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The pathophysiologic role of enhanced chemosensitivity to carbon dioxide and/or hypoxia has been underscored in several cardiovascular diseases, including heart failure. In the early stages of this syndrome, the chemoreflex acts as a compensatory mechanism. Later on, however, it contributes to sustain the sympathetic activation, with detrimental effects on cardiovascular function and prognosis.

Recent applications of frequency domain analysis to the variability of muscle sympathetic nerve activity (MSNA) have improved the comprehension of the relationship between cardiovascular oscillations and the autonomic nervous system. It has been observed that spectral analysis of MSNA is characterized by two major oscillatory components at low (LF) and high (HF) frequencies, similar to those detectable in the variability of cardiovascular signals. Pharmacological and non-pharmacological studies have shown that, at least within the physiological range, the two MSNA rhythms show a reciprocal behavior, similar to that already observed for cardiovascular oscillations. The oscillatory pattern of MSNA provides non-redundant but complementary information with respect to the time domain measures of MSNA (burst rate and amplitude) since it has been shown that completely different spectral profiles may be derived from various MSNA recordings. On the other hand, the latter are instead comparable in terms of mass activity. Due to the intrinsic characteristics of the signal, which represents the direct outflow of the central neural structures of the cardiovascular autonomic nervous system, this approach can be considered as a unique window over the central organization of excitatory and inhibitory neural mechanisms responsible for the genesis and the regulation of cardiovascular oscillations.

Dynamic 24-hour recordings were obtained in 10 healthy non hospitalized subjects. Spectral analysis of RR interval variabilities provided quantitative markers of sympatho-vagal balance throughout the day and night. The low frequency (0.1 Hz) component was considered a marker of sympathetic activity whereas the high frequency component (0.25 Hz) a marker of vagal tone. We observed an early morning rise in the sympathetic activity markers in all our patients, with a second smaller rise in the early afternoon. We believe this rise may be the trigger of the increased rate of major cardiovascular events reported to happen in the first hours of the morning.

Recent clinical observations suggest that adenosine may produce cardiac pain; even though the mechanisms involved still need defining, one of the most convincing hypotheses seems to be a direct adenosine stimulation of the sympathetic nerve endings present in the myocardium. In 10 decerebrate and artificially ventilated cats, single sympathetic afferent fibres innervating the left ventricle were isolated from the third white thoracic ramus communicans of the left sympathetic chain. After locations of the fibre receptor field on the cardiac surface, we evaluated the effects of the local epicardial application of adenosine (0.1, 1 and 10 mg/ml) on the nervous discharge activity. These results were compared with those obtained by application of bradykinin, a potent natural algogenic substance which activates sympathetic afferents, and by a mechanical stimulus such as a slight increase of systolic arterial pressure (46 +/- 6% from 113 +/- 18 mmHg) induced by partial occlusion of the thoracic aorta. In particular, adenosine (1 mg/ml) elicited a significant increase in impulse activity (from 0.11 +/- 0.02 to 0.36 +/- 0.06 imp/0.1 s) with a latency of 16 +/- 2 s. Bradykinin application (20 micrograms/ml), in the same way, produced a significant increase in impulse activity (from 0.11 +/- 0.01 to 0.86 +/- 0.16 imp/0.1 s) with a latency of 8 +/- 1 s. Neither situation showed significant hemodynamic changes. An increased neural discharge (from 0.11 +/- 0.02 to 0.26 +/- 0.04 imp/0.1 s) was also observed during aortic occlusion. After purinergic receptor blockade by aminophylline (5 mg/kg, iv), the response to adenosine was no longer observed, while responses to bradykinin and aortic occlusion were unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Unlabelled: The aim of our study was to seek out a possible different reactiveness to cardiovascular stimulation tests among normotensives with and without positive family history of essential hypertension. We have studied about 200 inhabitants of Ustica and 49 medicine students, all normotensives according to the World Health Organization and the Joint National Committee criteria. In an isolated room and in a supine position, blood pressure (BP) and heart rate were measured every 30 s for 15 min with an automatic sphygmomanometer. Averages of last 4 measurements were considered baseline values. Then we have carried out mental stress (MS), handgrip and active orthostatism test (AO) in the inhabitants of Ustica; cold pressor test and AO in students. Patients were divided in 2 groups, genetics and controls, on the basis of a positive family history of essential hypertension. The 2 groups, in every sample, were similar for sex, age, body mass index and alimentary and life habits., Results: a preliminary estimation of Ustica sample showed a different prevalence of positive history between hypertensives and normotensives (63.9% vs 46.61%; p less than 0.05) and no difference between hypertensive and borderline patients (63.9% vs 64.2%); BP and heart rate were slightly higher in controls; there was no statistical difference between genetics and controls., Conclusions: our results can be explained in various ways: pressor dysregulation in candidates for hypertension may be masked in a large group of normotensives; exaggerated pressor response do not exist in genetics or this pressor dysregulation is impossible to find out with the cardiovascular stimulation tests we have used; other mechanisms are responsible for genetic hypertension.

In order to discover more about the role of the sympathetic nervous and renin-angiotensin systems in the preservation of homeostasis during chronic reductions of salt intake, blood pressure, blood catecholamines and renin activity were measured in a group of healthy subjects in normal conditions and on a salt-free diet combined with blockade of the conversion enzyme by enalapril. The results confirmed the hypothesis advanced on an earlier occasion i.e. that both hormone systems contribute to pressure during salt depletion in the initial phase, while over the long term only the renin-angiotensin system is activated though when this is inhibited, the sympathetic nervous system will take over its function.

A review of current knowledge about the involvement of peripheral adrenergic mechanisms in the action of acupuncture is presented. Apart from its undeniable effects on these mechanisms, acupuncture seems to operate in two different ways: indirect stimulation due to an aspecific response to the stress of the acupuncture and direct stimulation or depression, mainly of noradrenaline increase according to the placing of the needles and the condition being treated. During electroacupuncture anesthesia the inhibition of peripheral adrenergic mechanisms is proportional to the effectiveness of the induction.

A brief account of the anatomical features of the smooth musculature of the entire bronchial tree is followed by an examination of the various components of the broncho-constrictor reflex. Stress is laid on the importance of the sympathetic and parasympathetic pathways in determining the reflex and the release of chemical mediators in the bronchi is discussed. Clinical situations leading to an enhanced reflex are described and their pathogenesis is explained. It is submitted, however, that existing knowledge of bronchospastic syndromes is still insufficiently clear. This explains the lack of success frequently encountered in their treatment.

The problem of the relationship between the thiamine and autonomic system drugs was studied about 30 years ago. To the vitamin was attributed an excitatory effect upon the peripheric section of parasympathetic nervous system and a synergic action with acetylcholine. Both an acetylcholine-like substance and thiamine are liberated at the nerve terminals after a stimulation. A similar synergic action of thiamine with adrenaline was also demonstrated. The study of the relationship between these drugs and the vitamin B1 is also now interesting. We want to stimulate a new series of experiments on this subject with the reprint of this review.

In ovariectomized rats treated with estradiol benzoate, the pre-treatment with bromocriptine or metergoline on increase of PRL secretion induced by some prostaglandins has been investigated. The PGs used were able to hinder the drop in PRL levels induced by metergoline, a blocker of 5-HT receptors, but not that produced by bromocriptine, a dopamine receptor agonist. Therefore it is possible to suppose that the PGs are involved in the monoaminergic hypothalamic regulation of the PRL secretion.