Showing papers by "Giuseppe Mancia published in 1990"

Sequential spectral analysis of 24-hour blood pressure and pulse interval in humans

Abstract: Blood pressure and pulse interval are characterized not only by erratic variations but also by rhythmic fluctuations at low-, mid-, and high-frequency (0.025-0.07, 0.07-0.14, and 0.14-0.35 Hz, respectively). However, information on these phenomena has largely been derived from analysis of short-term recordings taken in standardized laboratory conditions. In seven normotensive and 10 untreated mild essential hypertensive subjects, power spectrum analysis was performed on the intra-arterial blood pressure and pulse interval signal collected over a 24-hour period using the fast Fourier transform algorithm and splitting the recording into contiguous segments of 256 beats. About 70% of the segments were suitable for the analysis; the segments excluded for a nonstationary signal amounted to only 30%. All powers were characterized by a high segment-to-segment variability, but in each subject the mid- and high-frequency powers of diastolic blood pressure and the mid-frequency power of systolic blood pressure were markedly reduced during the night as compared with the daytime period, whereas the opposite occurred for the low- and high-frequency powers of the pulse interval. Over the 24-hour period, mid- and high-frequency powers of blood pressure were positively correlated to each other, but both accounted for less than 25% of the 24-hour blood pressure variance. No difference between mean normalized power values of normotensive and hypertensive subjects was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Sympathetic activation in congestive heart failure.

Abstract: This paper reviews the evidence that congestive heart failure is characterized by an increase in sympathetic nerve activity and that this may begin in an early symptomatic phase and progress with the severity of the disease. The sympathetic activation initially plays a compensatory role but eventually is outweighted by adverse consequences at both cardiac and vascular levels which may aggravate the clinical status and negatively affect prognosis. This is likely to depend on the fact that the sympathetic activation becomes excessive due to reduction in sensitivity of baroreflexes and cardiopulmonary reflexes restraining sympathetic tone (functional reflex denervation) and positive interactions between the sympathetic and the renin-angiotensin system. Therapeutic interventions may reduce the marked sympathetic activation which occurs in heart failure, and in some instances (particularly with digitalis compounds) may also improve the impaired sensitivity of reflex cardiovascular control.

Ambulatory blood pressure monitoring: research and clinical applications.

Abstract: Intra-arterial ambulatory blood pressure monitoring has shown that blood pressure undergoes a marked fall during sleep and marked repeated rises during emotional stimuli, including those elicited when blood pressure is assessed by the physician. This leads to an overestimate of blood pressure levels, which is so variable between patients, and so persistent and unpredictable that it seriously interferes with the diagnosis of hypertension. The ambulatory measurement technique has shown that, to a substantial degree, 24-h blood pressure variations can be attributed to neural influences triggered by environmental stimuli. However, blood pressure oscillates at different frequencies throughout the day and night and thus the overall blood pressure variability can be divided into a non-rhythmic and a rhythmic component, its size in each individual being buffered by the arterial baroreflex. In the light of these findings, ambulatory blood pressure monitoring is not only an important tool in cardiovascular research but also has potential for improving the diagnosis of hypertension and the evaluation of antihypertensive treatment. Ambulatory blood pressure data can be correlated, to a greater degree than clinic blood pressure, with the target-organ damage sustained by both treated and untreated hypertensive patients. However, widespread use of this approach in clinical practice must await the establishment of ambulatory blood pressure norms and demonstration of its prognostic superiority over traditional blood pressure assessments. Further, non-invasive ambulatory blood pressure monitoring (the only approach feasible on a routine basis) has limited accuracy and markedly increases the cost of dealing with hypertension.

Cardiovascular effects of smoking.

Abstract: Coronary heart disease (CHD) increases with smoking and this factor interacts with hypercholesterolemia and hypertension in raising the incidence of this condition in a greater than linear fashion. This can be explained by the adverse effect of smoking on plasma fibrogen, platelet turnover and lipid profile. It may also be accounted for, however, by the acute bradycardia, increase in blood pressure and generalized vasoconstriction accompanying smoking, due to a nicotine-dependent activation of the sympathetic nervous system. These effects (which in heavy smokers can raise blood pressure permanently) are only partly offset by beta-blockers and can only be abolished by opposing the cardiac and vascular sympathetic influences by alpha and beta-blockade combined.

Intra-arterial pressure alterations during tail-cuff blood pressure measurements in normotensive and hypertensive rats.

Abstract: The heating and restraint inherent to tail-cuff measurement of systolic blood pressure (SBP) in rats may alter SBP and introduce a 'biological' error in its estimation by this technique. This problem was examined in unanesthetized normotensive and hypertensive rats fitted with an arterial catheter. All SBP values recorded in unrestrained rats during a 2 h period were averaged by computer and compared with intra-arterial SBP measurements observed while the rat was being subjected to the tail-cuff procedure. With the latter procedure, SBP was 16 +/- 2 mmHg lower in normotensive rats (P less than 0.001) and 7 +/- 3 mmHg higher in hypertensive rats (P less than 0.05) than when the rats were unrestrained. The effects of heat and restraint, both separately and in combination, on SBP were evaluated during four additional 30-min monitoring periods. In both groups of rats, restraint failed to alter SBP and heat lowered it slightly. The two stimuli, combined, lowered SBP in normotensive rats, but raised it by 12 +/- 2 mmHg in hypertensive rats (P less than 0.01). Thus, tail-cuff SBP measurements represent under- and overestimates in normotensive and hypertensive rats, respectively, since the two groups respond to the procedure in opposite manners.

Clinical significance of "white coat" hypertension.

Abstract: This issue of Hypertension includes a report by Julius and colleagues on a topic of great importance for the diagnosis of hypertension, that is, the alerting reaction and blood pressure rise triggered by blood pressure measurements and commonly referred to as the "white coat" phenomenon. The first observation that blood pressure measurement may trigger an alerting reaction and a pressor response in the patient was made by Riva-Rocci in his original report on the sphygmomanometric technique, which was published near the end of the last century. This pressor response was then described in several other papers" and quantified in subjects in whom sphygmomanometric assessment of blood pressure by the physician was obtained during prolonged intra-arterial ambulatory blood pressure monitoring. The data showed that the peak increase in intra-arterial systolic and diastolic blood pressure occurring during the procedure was so pronounced that it averaged 27/14 mm Hg. However, although a blood pressure rise was observed in most subjects, the pressor response showed a pronounced interindividual variability, with the maximal increase in mean arterial pressure ranging from 2 to 53 mm Hg.

Atrial natriuretic factor and arterial baroreceptor reflexes in unanesthetized rats.

Abstract: The modulation exerted by atrial natriuretic factor (ANF) on the cardiac and vascular influences of arterial baroreceptors was investigated in two groups of unanesthetized, chronically instrumented normotensive rats. In group 1, the reflex control of heart rate was assessed by graded baroreceptor stimulations and deactivations obtained by intravenous boluses of phenylephrine and nitroprusside. Under either circumstance, baroreceptor reflex sensitivity was expressed as the linear regression slope relating the chronotropic responses to the drug-induced mean arterial pressure changes. In group 2, right common carotid occlusion was performed in rats with their aortic and left carotid sinus baroreceptors denervated to assess the baroreceptor control of blood pressure; the reflex response was quantitated as the peak blood pressure rise observed during the maneuver. The reflex studies were performed before and during atriopeptin III infusion (0.15-0.20 micrograms/kg/min for 60 minutes). ANF augmented the bradycardic response to phenylephrine by 102.5 +/- 29% (p less than 0.01), reduced the tachycardic response to nitroprusside by 67.7 +/- 6.4% (p less than 0.01), and failed to modify the pressor response to carotid occlusion (-6.8 +/- 2.1%, p = NS). In a separate group of rats infused with low dose nitroprusside, no change in the baroreceptor-heart rate reflex was observed. ANF infusion (0.20 micrograms/kg/min) performed in further separate groups of conscious rats raised plasma ANF to 480 +/- 58 fmol/ml. Values in control vehicle-infused rats were 50 +/- 8 fmol/ml. Vascular reactivity (pressor response to intravenous phenylephrine boluses in anesthetized, sinoaortic-denervated rats) was only minimally reduced by ANF.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood pressure variability: mechanisms and clinical significance.

Abstract: Studies have shown that the circadian blood pressure profile is similar in normotensive and hypertensive subjects, and that the observed increase in blood pressure variability in hypertensive patients is proportional to the increase over the normotensive baseline blood pressure, suggesting that transient blood pressure oscillations on a percentage basis are not altered by hypertension. It has also been found that although antihypertensive therapy tends to reduce mean arterial blood pressure (MAP), the tendency to oscillate around a mean pressure is modified to a lesser extent. The significance of this observation is unknown; however, this effect should possibly be considered and studied in view of the incomplete protection against cardiovascular complications that is afforded by the current management of hypertension.

Haemodynamic effects of ACE inhibitors

Abstract: 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 efects 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 quinaprill appears to share the haemodynamic effects of other ACE inhibitors with an improvement of cardiovascular function in congestive heart failure.

Cardiogenic reflexes and left ventricular hypertrophy.

Abstract: Studies performed in both animal and human species have shown that receptors anatomically located in the cardiac walls and in the pulmonary vascular bed exert a powerful influence on sympathetic vasoconstrictor tone and renin release from the kidney. This paper will review recent data collected by our group on the effects on this homeostatic reflex function of two different models of cardiac hypertrophy, i.e. that associated with arterial hypertension and that induced by prolonged physical training. It will also examine whether and to what extent cardiopulmonary reflex control of circulation can be restored after an effective antihypertensive pharmacological treatment has induced a regression of the structural alterations of the heart. The results of these studies suggest that cardiopulmonary reflex control of circulation is markedly impaired in the presence of cardiac hypertrophy, with (severe hypertensive subjects) or without (athletes) high blood pressure values. In hypertensives, furthermore, therapeutic regression of cardiac hypertrophy seems to restore, although not fully normalize, this reflex function. Taken together these findings suggest that cardiac hypertrophy, per se, is a condition characterized by the loss of the reflex functions exerted by cardiac receptors, with adverse consequences on cardiovascular homeostasis.

Haemodynamic Effects of the Multiple Action Antihypertensive Drug Urapidil

Abstract: This paper reviews the evidence that the antihypertensive effect of urapidil is due to a systemic vasodilatation with no change in cardiac output, no tachycardia and no under-perfusion of vital organs. Urapidil does not impair the cardiovascular control exerted by arterial baroreceptors and cardiopulmonary receptors. This is probably the reason why no orthostatic hypotension and derangement in blood pressure homeostasis follows its administration.