A NEW CONCEPT OF AUTONOMIC INTERACTIONS IN THE PERIPHERAL SYMPATHETIC NERVOUS SYSTEM.
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OBJECTIVE: In patients with coronary artery disease, the concomitant presence of renal function impairment is associated with decreased survival. We aimed to assess whether in coronary artery diseased patients renal function impairment is associated with systemic vascular function, functional parameters of the renin-angiotensin system, or inflammation as potential mediators for cardiovascular risk. METHODS AND RESULTS: We studied 125 patients, 87% male, with a mean age of 62.2+/-8.2 years; 72% had 3-vessel disease, and mean renal function was 74+/-13 mL/min per 1.73 m2. Internal thoracic artery rings were sampled during coronary bypass surgery and used for in vitro vascular measurements. We could not establish an association between endothelium-dependent vasorelaxation (response to methacholine) and renal function. In addition, vascular response to potassium chloride, phenylephrine, and angiotensin II were not associated with renal function. Finally, serum angiotensin-converting enzyme (ACE) activity, usage of ACE inhibitors, C-reactive protein, and soluble intercellular adhesion molecule 1 were not related to renal function. CONCLUSIONS: In coronary artery disease patients, mild renal function impairment is not associated with systemic vasomotor responsiveness, inflammation, or functional systemic parameters of the renin-angiotensin system. The relation between systemic endothelial dysfunction and mild renal insufficiency might be more complicated than previously thought.
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Noninvasive tests of four autonomic organ systems (vasomotor control, baroreceptor reflexes, sudomotor function and pupillary reflexes) were performed on nine patients with hereditary motor and sensory neuropathy (HMSN) type I and three patients with Lambert-Eaton myasthenic syndrome (LEMS). The results were compared with those of 33 control subjects. Autonomic dysfunction was considered present when at least two of the four organ system tests were abnormal. The three patients with LEMS had abnormal results in two or more different systems, whereas only one of the nine patients with HMSN type I had two abnormal test results. This study demonstrates that autonomic dysfunction is not a common finding in patients with HMSN type I and its presence should alert us to find the cause of this autonomic disorder.
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Male New Zealand White rabbits, Oryctolagus cuniculus, were stereotaxically implanted with a guide tube above the preoptic/anterior hypothalamus (PO/AH) for the injection of beta-endorphin (beta-E) or saline at ambient temperatures of 20 and 25 degrees C. Ear skin and PO/AH temperatures were recorded in loosely restrained control and beta-E-pretreated rabbits while radiant heat was applied to the dorsal skin. Without beta-E administration the ear skin temperature (Tear) underwent a rapid increase during back heating. Following beta-E administration there was a marked vasoconstriction along with a large reduction in responsiveness of ear skin temperature to radiant heat. The time to respond to radiant heat for beta-E-pretreated rabbits was significantly longer than that for control rabbits. In control animals, the increase in Tear in response to radiant heat exposure depended upon the initial ear temperatures. However, in beta-E-pretreated rabbits vasodilatation response to radiant heat exposure was nearly the same regardless of the initial Tear. These data suggest that there is a significant reduction in passage of temperature information from cutaneous thermal receptors to the PO/AH in beta-E-pretreated animals and that beta-E-induced reduction in sensitivity of the vasomotor system to radiant heat may account for the effectiveness of this opioid peptide to promote hyperthermia in the rabbit.
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Substantial evidence exists supporting the role of chronic exercise in reducing the incidence and severity of coronary vascular disease. Physical inactivity is an independent risk factor for coronary heart disease suggesting that the cardioprotective effect of exercise is due, in part, to an intrinsic adaptation within the coronary vasculature. Surprisingly, a paucity of information exists regarding the intrinsic cellular changes within the coronary vasculature associated with exercise training and even less is known regarding the effect of physical activity on long-term phenotypic modulation of coronary smooth muscle (CSM). The purpose of this symposium is to provide a concise update on the current knowledge regarding CSM adaptation to exercise training and the potential for these adaptations to contribute to exercise-induced cardioprotection. The potential role of CSM in exercise-induced cardioprotection will be approached from two perspectives. First, endurance exercise training effects on the regulation of coronary vasomotor tone via changes in CSM calcium regulation will be reviewed, i.e. short-term functional adaptation. Secondly, we will discuss potential long-term consequences of this altered calcium regulation, i.e. exercise-induced phenotypic modulation of CSM. We propose that exercise training alters CSM intracellular calcium regulation to reduce Ca2+-dependent activation of the contractile apparatus and Ca2+-dependent gene transcription and increase activation of sarcolemmal potassium channels. The overall effect is to increase the gain of the vasomotor system and maintain a stable, contractile CSM phenotype.
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A possible role of hypotension in the genesis of sudden or slowly developing sensorineural hearing loss has been outlined. In order to confirm this hypothesis, and to exclude other vascular risk factors, a prospective study was carried out within the "Brisighella Study", a wide and homogeneous group of subjects thoroughly examined from a metabolic and cardiovascular point of view. Among them, 20 participants aged 50 years or less (18 women, 2 men) with diastolic blood pressure < or = 60 mmHg and/or systolic blood pressure < or = 105 mmHg were selected and underwent otological and audiometric examinations. Patients with previous audiological, vestibular and otological diseases were excluded. The control group was represented by 100 subjects (60 women, 40 men), aged 50 years or less, randomly chosen from within a sample of the normal population in the same region. A statistically significant incidence of sensorineural hearing loss was recorded in the study group (7/20 subjects, all affected by low-frequency hearing loss), while hearing impairment was observed in only 3/100 participants in the control group. The mean values of the main metabolic parameters were normal. An alteration of the vasomotor system associated with a hypotensive condition could be responsible as a possible factor in the origin of a cochlear damage and the consequent sensorineural hearing loss.
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