Gonadal steroid hormones influence vascular tone and the development of hypertension. There are sex differences in the incidence of cardiovascular diseases, and great attention has been placed on the study of estrogen cardiovascular effects. However, there are only a few reports on the effects of testosterone on the vasculature. It is commonly accepted that the mechanism of the action of steroid hormones on target tissues is mediated through the binding of hormones to cytoplasmic or nuclear receptors. However, some studies indicate that steroid action can be extremely rapid and therefore unlikely to be through a genomic mechanism. The purpose of this study was to assess the effect of intravascularly confined testosterone on an isolated rat heart to demonstrate acute and possibly nongenomic effects of the steroid. Our results show that testosterone blocked the adenosine vasodilator effect and increased vascular resistance, even when its presence was restricted to the coronary vascular lumen. These effects were exerted rapidly and possibly through nongenomic mechanisms.

No abstract

Transmitter release at the nerve terminal is mediated by the influx of Ca2+ through voltage‐sensitive calcium channels (VSCCs). Many types of VSCCs have been found in neurons (T, N, L, and P), but uncertainty remains about which ones are involved in neuronal excitation‐secretion coupling. Specific ligands for the L‐ and N‐type VSCCs were used to determine which of these subtypes might be involved in the K+‐evoked [3H]noradrenaline release from superfused rat brain cortical and hippocampal synaptosomes. In cortical presynaptic terminals the 1,4‐dihydropyridine agonist Bay K 8644 enhanced the K+ (15 mM)‐evoked [3H]noradrenaline release. This effect was reversed by the 1,4‐dihydropyridine antagonists nimodipine and nitrendipine. The L‐type VSCC ligands had no effect on hippocampal synaptosomes. In contrast, the N‐type VSCC blocker ω‐conotoxin markedly reduced the K+‐evoked [3H]noradrenaline release in nerve terminals from both regions. Inhibition was greater in hippocampal synaptosomes. When applied together the inhibitory actions of nimodipine and ω‐conotoxin were approximately additive. These findings indicate that both L‐ and N‐type VSCCs participate in noradrenaline release in rat brain cortex and suggest that noradrenergic terminals in the two regions examined may have distinct populations of VSCCs: L type in cortex and N type in hippocampus.

The effectiveness of various antibiotics was tested in the eradication of a strain of methicillin-susceptible Staphylococcus aureus (MSSA) of cardiac vegetations, in an experimental model of endocarditis in rabbits. Twelve animals comprised the control group and 48 the treated ones. After inducing the experimental endocarditis, the animals were treated for three days; then mortality, blood cultures at 48 and 72 hours and the title of the colony forming units per gram of vegetation (CFU/g) were evaluated. Imipenem and the cloxacillin-gentamicin association were found to be as effective as cloxacillin in eradicating the microorganisms of the vegetation. Clindamycin in high doses was shown to be a valid alternative. Vancomycin, teicoplanin, rifampin and ciprofloxacin were less effective than cloxacillin. The experimental model seems to be an effective method for evaluating antimicrobial treatments in staphylococcal endocarditis.

Working with specific m‐learning apps is useful for learning/teaching purposes. However, its development requires advanced knowledge in programming mobile devices. We present a case study that evaluates the usefulness of App Inventor as a visual, blocks platform that allows teachers, without any advanced programming knowledge, to develop customized m‐learning apps.