessed in ms . mmHg-1 as the slope of the linear regressions relating the rise or fall in systolic blood pressure to the lengthening or shortening in St- (atrial stimulus artifact) Q interval (ECG recording). The study was performed before and 45 min after iv administration of digitalis (0.8 mg of Lanatoside C). Baroreflex sensitivity during baroreceptor stimulation was 2.9 +/- 1.1 ms . mmHg-1 (mean +/- SE) before digitalis, whereas after digitalis a significantly and markedly greater value of 5.6 +/- 1.5 ms . mmHg-1 was found. Baroreflex sensitivity during baroreceptor deactivation was 0.9 +/- 0.1 ms . mmHg-1 before digitalis, and was not significantly affected by the drug. Thus in man the baroreceptor control of atrio-ventricular conduction is strikingly potentiated by digitalis although this potentiation is only evident in the upper portion of the stimulus-response curve of the reflex.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

Mechanisms of antihypertensive action of beta-adrenergic blocking drugs: evidence against potentiation of baroreflexes.

A possibility that can be advanced to explain the antihypertensive effect of beta-blocking drugs is that they act through the baroreflex control of the cardiovascular system. In 38 essential hypertensive patients we measured 1) The lengthening and shortening in R-R interval caused by stimulation or deactivation of arterial baroreceptors (vasoactive drug technique); 2) The fall and rise in blood pressure caused by stimulation and deactivation of carotid baroreceptors (neck chamber); 3) The rise in forearm vascular resistance caused by deactivation of cardiopulmonary receptors (lower body suction). The study was made before and after 6-10 days' administration of nadolol (80-360 mg once a day) or acebutolol (200-600 mg t.i.d.). Nadolol and acebutolol similarly reduced blood pressure and heart rate. Either drug increased heart rate responses to arterial baroreceptor manipulation but the increase fell short of statistical significance. Blood pressure and vasomotor responses to carotid baroreceptor and cardiopulmonary receptor manipulation were also not significantly modified by beta blockade. The baroreceptor control of heart rate and blood pressure showed a modification, however, insofar as a resetting towards the lower blood pressure values occurred. These findings demonstrate that arterial baroreceptor and cardiopulmonary receptor control of circulation is not potentiated by beta-blocking drugs, and that therefore this mechanism cannot account for their antihypertensive effect. The resetting of the baroreflex that occurs during beta blockade may, however, contribute to maintain the hypotension obtained.

Adrenergic beta-Antagonists↗
PubMed1982

Modification of arterial baroreflexes by captopril in essential hypertension.

Captopril lowers blood pressure without increasing heart rate and plasma norepinephrine, which suggests that this drug may potentiate arterial baroreflexes. In eight subjects with untreated essential hypertension, blood pressure was monitored intraarterially and the effects of baroreceptor stimulation or deactivation were assessed by measuring (1) the slopes of the relations between increase or reduction in systolic pressure (intravenous phenylephrine or nitroglycerin) and the resulting lengthening or shortening in R-R interval, and (2) the increase or decrease in mean arterial pressure induced by increasing and decreasing carotid transmural pressure (neck chamber). The measurements were made before and after a hypotensive oral dose of captopril (50 mg). Before captopril, the slopes of the R-R interval changes with increase and reduction in systolic pressure were 8 and 4 ms/mm Hg, respectively. The slopes of the mean arterial pressure changes with increase and reduction in carotid transmural pressure were 0.51 and 0.40 mm Hg, respectively. After captopril, the responses to baroreceptor stimulation were unaltered but those to baroreceptor deactivation were augmented. The pressor and heart rate responses to hand-grip and cold exposure were unchanged by captopril. Administration of captopril is accompanied by a baroreflex potentiation which involves the lower portion of the stimulus-response curve of the reflex. This phenomenon (which may originate at the afferent baroreceptor fibers or centrally) may avoid a reduction in the tonic baroreflex influence during captopril-induced hypotension, thus contributing to the hemodynamic effects of the drug.

Adult↗
PubMed1982

Blood pressure response to labetalol in twice and three times daily administration during a 24-hour period.

1 The anti-hypertensive effect of labetalol given twice or three times daily was evaluated in ambulant subjects with essential hypertension by recording blood pressure directly for 24 h before and after 15 d of labetalol administration (daily dose 600-1800 mg). 2 Labetalol reduced 24 h systolic and diastolic blood pressures by about 20%. The reduction was evident throughout the whole 24 h period, although it was less marked during sleep. The hypotensive effect was similar when the drug was given twice or three times daily. 3 The 24 h heart rate was reduced during labetalol treatment. However, this effect was less marked than the hypotensive effect and was not present in all subjects. 4 There was a reduction in the standard deviations of blood pressure and heart rate values. However, in neither case was the coefficient of variation altered, indicating that labetalol did not have any significant effect on the shape of the 24 h blood pressure measurements.

Adult↗
PubMed1981

Carotid sinus reflex control of renin release in hypertensive subjects with high renin secretion.

1. Carotid baroreceptor manipulation (neck-chamber technique) and passive head-up tilting were used in ten patients with renovascular hypertension and in five subjects with essential hypertension under diuretic treatment to study reflex control of renin secretion at high basal-renin production rates. 2. Reflex effects of carotid baroreceptor manipulation on renin secretion were only minor. During baroreceptor deactivation there was a moderate increase in mean arterial pressure, but an inconsistent change in the renal venous--arterial difference in plasma renin activity (PRA). 3. During baroreceptor stimulation there was a modest fall in mean arterial pressure and a marked rise in the renal venous--arterial difference in PRA. This was opposite to the fall which might have been predicted as a result of the sympathetic depressor influence of the baroreceptor stimulus. Conversely, tilting increased the venous--arterial PRA difference by about 200%. 4. It is concluded that when renin production rate is high carotid baroreceptors exert little control over renin release, just as when renin production is low. Reflex control of renin, however, is very active in subjects with a high renin production, probably due to receptors in the cardiopulmonary region.

Adult↗
PubMed1981

Digitalis and baroreceptor reflexes in man.

Data in animals indicate that large amounts of digitalis potentiate arterial baroreflexes and that this factor may be important for the cardiovascular effects of the drug. To determine if arterial baroreflex potentiation also exists after administration of therapeutic doses of digitalis in man, we studied how stimulation and deactivation of arterial baroreceptors by phenylephrine and nitroglycerin injection affect heart rate and how stimulation and deactivation of carotid baroreceptors by neck suction and pressure affects blood pressure and heart rate. The study was performed in 29 normotensive or hypertensive subjects before and after injection of Lanatoside C (0.8 mg i.v.). Baroreceptor stimulation reduced heart rate and blood pressure, while baroreceptor deactivation increased both of these variables. The bradycardic and hypotensive effect of baroreceptor stimulation increased significantly after digitalis both in normotensive and hypertensive subjects. However, the tachycardic and hypertensive responses to baroreceptor deactivation were not affected by digitalis. Thus, therapeutic doses of digitalis in man enhance baroreceptor reflexes, and both the heart rate and the blood pressure reflex effects are involved. However, the enhancement occurs to a marked degree only with baroreceptor stimulation and is not evident with baroreceptor deactivation.

Adult↗