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Biomedical subjects

A Zanchetti

Publications and source records attributed to A Zanchetti.

At least 433 records · Page 24Linked to original sources
PubMed1977

The variable-pressure neck-chamber method for studying the carotid baroreflex in man.

1. The variable-pressure neck-chamber method was analysed in ten healthy volunteer subjects to determine its suitability for the study of the carotid baroreceptor reflex in man. 2. Positive and negative pressures applied to the neck (range +/- 60 mmHg) were always transmitted linearly to a tissue catheter outside the carotid sinus, but only 86% of positive pressure, and 64% of negative pressure. Tissue pressures were confirmed by simultaneous measurement in the internal jugular vein adjacent to the carotid sinus. 3. Positive and negative pressure changes within the above range did not alter PO2 of internal jugular venous blood, suggesting that cerebral blood flow was unaltered. 4. Positive pressure changes induced reflex pressor responses of similar magnitude at arterial PO2 12-8 and 70-1 kPa (96 and 527 mmHg), suggesting that the carotid chemoreceptors were not involved. 5. It is concluded that the variable-pressure neck chamber is a valid method for selectively studying the carotid baroreceptor reflex in man. However, transmission of external pneumatic pressure to the carotid sinus is imperfect and greater for positive than for negative pressure. This must be recognized to avoid underestimation of gain and distortion of shape of the reflex.

Adult↗
PubMed1977

Effects of renal denervation on renin release in response to tilting and furosemide.

In anesthetized cats head-up tilting for 30 min and infusion of furosemide at 0.75 mg/kg in 30 min significantly raised renin release from the innervated kidney (increments of 90.7 +/- 21.4 ng/min on tilting and 105.4 +/- 26.4 ng/min after furosemide); a small and inconstant increase from the contralateral denervated kidney (increments of 16.8 +/- 16.0 and 16.3 +/- 17.7 ng/min, respectively) was abolished by acute bilateral adrenalectomy. Larger doses of furosemide (6.0 mg/kg) could release renin from the denervated kidney also, but the response was still more marked on the innervated side especially in the early period of infusion (increments of 132.7 +/- 23.8 and 33.7 +/- 23.8 ng/min of innervated and denervated sides at 10 min). The response of the denervated kidney to 6.0 mg furosemide/kg was not affected by adrenalectomy. Stimulation of juxtaglomerular cells by tilting is entirely due to sympathoadrenergic activation; stimulation by furosemide is also entirely neural when the diuretic drug is given in moderate doses, but is partly independent of innervation when larger doses are administered.

Adrenalectomy↗
PubMed1977

Circulatory reflexes from carotid and extracarotid baroreceptor areas in man.

The carotid sinus baroreceptor reflex was studied in 11 normotensive subjects, using a variable pressure neck chamber and correcting for imperfect pressure transmission to the carotid sinus. Decreased carotid baroreceptor stimulation caused a sustaineded rise in arterial pressure, and increased carotid baroreceptor stimulation caused a sustain fall. The responses were in linear relation to the stimulus, and, after reaching the steady state, greater for the reduced than for the increased baroreceptor stimulation. Thus the carotid sinus baroreceptor reflex of the normotensive man is an effective antihypotensive and antihypertensive feedback system, though the former function may have more sensitivity. The increased and decreased baroreceptor stimulation by the neck chamber also caused bradycardia and tachycardia which were modest in magnitude and often transient. In eight subjects the reflex changes in heart rate induced by the neck chamber were compared with those induced by altering transmural pressure not merely at the carotid sinus but throughout the arterial tree (injection of phenylephrine and trinitroglycerin). The slopes of these relations were 3 times as great in the latter circumstance. Thus the carotid baroreceptors play a lesser role in heart rate control than do extracarotid baroreceptors.

Adult↗
PubMed1976

Control of renin release: a review of experimental evidence and clinical implications.

Present knowledge of the mechanisms regulating release of renin is reviewed with particular emphasis on neural factors. Evidence is given for a direct effect of renal innervation on beta adrenergic receptors in juxtaglomerular cells, and for the involvement of reflex release of renin in conditions such as tilting and acute salt depletion. Participation of neural and nonneural mechanisms of control is also shown to occur in other conditions, such as aortic constriction and hemorrhage. The view is held that neural sympathetic factors might explain some of the renin disturbances found in essential hypertension. First, in patients with high renin hypertension part of the hypertension is renin-dependent, and these pressor levels of renin seem to be neurally induced since they can commonly be suppressed by beta adrenoreceptor blocking agents. Second, the hypothesis is presented that patients with low renin hypertension, at least those who have no volume disturbance, have a blunted sympathetic control of renin release. Therefore a sufficiently precise test of sympathetic activity, and possibly of body fluid volumes, should be associated with renin profiles for a better understanding of the pathophysiology of arterial hypertension and as a better guide to therapeutic management. Indeed, most of the available antihypertensive drugs act on sympathetic activity, body fluid volume or renin, and this multifaceted profile would provide more rational guidelines for treatment.

Adrenergic beta-Antagonists↗
PubMed1976

Neural factors contributing to renin release during reduction in renal perfusion pressure and blood flow in cats.

1. The participation of neural mechanisms in mediating the renin release induced by reduction of renal perfusion pressure was explored in anaesthetized cats by comparing renin release from the two kidneys, one acutely denervated and the other intact. 2. Suprarenal aortic stenosis of 10 min duration reduced renal perfusion pressure to 50 mmHg and halved blood flow to both kidneys, but cause a greater release of renin from the innervated kidney than from the contralateral denervated one (increments of 72 +/- 17 and 29 +/-20 pmol/min respectively). 3. A study of the time-course of the response during aortic stenosis of 30 min duration showed early release of renin from the innervated kidney at a time (5 min) when little release occurred from the denervated one. In later samplings (15 and 30 min) the response of the innervated kidney levelled out at somewhat lower values, and that of the denervated organ progressively increased, but remained smaller than on the side with intact nerves. 4. There was no parallelism between renin release and renal vasomotor changes induced by aortic stenosis, as vasomotor changes were equal in the two kidneys and remained constant from beginning to end of stenosis. It is concluded that a significant part of the renin release induced by aortic stenosis is dependent on neural mechanisms: the neural differs from the non-neural component in being of more rapid onset and probably of shorter duration.

Animals↗
PubMed1976

Role of the renal nerves in renin release during suprarenal aortic stenosis in cats.

1. Renin release from an intact, innervated kidney and from the contralateral denervated kidney was measured before and during a period of suprarenal aortic stenosis. 2. Aortic stenosis of 10 min duration reduced renal perfusion pressure to 50 mmHg and increased renin release from both kidneys, but the response from the innervated kidney was greater. 3. A study of the time-course of the response during 30 min of aortic stenosis showed that the difference in rate of renin release between the innervated and the denervated kidney is greatest during the first few minutes of aortic stenosis.

Animals↗
PubMed1976

Carotid baroreceptor reflex in normotensive and hypertensive subjects.

1. A graded decrease and increase in carotid baroreceptor activity (induced by a varying pressure in a neck chamber) caused a linearly related increase and decrease in arterial blood pressure. This occurred in both normotensive and hypertensive subjects. 2. Decrease of carotid baroreceptor activity caused a greater increase of blood pressure in normotensive than in hypertensive subjects. Increasing the activity caused changes of similar magnitude in the two groups. 3. Decrease of baroreceptor activity also caused an increase in heart rate although increasing the activity of the reflex had little effect on heart rate, particularly in normotensive subjects. Thus the carotid baroreceptor effect on blood pressure does not always reflect that on heart rate and inference of one reflex response from measurement of the other may be in error.

Blood Pressure↗
PubMed1976

Factors influencing the carotid baroreceptor response to pressure changes in a neck chamber.

1. Transmission of pneumatic pressure from a neck chamber to the region of the carotid sinus is imperfect and asymmetric (86% of positive pressure, 64% of negative pressure). This has to be taken into account in the correct analysis of the carotid baroreceptor reflex. 2. There is no evidence for a reduction in cerebral blood flow nor of carotid chemoreceptor stimulation in response to an increase in neck chamber pressure of about 45 mmHg. Thus it is likely that the pressor response to this manoeuvre is in fact due to reduction in carotid baroreceptor activity.

Carotid Sinus↗
PubMed1976

Interplay of sino-aortic reflexes and haemodynamic changes during natural sleep in the cat.

1. When the sino-aortic afferents are intact, desynchronized sleep causes a small decrease in the blood pressure, a vasodilation in the mesenteric and renal beds, and a vasoconstriction in the external iliac bed. 2. After sino-aortic deafferentation desynchronized sleep causes a larger fall in the blood pressure, a greater vasodilatation in the mesenteric and renal beds, and a vasodilatation replaces the vasoconstriction in the external iliac bed. 3. The sino-aortic reflexes play an active role in controlling circulation during desynchronized sleep by opposing the centrally induced reduction in adrenergic sympathetic tone. This effect of sino-aortic reflexes is similar on both visceral and muscular vessels. In addition, the muscular bed, but not the visceral one, is regulated by a spinal reflex vasoconstriction mechanism which is apparent only when the sino-aortic reflexes are intact.

Animals↗
PubMed1976

Haemodynamic responses and renin release during stimulation of afferent renal nerves in the cat.

1. Experiments were done on anaesthetized cats to study the effect of electrical stimulation of afferent renal nerves on the circulatory system and on the release of renin from the kidney. 2. Stimulation of afferent renal nerves over a wide range of parameters consistently elicited an increase in arterial pressure and heart rate. This response was still present in paralysed animals and was not accompanied by changes in respiration or in sympathetic autonomic activity usually associated with painful stimulation. Mesenteric and iliac vasoconstriction was observed concomitantly with the increase in arterial pressure. 3. Release of renin from the contralateral innervated kidney was not significantly changed by stimulation of afferent renal nerves. 4. The existence of renal vascular mechanoreceptors was investigated by altering renal circulation. Stenosis of the renal artery or a marked reduction in renal perfusion pressure elicited an increase in arterial pressure while stenosis of the renal vein elicited a decrease in arterial pressure. These responses, however, were not affected by denervation of the kidney and were therefore interpreted as not being due to neural mechanisms. 5. The precise nature, location and physiological role of renal receptors involved in the cardiovascular responses observed during electrical stimulation of afferent renal nerves remain to be determined.

Animals↗
PubMed1976

Interactions between sino-aortic reflexes and cardiovascular effects of sleep and emotional behavior in the cat.

The role of sino-aortic reflexes in the control of circulation during normal behavior was investigated by comparing cardiovascular reactions during various but reproducible types of behavior before and after bilateral sino-aortic deafferentation. Chronic deafferentation caused little change in baseline blood pressure, but a subtler, important role of sino-aortic reflexes was revealed by examining the integrated cardiovascular responses to behavioral stimuli. During desynchronized sleep, the buffering action of sino-aortic reflexes prevented a marked and diffuse vasodilation, with an action that was particularly evident on muscle blood vessels. During emotional behavior, especially when emotion was accompanied by movement, sino-aortic reflexes opposed the consequences of muscle vasodilation by inducing tachycardia and vasoconstriction in the viscera and in noncontracting muscles. A reciprocal type of interaction between behavior and sino-aortic reflexes was shown by testing the amplitude of the carotid occlusion response before and during desynchronized sleep; the latter condition was consistently associated with decreased effectiveness of the reflex response. The possibility is considered that this might indicate central suppression of the carotid sinus reflex during desynchronized sleep and that a similar inhibitory interference might occur during emotional behavior. Alternatively, reduction of the reflex response might result from a shift of the stimulus-response curve on either side of its steep portion.

Animals↗