Showing papers on "Autonomic nervous system published in 1988"
TL;DR: The frequency characteristics of HR fluctuations in patients with severe CHF are consistent with abnormal baroreflex responsiveness to physiologic stimuli, and suggest that there is diminished vagal, but relatively preserved sympathetic, modulation of HR.
Abstract: Neurohumoral modulation of cardiovascular function is an important component of the hemodynamic alterations in patients with chronic congestive heart failure (CHF). Analysis of heart rate (HR) variability is a noninvasive means of investigating the autonomic control of the heart. The variability of HR and respiratory signals, both derived from ambulatory electrocardiographic recordings, were analyzed with power spectral analysis to evaluate autonomic control in 25 patients with chronic stable CHF (class III or IV) and 21 normal control subjects. In the patients with CHF, HR spectral power was markedly reduced (p less than 0.0001) at all frequencies examined (0.01 to 1.0 Hz, period 1 to 100 seconds) and virtually absent at frequencies greater than 0.04 Hz. Heart rate fluctuations at very low frequencies (0.01 to 0.04 Hz) less effectively differentiated CHF patients from control subjects, due to discrete (about 65 seconds, 0.015 Hz) oscillation in HR, which was associated with a similar pattern in respiratory activity in many of the patients with CHF. These findings demonstrate a marked derangement of HR modulation in patients with severe CHF. The frequency characteristics of HR fluctuations in these patients are consistent with abnormal baroreflex responsiveness to physiologic stimuli, and suggest that there is diminished vagal, but relatively preserved sympathetic, modulation of HR.
743 citations
TL;DR: Physiologists have hypothesized that the sympathetic nervous and renin-angioten causes an increase in loading conditions in ventricle and may accelerate progression of lying disease, which may underlie the path ventricular arrhythmias.
Abstract: When cardiac output falls after an insult t cardium, a number of neurohormonal mecd activated to preserve circulatory homeo though originally viewed as a beneficial coI response, the endogenous release of vasc neurohormones appears to play a deleteriou development of congestive heart failure. A( the sympathetic nervous and renin-angioten causes an increase in loading conditions in ventricle and may accelerate progression of lying disease. These neurohormones may ir (and exacerbate) the electrolyte abnormalit heart failure, which may underlie the path ventricular arrhythmias. By these mechan rohormonal activation contributes importa symptoms of heart failure as well as to the tality of patients with this disorder.' Why are these neurohormones released with heart failure when their effects are so d Physiologists have hypothesized that the ci limited in its capacity to respond to circul; (e.g., a reduction in cardiac output). Accor theory, the mechanisms that are activated ir
526 citations
TL;DR: It is suggested that autonomic alterations are important in human obesity, as they are in animal obesity, because a disordered homeostatic mechanism may promote excessive storage of energy by decreasing sympathetic activity, while defending against weight gain by decreasing parasympathetic activity.
Abstract: The cause of most cases of human obesity is unknown. Specific alterations in the activity of the autonomic nervous system may mediate and perhaps cause obesity in animal models. We therefore looked for alterations in autonomic activity in human obesity. Fifty-six healthy men with various percentages of body fat underwent autonomic testing while at rest. Significant correlations were found between the percentage of body fat and the variation in the R–R interval after beta-adrenergic blockade (r = -0.30, P<0.03), the heart rate (r = 0.30, P<0.03), the plasma norepinephrine concentration (r = -0.30, P<0.05), the plasma epinephrine concentration (r = -0.49, P<0.001), and the pupillary latency period (r = 0.39, P<0.01). Each of these variables reflects the activity of the sympathetic nervous system or parasympathetic nervous system or both. Depressions in sympathetic and parasympathetic activity were significantly but weakly associated with increasing percentages of body fat. These associations indica...
420 citations
TL;DR: Quantitative studies of a simple part of the nervous system in mammals provide evidence that neuronal geometry and innervation are regulated by long-term trophic interactions between neurons and their targets.
Abstract: A remarkable feature of nerve cells is the complex and variable pattern of their axonal and dendritic branches. Quantitative studies of a simple part of the nervous system in mammals provide evidence that neuronal geometry and innervation are regulated by long-term trophic interactions between neurons and their targets. This trophic linkage may explain how nerve cells adjust their function to the needs of bodies that vary markedly in size and form.
352 citations
01 Jan 1988
TL;DR: The question of whether there are different patterns of autonomic nervous system responses for different emotions is examined in the context of the development of research methods appropriate for studying this question as mentioned in this paper.
Abstract: The question of whether there are different patterns of autonomic nervous system responses for different emotions is examined. Relevant conceptual issues concerning both the nature of emotion and the structure of the autonomic nervous system are discussed in the context of the development of research methods appropriate for studying this question. Are different emotional states associated with distinct patterns of autonomic nervous system (ANS) activity? This is an old question that is currently enjoying a modest revival in psychology. In the 1950s autonomic specificity was a key item on the agenda of the newly emerging discipline of psychophysiology, which saw as its mission the scientific exploration of the mind-body relationship using the tools of electrophysiological measurement. But the field of psychophysiology had the misfortune of coming of age during a period in which psychology drifted away from its physiological roots, a period in which psychology was dominated by learning, behaviourism, personality theory and later by cognition. Psychophysiology in the period between 1960 and 1980 reflected these broader trends in psychology by focusing on such issues as autonomic markers of perceptual states (e.g. orienting, stimulus processing), the interplay between personality factors and ANS responsivity, operant conditioning of autonomic functions, and finally, electrophysiological markers of cognitive states. Research on autonomic specificity in emotion became increasingly rare. Perhaps as a result of these historical trends in psychology, or perhaps because research on emotion and physiology is so difficult to do well, there 18 SOCIAL PSYCHOPHYSIOLOGY AND EMOTION exists only a small body of studies on ANS specificity. Although almost all of these studies report some evidence for the existence of specificity, the prevailing zeitgeist has been that specificity has not been empirically established. At this point in time a review of the existing literature would not be very informative, for it would inevitably dissolve into a critique of methods. Instead, what I hope to accomplish in this chapter is to provide a new framework for thinking about ANS specificity, and to propose guidelines for carrying out research on this issue that will be cognizant of the recent methodological and theoretical advances that have been made both in psychophysiology and in research on emotion. Emotion as organization From the outset, the definition of emotion that underlies this chapter should be made explicit. For me the essential function of emotion is organization. The selection of emotion for preservation across time and species is based on the need for an efficient mechanism than can mobilize and organize disparate response systems to deal with environmental events that pose a threat to survival. In this view the prototypical context for human emotions is those situations in which a multi-system response must be organized quickly, where time is not available for the lengthy processes of deliberation, reformulation, planning and rehearsal; where a fine degree of co-ordination is required among systems as disparate as the muscles of the face and the organs of the viscera; and where adaptive behaviours that normally reside near the bottom of behavioural hierarchies must be instantaneously shifted to the top. Specificity versus undifferentiated arousal In this model of emotion as organization it is assumed that each component system is capable of a number of different responses, and that the emotion will guide the selection of responses from each system. Component systems differ in terms of the number of response possibilities. Thus, in the facial expressive system a selection must be made among a limited set of prototypic emotional expressions (which are but a subset of the enormous number of expressions the face is capable of assuming). A motor behaviour must also be selected from a similarly reduced set of responses consisting of fighting, fleeing, freezing, hiding, etc. All major theories of emotion would accept the proposition that activation of the ANS is one of the changes that occur during emotion. But theories differ as to how many different ANS patterns constitute the set of selection possibilities. At one extreme are those who would argue that there are only two ANS patterns: 'off' and 'on'. The 'on' ANS pattern, according to this view, consists EMOTION AND THE AUTONOMIC NERVOUS SYSTEM 19 of a high-level, global, diffuse ANS activation, mediated primarily by the sympathetic branch of the ANS. The manifestations of this pattern rapid and forcefulcontractions of the heart, rapid and deep breathing, increased systolic blood pressure, sweating, dry mouth, redirection of blood flow to large skeletal muscles, peripheral vasoconstriction, release of large amounts of epinephrine and norepinephrine from the adrenal medulla, and the resultant release of glucose from the liver are well known. Cannon (1927) described this pattern in some detail, arguing that this kind of high-intensity, undifferentiated arousal accompanied all emotions .. Among contemporary theories the notion of undifferentiated arousal is most clearly found in Mandler's theory (Mandler, 1975). However, undifferentiated arousal also played a major role in the extraordinarily influential cognitive/physiological theory of Schachter and Singer (1962). According to this theory, undifferentiated arousal is a necessary precondition for emotionan extremely plastic medium to be moulded by cognitive processes working in concert with the available cues from the social environment. At the other extreme are those who argue that there are a large number of patterns of ANS activation, each associated with a different emotion (or subset of emotions). This is the traditional specificity position. Its classic statement is often attributed to James (1884), although Alexander (1950) provided an even more radical version. The specificity position fuelled a number of experimental studies in the 1950s and 1960s, all attempting to identify some of these autonomic patterns (e.g. Averill, 1969; Ax, 1953; Funkenstein, King and Drolette, 1954; Schachter, 1957; Sternbach, 1962). Despite these studies, all of which reported support for ANS specificity, the undifferentiated arousal theory, especially as formulated by Schachter and Singer (1962) and their followers, has been dominant for a great many years. Is the ANS capable of specific action No matter how appealing the notion of ANS specificity might be in the abstract, there would be little reason to pursue it in the laboratory if the ANS were only capable of producing one pattern of arousal. There is no question that the pattern of high-level sympathetic arousal described earlier is one pattern that the ANS can produce. Cannon's arguments notwithstanding, I believe there now is quite ample evidence that the ANS is capable of a number of different patterns of activation. Whether these patterns are reliably associated with different emotions remains an empirical question, but the potential is surely there. A case in support of this potential for specificity can be based on: (a) the neural structure of the ANS; (b) the stimulation neurochemistry of the ANS; and (c) empirical findings. 20 SOCIAL PSYCHOPHYSIOLOGY AND EMOTION
276 citations
TL;DR: Vagal tone, as measured by the amplitude of respiratory sinus arrhythmia extracted from heart period data, was significantly reduced during the severe stress of circumcision, and these reductions were paralleled by significant increases in the pitch of the infants' cries, emphasizing the potential role of vagal control of the autonomic nervous system during stress.
Abstract: Clinical studies have demonstrated that the cries of chronically stressed, medically compromised infants are characteristically higher and more variable in pitch than those of healthy infants. Other studies have indicated that the vagal tone of chronically stressed infants is significantly reduced in comparison to that of normal infants. A neural model of cry production has been proposed which suggests that decreased vagal tone among infants at risk may, in fact, be related to these increases in cry pitch. Using routine, unanesthetized circumcision as a model of stress, we were able to examine the relation between cry acoustics and vagal tone in normal, healthy newborns undergoing an acutely stressful event. Vocalizations, heart, and respiratory waveforms were continuously recorded from 49 (32 experimental; 17 control) 1-2-day-old, full-term infants during preoperative, surgical, and postoperative periods. Vagal tone, as measured by the amplitude of respiratory sinus arrhythmia extracted from heart period data, was significantly reduced during the severe stress of circumcision, and these reductions were paralleled by significant increases in the pitch of the infants' cries. In addition, individual differences in vagal tone measured prior to circumcision surgery were predictive of physiological and acoustic reactivity to subsequent stress. These results emphasize the potential role of vagal control of the autonomic nervous system during stress.
243 citations
TL;DR: There were important qualitative differences in the effects of CAR and CDM on reactions to handling and the reflex tests in that CDM increased excitability and enhanced responses to several stimuli but CAR either had no effect or decreased these measures.
238 citations
TL;DR: Ablation of capsaicin-sensitive afferent neurons enhances experimentally induced ulceration in the rat gastric mucosa, which suggests that these neurons are involved in Gastric mucosal protection as mentioned in this paper.
229 citations
146 citations
TL;DR: It is concluded that CRF acts within the central nervous system to delay gastric emptying, to inhibit small bowel transit, and to increase large bowel transit in freely moving rats and CRF exerts these biological actions by modulation of the autonomic nervous system and, in part, by opioid pathways.
142 citations
TL;DR: The one outstanding piece of evidence required to confirm that ATP is an excitatory neurotransmitter released from sympathetic nerves in blood vessels is the unequivocal demonstration that it is, in fact, released from the sympathetic nerves when they are stimulated.
TL;DR: The results of this study suggest that activation of the sympathetic nervous system plays a role in CRF-induced suppression of NK cytotoxicity.
Abstract: Corticotropin-releasing factor (CRF) acts within the brain to elicit changes in neuroendocrine, autonomic, and behavioral activity similar to those observed after stress. A reduction of immune function has also been described following central administration of CRF. In this study, we examined whether autonomic nervous system activation plays a role in CRF-induced suppression of natural killer (NK) cytotoxicity. synthetic rat CRF (1.0 microgram) microinjected into the lateral ventricle significantly increased plasma concentrations of norepinephrine and reduced splenic NK cell activity in the rat. Pretreatment of the animals with the ganglionic-blocking agent chlorisondamine completely abolished the CRF-induced increase in plasma norepinephrine levels and reduction in NK activity. However, CRF-induced elevations in plasma levels of adrenocorticotropic hormone and corticosterone were not affected by chlorisondamine. The results of this study suggest that activation of the sympathetic nervous system plays a role in CRF-induced suppression of NK cytotoxicity.
TL;DR: 5HT intraspinal neurons are the probable source of the biochemically detectable 5HT that remains in the spinal cord distal to a spinal transection and it is unknown if they are preganglionic in nature.
TL;DR: The results support the conclusion that the Ce contains several peptides that could be involved in the regulation of cardiovascular and autonomic nervous system function.
TL;DR: It is shown that hyperglycemia can be produced by chemical stimulation of the brain with morphine as well as with a variety of endogenous neuropeptides and can be abolished by bilateral adrenalectomy.
Abstract: Many investigators have begun to speculate that the sympathetic nervous system is involved in the pathophysiology of type II (noninsulin-dependent) diabetes mellitus (1–4). Recalling the early observations of Claude Bernard, who found that hyperglycemia could be produced in normal rabbits by lesioning the area of the hypothalamus, several groups have noted that hyperglycemia can be produced by chemical stimulation of the brain with morphine as well as with a variety of endogenous neuropeptides and can be abolished by bilateral adrenalectomy (1,5). Similarly, hyperglycemia has been shown to result from slow intravenous infusion of epinephrine (6) as well as from certain forms of stress that produce prolonged sympathetic discharge (7).
TL;DR: Results suggest a role for central oxytocin in autonomic efferent activity and show that oxytocIn antagonist microinjected into the dorsal motor nucleus of the vagus nerve blocks gastric and cardiac effects caused by stimulation of the hypothalamic paraventricular nucleus.
TL;DR: Ocular sympathetic function, facial flushing and the presence or absence of lachrymation and rhinorrhoea were examined in 30 patients during spontaneous or nitroglycerin-induced cluster headache as mentioned in this paper.
Abstract: Ocular sympathetic function, facial flushing and the presence or absence of lachrymation and rhinorrhoea were examined in 30 patients during spontaneous or nitroglycerin-induced cluster headache. In 27 cases measurements were also obtained during the headache-free interval. Ocular sympathetic function was impaired on the symptomatic side between cluster attacks and function was reduced further during cluster headache. Greater heat loss from the orbital region on the symptomatic side was associated with ocular sympathetic dysfunction both during and between attacks, and with lachrymation during attacks. Heat loss from the cheek and side of the nose was greater on the symptomatic side in patients whose attack was accompanied by lachrymation, but heat loss from these areas was unrelated to the extent of ocular sympathetic deficit. These findings suggest that parasympathetic overactivity in the greater superficial petrosal nerve provokes facial flushing and lachrymation. Parasympathetic overactivity could also cause dilatation of the internal carotid artery and compression of the periarterial plexus of sympathetic fibres, producing a sympathetic deficit with release of vasoconstrictor tone in the eye. Thus autonomic disturbances in cluster headache may be explained by the unitary hypothesis of parasympathetic hyperactivity being responsible for ocular sympathetic deficit.
TL;DR: It is concluded that, although NPY is associated with sympathetic perivascular neurons, the majority of the pancreatic NPY-containing nerve fibers are likely to belong to the parasympathetic division of the autonomic nervous system.
Abstract: Several lines of evidence have connected neuropeptide Y (NPY), a 36-residue polypeptide, to the sympathetic division of the autonomic nervous system. We studied the localization, the molecular characteristics, and the release of NPY and norepinephrine (NE) in the porcine pancreas. Immunohistochemical investigations revealed that NPY nerves around blood vessels were likely to be of adrenergic nature, whereas NPY-immunoreactive fibers close to exocrine and endocrine cells may originate from local ganglia also containing VIP (vasoactive intestinal peptide) and PHI (peptide histidine isoleucine). Electrical stimulation of the splanchnic nerve supply to the isolated perfused pig pancreas resulted in a corelease of NPY and NE into the venous effluent. Stimulation of the vagal nerves caused a sevenfold larger release of NPY without affecting the NE secretion. Characterization of the NPY immunoreactivity in the pancreatic tissue and in the venous effluent by gel filtration, high-performance liquid chromatography, and isoelectric focusing showed that the immunoreactive NPY was indistinguishable from synthetic porcine NPY. It is concluded that, although NPY is associated with sympathetic perivascular neurons, the majority of the pancreatic NPY-containing nerve fibers are likely to belong to the parasympathetic division of the autonomic nervous system.
TL;DR: This study has demonstrated a significant association betweenretinal vessel calibre and systemic autonomic nerve stimulation and the possible mechanisms for the retinal vessel constriction observed in this study are discussed.
Abstract: The retinal vessel calibre responses to controlled stimulation of the autonomic nervous system were studied in 10 healthy subjects, using sustained isometric muscle contraction as stimulus. Each subject was studied twice using different mydriatic agents, (1) g.tropicamide 1% a parasympatholytic agent and (2) g. phenylephrine 10% a sympathetic agonist. In the tropicamide study, there was a mean arteriolar constriction of 8.1% (SEM 1.67, p 0.05) or between the two mydriatic agents on vessel responses (p>0.05). There was no correlation between the rise in diastolic blood pressure and the degree of retinal vessel constriction, during handgrip contraction in either study. This study has demonstrated a significant association between retinal vessel calibre and systemic autonomic nerve stimulation. The possible mechanisms for the retinal vessel constriction observed in this study are discussed.
TL;DR: The blood pressure response to sustained handgrip was diminished and the pupillary light reflex latency was increased in the HD group, which may indicate involvement of the pretectal or Edinger-Westphal nuclei in HD.
Abstract: • Autonomic nervous system function was studied by means of a series of standardized tests in 11 patients with Huntington's disease (HD) and in 11 ageand sex-matched controls. Two statistically significant differences were found. The blood pressure response to sustained handgrip was diminished and the pupillary light reflex latency was increased in the HD group. The former probably reflects diminished input from higher centers on an otherwise intact sympathetic nervous system. The latter may indicate involvement of the pretectal or Edinger-Westphal nuclei in HD. No further signs of autonomic nervous system dysfunction were found.
TL;DR: It is demonstrated that ventricular repolarization is directly altered by the volatile anesthetics independent of changes in autonomic nervous tone, whether or not such effects are additive with other congenital or acquired forms of QTc, prolongation has yet to be examined.
Abstract: The influence of volatile anesthetics on ventricular repolarization in vivo (QT interval) has not been studied in a systematic fashion. The purpose of this investigation was to characterize the electrocardiographic and hemodynamic actions of the volatile anesthetics halothane, isoflurane, and enflurane in chronically instrumented dogs. Because autonomic nervous system tone may influence ECG findings, experiments were completed with and without concomitant pharmacologic autonomic nervous system blockade. In six groups comprising 50 experiments with 21 instrumented dogs, anesthesia was mask-induced with nitrous oxide, oxygen, and one of the volatile anesthetics and maintained with the volatile anesthetic in 100% oxygen for 2 hours. Changes in the ECG and in hemodynamics were compared to the conscious state. In the absence of autonomic nervous system blockade, halothane and isoflurane significantly prolonged the QT interval (0.24 +/- 0.01 to 0.30 +/- 0.01 second and 0.22 +/- 0.01 to 0.28 +/- 0.01 second, respectively), whereas enflurane produced no change in ventricular repolarization (0.24 +/- 0.01 to 0.26 +/- 0.01 second). All of the volatile anesthetics increased the QT interval corrected for changes in basal heart rate (QTc), and all agents decreased intravascular pressure and dP/dt. Following autonomic nervous system blockade, halothane, isoflurane, and enflurane significantly increased the QT interval and QTc. The results demonstrate that ventricular repolarization is directly altered by the volatile anesthetics independent of changes in autonomic nervous tone. Whether or not such effects are additive with other congenital or acquired forms of QTc prolongation has yet to be examined. The present results indicate that caution should be used during the administration of volatile anesthetics to patients with abnormalities of the QT interval.
TL;DR: Using a subsample of subjects from the Copenhagen schizophrenia high-risk project, results are presented as a preliminary indication of an association between third ventricle enlargement and reduced autonomic nervous system activity.
Abstract: Using a subsample of subjects from the Copenhagen schizophrenia high-risk project, we investigated the relationship between enlargement of the third ventricle and phasic electrodermal activity, as measured by amplitude and frequency of responses to orienting, unconditioned, conditioned, and generalization stimuli Subjects with enlarged third ventricles evidenced significant overall reductions in amplitude and frequency of response, and significantly lower response levels to orienting, conditioned, and generalization stimuli These effects were independent of psychiatric diagnosis and enlargement of the lateral cerebral ventricles Difficulties in interpretation posed by the index of atrophy employed and by the 18-year time interval between the electrodermal and brain measures are discussed The results are presented as a preliminary indication of an association between third ventricle enlargement and reduced autonomic nervous system activity
TL;DR: The functional significance of the relationship between the hypothalamus and the hepatic autonomic nerve in regulation of glucose metabolism in the liver are discussed and stimulation and lesion of this area produced a strong inhibition of vagal nerve activity and facilitation of splanchnic nerve activity.
TL;DR: In this article, the authors investigated autonomic nervous system involvement in cluster headache (CH) and migraine, compared the cardiovascular reflex responses of common migraine and CH subjects to a group of controls.
Abstract: SYNOPSIS
To investigate autonomic nervous system involvement in cluster headache (CH) and migraine, we compared the cardiovascular reflex responses of common migraine and CH subjects to a group of controls. A battery of 5 well-codified autonomic tests was applied: (1) deep breathing test (DB); (2) lying to standing test (LS); (3) Valsalva manoeuvre (VAL); (4) postural hypotension test (PH); (5) blood pressure response to sustained handgrip (SHG). Our data confirm an autonomic dysfunction in CH, mainly affecting the parasympathetic system. Evidence for an impairment of sympathetic cardiovascular reflex regulation was obtained in the common migraine group.
TL;DR: The above findings indicate that hyperalgesia in SART-stressed animals apparently bears little relation to the parasympathetic nervous system, but is associated relatively more with reduced tone in the sympathetic nervous system.
Abstract: 1. The mechanism of hyperalgesia observed in SART (repeated cold)-stressed animals (mice and rats) was studied in relation to the autonomic nervous system. 2. SART stress reduced the nociceptive threshold previously increased in vagotomized mice, but failed to change the threshold previously decreased in sympathectomized mice. 3. The nociceptive threshold previously decreased in SART-stressed mice was elevated by vagotomy, but decreased still more by sympathectomy. 4. Lesion of ventromedial (VMH), anterior (AH) or posterior hypothalamus (PH) prevented decrease in the nociceptive threshold of rats by SART stress, but lesion of the lateral hypothalamus (LH) had no such effect. 5. The nociceptive threshold previously decreased in stressed rats did not change by VMH, AH or PH lesion, but increased by LH lesion. 6. The above findings indicate that hyperalgesia in SART-stressed animals apparently bears little relation to the parasympathetic nervous system, but is associated relatively more with reduced tone in the sympathetic nervous system.
TL;DR: These post-maturation changes occurring throughout adult life reveal a continued dynamism of sympathetic neurons into old age as well as revealing further differences between populations of sympathetic neuron.
Journal Article•
TL;DR: The vasoconstrictor actions of arginine vasopressin (AVP) have been shown to occur in concentrations much lower than previously thought, and it appears likely that it has an important permissive action in the development of sodium-dependent forms of hypertension.
Abstract: The vasoconstrictor actions of arginine vasopressin (AVP) have been shown to occur in concentrations much lower than previously thought. Pressor responses to AVP are a poor index of vasoconstrictor activity since, in contrast to other vasoconstrictor agents, the expected rise of pressure is offset by dose-dependent decreases of cardiac output. The mechanisms for this appear to be, in large part, modulation of the autonomic nervous system whereby AVP enhances vagal nerve activity and reduces peripheral sympathetic nerve activity. AVP enhancement of baroreceptor reflex gain is in part responsible for these changes in some species (dog and rabbit), but not in others (rat). The release of AVP appears to contribute significantly to the normalization of arterial pressure in volume-depleted and hypotensive states. The link between plasma AVP and hypertension remains unclear, but it appears likely that it has an important permissive action in the development of sodium-dependent forms of hypertension.
TL;DR: Although specific diagnostic testing can be useful in defining abnormalities in each of these systems, treatment of sexual dysfunction in the setting of hypertension in the elderly patient remains a challenge.
Abstract: The incidence of sexual dysfunction increases with age and in the presence of systemic hypertension. An interplay between endocrine, neurologic and vascular systems mediates normal male sexual function. Androgens primarily regulate libido and maintenance of genital tissue, while the autonomic nervous system and arterial blood flow play key roles in the physiology of the male sexual response, particularly penile erection. Vascular disease related to hypertension, diabetes mellitus and atherosclerosis may be the main factor contributing to the sexual dysfunction that occurs with aging. Hormonal alterations probably play less of a role. The importance of neurologic abnormalities remains to be determined. Although specific diagnostic testing can be useful in defining abnormalities in each of these systems, treatment of sexual dysfunction in the setting of hypertension in the elderly patient remains a challenge.