Showing papers by "Giuseppe Mancia published in 1979"

Control of blood pressure by carotid sinus baroreceptors in human beings

Abstract: Most techniques available for studying arterial baroreflexes in man are unsuitable for analysis of the primary function of these reflexes, that is, arterial pressure control. Such control can be evaluated during increases and decreases in carotid baroreceptor activity obtained with a variable pressure neck chamber. This study reviews some technical aspects of the technique and describes the influence the carotid baroreceptors exert on arterial pressure in normotensive subjects and in those with essential hypertension. Major differences can be found in the two populations. In normotensive subjects the change in blood pressure is greater with a decrease than with an increase in baroreceptor activity. The former response becomes progressively less and the latter progressively greater with increasingly high blood pressure, so that in severe hypertension the reflex shows an asymmetry opposite to that in normotensive subjects, the change in blood pressure being greater with an increase than with a decrease in baroreceptor activity. These results imply that in human hypertension the carotid baroreflex mechanism controlling blood pressure undergoes a very marked resetting but shows no major reduction in sensitivity. In hypertensive subjects cardiac output and peripheral resistance were also measured. It was found that the depressor response to an increase in carotid baroreceptor activity depends on both a reduction in cardiac output and a systemic vasodilatation. However, peripheral vasoconstriction is the only factor accounting for the pressor response to reduced baroreceptor activity.

Baroreceptor control of atrioventricular conduction in man.

Abstract: Although human baroreflexes are known to exert a powerful physiological control on heart rate, little information exists on the physiological control they exert on the atrioventricular conduction system. In 11 normotensive subjects with normal atrioventricular conduction, we altered baroreceptor activity by injection of pressor and depressor drugs (phenylephrine and trinitroglycerin) and recorded mean arterial pressure (MAP, catheter measurements), R-R interval, and pre-His and post-His intervals (A-H and H-V, His bundle recording). With the subjects in sinus rhythm, increasing MAP by 21+/- 1 mm Hg caused a marked lengthening (250 +/- 28 msec), and decreasing MAP by 17 +/- 2 mm Hg a marked shortening (142 +/- 16 msec) of the R-R interval. There was little change in the A-H interval and no change at all in the H-V interval. However, when the R-R interval was kept constant in these subjects by atrial pacing, a similar increase and decrease in MAP caused, respectively, a marked lengthening (49 +/- 6 msec) and shortening (19 +/- 3 msec) of the A-H interval, although the H-V interval remained unaffected. Thus physiological ranges of baroreceptor activation have a marked influence on the atrioventricular node but apparently not on the ventricular portion of the atrioventricular conduction system. This influence is unmasked when pacing prevents the baroreceptor influence on the sinoatrial node.

Clonidine and carotid baroreflex in essential hypertension.

Abstract: Clonidine is believed to reduce blood pressure by a neural action and animal experiments suggest that this consists in potentiation of baroreflexes. In 16 patients with essential hypertension we studied the effects of alterations in carotid sinus baroreceptor activity (neck chamber technique) on arterial blood pressure (catheter measurements) and heart rate, before and after intravenous administration of 150 microgram and 300 microgram of clonidine. The magnitude of the reflex responses was assessed by the slope of the linear regressions relating applied increase and decrease in tissue pressure at the carotid sinus (and therefore applied decrease and increase in carotid sinus transmural pressure) and resulting changes in mean arterial pressure and R-R interval. Clonidine caused a marked reduction in mean arterial pressure (-26 +/- 3 mm Hg) and a slight but significant reduction in heart rate (-5 +/- 1 b/min). There was no evidence for a potentiation of the baroreceptor influence on blood pressure, although a slight potentiation of the baroreceptor influence on heart rate was observed in few instances. We conclude that in man clonidine can exert a pronounced hypotensive effect without potentiating baroreceptor influence on blood pressure. Therefore this mechanism does not play a prominent role in the clinical antihypertensive action of the drug.

Plasma Catecholamines and Blood Pressure Responses to the Carotid Baroreceptor Reflex in Essential Hypertension

Abstract: 1. Slight decreases and increases in carotid baroreceptor activity were induced in subjects with essential hypertension by slight alterations in carotid transmural pressure (variable pressure neck-chamber technique) in order to obtain limited increases and reductions in sympathetic adrenergic activity. 2. When sympathetic activity was reflexly increased there was a rise in arterial pressure but no significant increase in plasma catecholamines. Likewise when sympathetic activity was reflexly reduced there was a fall in arterial pressure but no significant reduction in plasma catecholamines. 3. Plasma noradrenaline and adrenaline significantly and markedly increased in the same subjects when sympathetic activity was increased by activation of both arterial and low pressure baroreceptor reflexes with tilting. 4. It is suggested that measurements of catecholamines in systemic plasma may reveal marked degrees of sympathetic activation but may not be a sensitive index of more moderate changes in sympathetic tone.