Pheromone reception in mammals.

Pheromonal communication is the most convenient way to transfer information regarding gender and social status in animals of the same species with the holistic goal of sustaining reproduction. This type of information exchange is based on pheromones, molecules often chemically unrelated, that are contained in body fluids like urine, sweat, specialized exocrine glands, and mucous secretions of genitals. So profound is the relevance of pheromones over the evolutionary process that a specific peripheral organ devoted to their recognition, namely the vomeronasal organ of Jacobson, and a related central pathway arose in most vertebrate species. Although the vomeronasal system is well developed in reptiles and amphibians, most mammals strongly rely on pheromonal communication. Humans use pheromones too; evidence on the existence of a specialized organ for their detection, however, is very elusive indeed. In the present review, we will focus our attention on the behavioral, physiological, and molecular aspects of pheromone detection in mammals. We will discuss the responses to pheromonal stimulation in different animal species, emphasizing the complicacy of this type of communication. In the light of the most recent results, we will also discuss the complex organization of the transduction molecules that underlie pheromone detection and signal transmission from vomeronasal neurons to the higher centers of the brain. Communication is a primary feature of living organisms, allowing the coordination of different behavioral paradigms among individuals. Communication has evolved through a variety of different strategies, and each species refined its own preferred communication medium. From a phylogenetic point of view, the most widespread and ancient way of communication is through chemical signals named pheromones: it occurs in all taxa, from prokaryotes to eukaryotes. The release of specific pheromones into the environment is a sensitive and definite way to send messages to other members of the same species. Therefore, the action of an organism can alter the behavior of another organism, thereby increasing the fitness of either or both. Albeit slow in transmission and not easily modulated, pheromones can travel around objects in the dark and over long distances. In addition, they are emitted when necessary and their biosynthesis is usually economic. In essence, they represent the most efficient tool to refine the pattern of social behaviors and reproductive strategies.

How mammals detect pheromones.

One of the most intriguing discoveries in mammalian pheromone research is the report that a short exposure of women to volatile compounds from sweat can significantly alter their menstrual cycle. This work suggests that specific molecules are produced by women at different stages of the menstrual cycle and that this putative 'pheromonal' blend has effects on the timing of the cycle in women that were briefly exposed to it. What human pheromones are and how they work are not known, however a considerable progress has been made in understanding how other mammals are likely to detect pheromones with the discovery of pheromone receptors. Even though it is proved that pheromones affect human responses, it remains unlikely that similar receptors account for these effects.

Brain magnetic resonance imaging and manganese exposure.

Due to its paramagnetic properties, manganese (Mn) can be effectively visualized by MRI. Mn accumulates selectively in the globus pallidus of basal ganglia, where it can produce high signals at brain magnetic resonance. These hyperintensities are bilateral, symmetrical, and visible in T1-weighted magnetic resonance imaging of different manganese overload conditions. A review of the literature shows identical findings in manganese exposed workers, hepatopatic patients, and patients undergoing total parenteral nutrition with excessive amount of manganese. Two indicators of exposure and hyperintensity were considered, represented respectively by the concentration of Mn in total blood (MnB), and the pallidal index (PI). These two indicators show a positive association, which indicates a possible continuum from normality to clinical stages both in workers occupationally exposed to Mn and in patients suffering from chronic liver disease. Since both MnB and PI show a high degree of variability, further research should be focused on the identification of more accurate indicators.

Relationship between initial cardiovascular structural changes and daytime and nighttime blood pressure monitoring.

It has been shown that in hypertensive patients the degree of target organ damage correlates more closely with average blood pressure as recorded by ambulatory monitoring (ABPM) throughout 24 h than with clinic blood pressure. We examined a group of 91 clinically healthy subjects, 23 normotensives and 68 hypertensives according to clinic blood pressure. Cardiac anatomy was investigated by echocardiography. As an index of arterial structural changes forearm minimal vascular resistance was calculated from mean arterial pressure and maximal postischemic blood flow, as assessed by venous occlusion plethysmography. The results were correlated to clinic blood pressure or ABPM values (measured by noninvasive ABPM ICR 5200, Spacelabs, Bellevue, CA). Left ventricular mass was correlated more closely with the average blood pressure recorded during 24 h, or during daytime or nighttime periods, than with clinic blood pressure. Minimal vascular resistance was also significantly correlated to ABPM values, but the correlation was similar to that observed with clinic blood pressure. Minimal vascular resistance was significantly correlated to blood pressure variability, as evaluated by the standard deviation of the mean. Minimal vascular resistance and left ventricular mass were higher in a subgroup of patients in whom blood pressure was not significantly reduced during the night. The results of this study confirm that elevated average ABPM values are associated to higher left ventricular mass; in addition, they suggest that increased blood pressure variability may be associated with vascular structural changes, as evaluated by minimal vascular resistance. It remains to be clarified whether cardiac hypertrophy and/or vascular structural changes are a cause or consequence of increased blood pressure values and variability.

ACTH and beta-endorphin responses to physical exercise in adolescent women tested for anxiety and frustration.

Thirty healthy adolescent women (age: 14 years), high school students without clinical signs of psychiatric or major affective disorders, received psychological and endocrinological examinations. Two psychological tests were used: the Anxiety Score Test for Adolescents and the Pictures Frustration Test for Adolescents of Rosenzweig. On the basis of the results of these tests, subjects were divided into two groups: A (n = 21), normal subjects; B (n = 9), subjects with evidence of anxiety (n = 1), frustration (n = 1), or both (n = 7). Plasma levels of adrenocorticotropic hormone (ACTH) and beta-endorphin were measured under basal conditions and after physical exercise (Step Test) in all subjects. Hormonal responses in groups A and B were compared. Basal concentrations of ACTH and cortisol were similar in the two groups, whereas basal beta-endorphin levels were significantly higher in group B than in group A. Exercise induced a slight but significant increase in plasma concentrations of both ACTH (32% increase) and beta-endorphin (60% increase) in group A. A striking increase in plasma ACTH (100% increment) and a slight increase of beta-endorphin (60% increment) levels were observed in group B after exercise. Absolute levels of ACTH and beta-endorphin after physical exercise were significantly higher in group B than in group A. These findings indicate increased levels of adrenocorticotropic and opioid activity in adolescent women with high scores on psychological measures of anxiety and frustration.

Antidiuretic hormone and atrial natriuretic peptide during lower body negative or positive pressure in hypertensive patients with and without left ventricular hypertrophy.

Aim of the study was to evaluate the effect of cardiopulmonary receptors activation and deactivation on antidiuretic hormone (ADH) and atrial natriuretic peptide (ANP) incretion in hypertensive and normotensive subjects. Twenty-one male subjects, 7 normotensives and 14 mild hypertensives, 7 without and 7 with left ventricular hypertrophy (LVH) were admitted to the study. Each subject underwent selective loading and unloading of cardiopulmonary receptors, by application of a positive (LBPP) or negative (LBNP) pressure to the lower body. Blood samples were taken for measurement of ANP, ADH, PRA, immunoreactive renin, aldosterone, noradrenaline and adrenaline. ADH plasma concentration increased during cardiopulmonary receptors inhibition, but this increase became statistically significant (p less than 0.05) at a step of LBNP (-40 mm Hg), in which an involvement of the sinoaortic receptors cannot be excluded. ANP plasma levels increased progressively during LBPP (p less than 0.05 at least). These changes were significantly reduced in hypertensive patients with LVH.

[Increase by ANP and ADH of the duration of activation and deactivation of the cardiopulmonary baroreceptor reflex: modification in the presence of left ventricular hypertrophy]. / Increzione di ANP e ADH durante attivazione e deattivazione dei barocettori cardiopolmonari: modificazioni in presenza di pertrofia ventricolare sinistra.

The involvement of cardiopulmonary and arterial sinoaortic receptors in the control of antidiuretic hormone (ADH) and atrial natriuretic peptide (ANP) release is still controversial in humans. Moreover, it is not clear if this control may be impaired in hypertensive patients with left ventricular hypertrophy (LVH). We studied 17 male subjects, age 18-58 (6 normotensives and 9 mild hypertensives, 5 without and 4 with LVH). Each subject underwent selective loading and unloading of cardiopulmonary receptors, in a randomized sequence, by application of a positive (LBPP) or negative (LENP) pressure to the lower body (steps: +10, +20, +40, -10, -40 mmHg, each for about 30 min), through a plexyglass-constructed tubular apparatus with a rubber adhesion round the patients' waist. Blood samples were taken at the end of every step for measurement of ADH, ANP, PRA, immunoreactive renin, aldosterone, noradrenaline and adrenaline. Cuff arterial pressure was measured every 5 min, while heart rate was evaluated by continuous ECG recording. Hypertensive subjects underwent right atrial pressure measurement by an iv catheter and forearm blood flow evaluation at rest and during the different steps (venous occlusion plethysmography). During LBNP, ADH plasma levels increased progressively, but the increase became statistically significant only at the step of -40 mmHg. ANP increased significantly during LBPP. Taking into account only hypertensive patients, a consistent reduction in the changes of ADH and ANP plasma levels, respectively during LBNP and LBPP in patients with LVH in respect to those without LVH was found.(ABSTRACT TRUNCATED AT 250 WORDS)

Relation between cardiac hypertrophy and forearm vascular structural changes before and during long-term antihypertensive treatment.

In patients with hypertension, structural changes develop in the heart and in the systemic arteries that have a significant role in the maintenance and gradual worsening of the hypertensive disease. Blood pressure, basal and post-ischemic "maximal" forearm blood flow (strain-gauge venous occlusive plethysmography), and echocardiographic left ventricular mass index were measured in 28 hypertensive patients (WHO class I or II, 23 men and five women, aged 26 to 59 years). Minimal vascular resistance (mean arterial pressure/peak blood flow) was taken as an index of vascular structural changes. The same measurements were made in a group of 14 patients before and after long-term antihypertensive treatment: in eight patients after six and 12 months of treatment with captopril (50 mg twice a day, plus 25 mg of hydrochlorothiazide per day if necessary) and in six patients after six months of treatment with nitrendipine (20 mg per day, plus 50 mg of atenolol per day if necessary). A significant but weak direct correlation was found between the degree of left ventricular hypertrophy and mean arterial pressure (r = 0.41) or minimal vascular resistance (r = 0.31). Thus, patients were categorized according to whether they had left ventricular hypertrophy or impaired blood flow; the results suggested that left ventricular hypertrophy may be detected earlier than increased minimal vascular resistance. After six months of treatment, both captopril and nitrendipine significantly reduced left ventricular mass index and minimal vascular resistance. Left ventricular mass index was normalized in 50 percent of the patients, whereas minimal vascular resistance was normalized in one patient only. After 12 months of treatment, left ventricular mass index was normalized in all patients; minimal vascular resistance was on the average further reduced but normalized in only one additional patient. Thus, regression of cardiovascular structure also seems to occur earlier in the heart.