Antibodies (Ab) recognizing G-protein coupled receptors, such as β 1 and β 2 adrenergic (anti-β 1-AR and anti-β 2-AR, respectively) and muscarinic cholinergic receptors (anti-M2-CR) may contribute to cardiac damage, however their role in chronic chagasic cardiomyopathy is still controversial. We describe that Trypanosoma cruzi-infected C3H/He mice show increased P and QRS wave duration, and PR and QTc intervals, while the most significant ECG alterations in C57BL/6 are prolonged P wave and PR interval. Echocardiogram analyses show right ventricle dilation in infected animals of both mouse lineages. Analyses of heart rate variability (HRV) in chronically infected C3H/He mice show no alteration of the evaluated parameters, while C57BL/6 infected mice display significantly lower values of HRV components, suggesting autonomic dysfunction. The time-course analysis of anti-β 1-AR, anti-β 2-AR and anti-M2-CR Ab titres in C3H/He infected mice indicate that anti-β 1-AR Ab are detected only in the chronic phase, while anti-β 2-AR and anti-M2-CR are observed in the acute phase, diminish at 60 dpi and increase again in the chronic phase. Chronically infected C57BL/6 mice presented a significant increase in only anti-M2-CR Ab titres. Furthermore, anti-β 1-AR, anti-β 2-AR and anti-M2-CR, exhibit significantly higher prevalence in chronically T. cruzi-infected C3H/He mice when compared with C57BL/6. These observations suggest that T. cruzi infection leads to host-specific cardiac electric alterations.

In pregnancies complicated by placental insufficiency (PI), fetal hypoglycemia and hypoxemia progressively worsen during the third trimester, which increases circulating norepinephrine (NE). Pharmacological adrenergic blockade (ADR-block) at 0.9 gestation revealed that NE inhibits insulin secretion and enhanced β-cell responsiveness in fetuses with PI-induced intrauterine growth restriction (IUGR). NE concentrations in PI fetuses at 0.7 gestation were threefold greater compared with age-matched controls, but the levels were similar to near-term controls. Therefore, our objective was to determine whether elevations in plasma NE concentrations inhibit insulin secretion and produce compensatory β-cell responsiveness in PI fetuses at 0.7 gestation. Fetal insulin was measured under basal, glucose-stimulated insulin secretion (GSIS) and glucose-potentiated arginine-stimulated insulin secretion (GPAIS) conditions in the absence and presence of an ADR-block. Placental weights were 38% lower (P < 0.05) in PI fetus than in controls, but fetal weights were not different. PI fetuses had lower (P < 0.05) basal blood oxygen content, plasma glucose, insulin-like growth factor-1 and insulin concentrations and greater plasma NE concentrations (891 ± 211 v. 292 ± 65 pg/ml; P < 0.05) than controls. GSIS was lower in PI fetuses than in controls (0.34 ± 0.03 v. 1.08 ± 0.06 ng/ml; P < 0.05). ADR-block increased GSIS in PI fetuses (1.19 ± 0.11 ng/ml; P < 0.05) but decreased GSIS in controls (0.86 ± 0.02 ng/ml; P < 0.05). Similarly, GPAIS was 44% lower (P < 0.05) in PI fetuses than in controls, and ADR-block increased (P < 0.05) GPAIS in PI fetuses but not in controls. Insulin content per islet was not different between treatments. We conclude that elevations in fetal plasma NE suppress insulin concentrations, and that compensatory β-cell stimulus-secretion responsiveness is present before IUGR.

Alpha (α)- and beta (β)-adrenergic receptors in the bovine mammary gland are mainly present in the teat muscles and in the region where large milk ducts reach the cisternal cavities. The aim of the study was to test the hypothesis that the region of the large mammary ducts is the most important location of α- and β-adrenergic receptor stimulation affecting milk ejection and milk removal. Effects of α- and β-adrenergic receptor stimulation and of oxytocin (OT) receptor blockade on milking characteristics were tested in six cows. Milk flow was measured before and after the distal part of one teat, including the teat canal and teat sphincter, had been partly amputated. Before the operation, milk yield and peak flow rate decreased during α-adrenergic receptor stimulation and during the OT receptor blockade, and increased during β-adrenergic stimulation. After removal of the teat tip, relations of milk yield and peak flow rates after administration of α- and β-agonists and after application of an OT receptor blocking agent were similar to those before operation. Only total milk yield had decreased in the teat-amputated quarter owing to unhindered flow of cisternal milk before cluster attachment. Since responses to α- and β-adrenergic receptor stimulation as well as to OT receptor blockade do not differ with or without the teat sphincter, it is concluded that milk flow is mainly influenced by the muscle tone of the large mammary ducts.

Milk ejection and milk removal is considerably influenced by the sympathetic nervous system. Stimulation of α-adrenergic receptors by administration of α-adrenergic agonists inhibits alveolar milk ejection and milk removal in dairy cows due to smooth muscle contraction (Blum et al. 1989; Bruckmaier et al. 1991). However, contraction of the teat in response to α-adrenergic receptor stimulation has no influence on milk flow as long as milk is available in the cistern (Bruckmaier et al. 1997). Therefore, α-adrenergic stimulation causes inhibition of transport of alveolar milk into the cistern. On the contrary, the stimulation of β-adrenergic receptors facilitates milk ejection and milk removal in dairy cows (Bernabé & Peeters, 1980; Bruckmaier et al. 1991) because of muscle relaxation. Therefore, the distribution of α- and β-adrenergic receptors plays an important role in the milkability of dairy cows. However, from these in vivo studies it is not possible to distinguish between the different α1- and α2- and β2-receptor subtypes owing to the non-specific nature of the pharmacological agents used.

To date, the precise tissue distribution of these different subtypes, in bovine mammary tissue, is unknown. Using molecular techniques, we were interested in the expression of genes that encode α1c and β2 as a preliminary study towards the understanding of noradrenergic receptor-gene expression and regulation in this important system.

In addition, α1c- and β2-adrenergic receptors were determined in front and rear quarters of the mammary gland to investigate differences in receptor distribution within the udder and possible relations between adrenergic receptor distribution and the higher milk flow rates in rear than in front quarters (Rothenanger et al. 1995).