Showing papers by "Giuseppe Mancia published in 1981"
TL;DR: It is concluded that SR clonidine is an effective antihypertensive agent and that a single administration of this drug can produce a clear-cut reduction in the blood pressure values of hypertensive patients for a 24-h period.
Abstract: The antihypertensive effect of a slow-release (SR) clonidine preparation was evaluated in hypertensive patients not confined to bed using a 24-h intraarterial blood pressure monitoring (Oxford) method. The monitoring was carried out during placebo administration and after 7-10 days of daily administration of SR clonidine in a single oral dose (250 or 500 microgram). An analysis of all the blood pressure values obtained was performed by computer. The results were as follows: (a) SR clonidine significantly reduced the 24-h systolic and diastolic arterial pressure by 16 and 10 mm Hg, respectively (mean +/- SE). (b) The reduction was well evident throughout the 24-h period, the average decrease in mean arterial pressure observed during the first, second, and third 8-h period after the administration of the drug being 11, 14, and 14 mm Hg, respectively. (c) The blood pressure reduction was similar during the daytime and the nighttime, despite the lower base-line value that occurred in the latter condition. (d) There was no consistent change in blood pressure variability, as measured in each patient by the standard deviation of the blood pressure values, with SR clonidine. SR clonidine caused a reduction in heart rate that, as that in blood pressure, was well evident throughout the 24 h. It is concluded that SR clonidine is an effective antihypertensive agent and that a single administration of this drug can produce a clear-cut reduction in the blood pressure values of hypertensive patients for a 24-h period.
14 citations
TL;DR: 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, while reflex control of renin is very active in subjects with a high reninProduction, probably due to receptors in the cardiopulmonary region.
Abstract: 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.
8 citations
TL;DR: AV conduction normally is modulated by inhibitory influences but also by powerful excitatory stimuli, which are seen mainly at constant heart rate and are limited to the AV node with no effect on the His-Purkinje fibers.
Abstract: In humans, arterial baroreceptow depress atrioventricular (AV) conduction through vagal influences on the AV node but not on the His-Purkinje fibers. We investigated the influence on AV conduction of an excitatory neural influence, i.e., isometric exercise (handgrip). In subjects with normal AV conduction, blood pressure was measured by an intra-arterial catheter, R-R interval by an electrocardiogram, and A-H and H-V intervals (representing conduction, respectively, through the AV node and the His-Purkinje fibers) by His bundle recording. Handgrip raised blood pressure markedly, it shortened R-R interval, and caused no change in A-H and H-V intervals. Because prior studies had demonstrated that autonomic influences over AV conduction can be quantified accurately only when heart rate is constant, the subjects also were studied during atrial pacing. Under this condition, handgrip again caused a marked pressor response but also induced a marked shortening in the A-H interval (30%) whereas the H-V interval still wax unaffected. The handgrip-induced shortening in the A-H Interval was less pronounced after atropine but it was also Impaired by propranolol. Thus AV conduction normally is modulated by inhibitory influences but also by powerful excitatory stimuli. Like the inhibitory influences, the excitatory ones are seen mainly at constant heart rate and are limited to the AV node with no effect on the His-Purkinje fibers. Unlike the Inhibitory Influences, however, the excitatory modulation is substantially mediated via the cardiac sympathetic nerves.
7 citations
01 Jan 1981
TL;DR: It is suggested that an arterial baroreflex disfunction plays a role either as a maintaining and/or an initiating factor in the genesis of essential hypertension.
Abstract: Publisher Summary There are several studies on the control of heart rate exerted by the arterial baroreceptors in human beings. These studies have shown that the baroreceptors have a considerable influence on this variable in normotensive subjects and that this influence undergoes two major modifications in subjects with an established essential hypertension. First, in this pathological condition, the operating range of the arterial baroreceptor influence on heart rate is shifted toward the elevated blood pressure levels, a phenomenon known as resetting of the baroreceptors since its first demonstration in experimental animals. Second, the magnitude of the reflex changes in heart rate for comparable alterations in baroreceptor activity is much less pronounced in the hypertensive subjects as compared to the normotensive controls, a phenomenon indicating that in this disease, there is a reduction in the sensitivity of the baroreflex function. These results have suggested that an arterial baroreflex disfunction plays a role either as a maintaining and/or an initiating factor in the genesis of essential hypertension. A major limitation of the studies is the absence of any information on the influence that the arterial barereceptors exert on blood pressure. This limitation is of an utmost importance not only because the primary role of the arterial baroreceptors is blood pressure control but also because this control cannot be easily extrapolated from the heart rate data, due to a nonuniform baroreceptor influence on different cardiovascular areas.