Antispasmodic effect of Mentha piperita essential oil on tracheal smooth muscle of rats.

AIM OF THE STUDY: Mentha piperita is a plant popularly known in Brazil as "hortelã-pimenta" whose essential oil is used in folk medicine for its anti-inflammatory, antispasmodic, expectorant actions and anti-congestive. Here, it was investigated the effect of Mentha piperita essential oil (peppermint oil) in rat tracheal rings along with its mechanism of action. MATERIALS AND METHODS: Tracheal tissue from male Wistar rats (250-300 g) were used. Peppermint oil was added in cumulative concentrations [1-300 microg/ml] to the tissue basal tonus or pre-contracted by carbachol [10 microM] at 10 min intervals, incubated or not with indomethacin [10 microM], L-N-metyl-nitro-arginine [100 microM], hexamethonium [500 microM], or tetraethylammonium [5 mM]. RESULTS: Peppermint oil [100 and 300 microg/ml] inhibited the contractions induced by carbachol, which was reversed by indomethacin, L-N-metyl-nitro-arginine and hexamethonium, but not by tetraethylammonium. These data suggest the participation of prostaglandin E(2), nitric oxide and autonomic ganglions in the peppermint oil relaxant effect and may be correlated with its popular use in respiratory diseases. CONCLUSIONS: Peppermint oil exhibited antispasmodic activity on rat trachea involving prostaglandins and nitric oxide synthase.

Administration of noradrenaline in the autonomic ganglia modifies the testosterone release from the testis using an ex vivo system.

The male gonad receives nerve fibres from the autonomic ganglionic system. These fibres converge on the testis along two pathways, the superior and the inferior spermatic nerves. The superior spermatic nerve runs from the superior mesenteric ganglion alongside the testicular artery, whereas the inferior spermatic nerve originates in inferior mesenteric ganglion, accompanies the vas deferens and penetrates the inferior pole of the testis. The aim of this work was to evaluate androgen release after the addition of noradrenaline or adrenoreceptor antagonists (propranolol or phentolamine) to the ganglionic compartment. An ex vivo system used in a previous work was incubated in two separate containers, one for the testis and the other for the ganglion. Both organs remain interconnected (as in vivo) by the respective spermatic nerve. When noradrenaline was added to the inferior mesenteric ganglion, testosterone release in the gonad container underwent a progressive and significant increment. Propranolol diminishes and phentolamine increases the androgen release. When using the superior mesenteric ganglion, no changes were observed. These results indicate that the ganglionic stimulation of the autonomic system clearly participates in testosterone release from the testis. This effect depends on the ganglion involved. These results make it evident that not only the classical and well-known hypothalamus-hypophysial axis, but also the peripheral nervous system, via the autonomic ganglia, are directly involved in the endocrine control of the testis.

Effects of ACE inhibition and beta-blockade on plasminogen activator inhibitor-1 and transforming growth factor-beta1 in carotid glomus and autonomic ganglia in hypertensive rats.

BACKGROUND: Previous studies have demonstrated a high correlation between arterial hypertension and the development of lesions in the carotid glomus (CG) and autonomic ganglia (AG), characterized by extracellular matrix (ECM) expansion and reduction in the number of AG neurons. Because lowering blood pressure (BP) is the first step in controlling the deleterious effects of arterial hypertension, the objective was to evaluate possible differences between the beta-blocker atenolol (AT) and the angiotensin-converting enzyme (ACE) inhibitor ramipril (RAM) regarding a protective role on CG and AG, as target organs in the spontaneously hypertensive rat (SHR). METHODS: Male 12-week-old SHR and Wistar-Kyoto rats (WKY) were divided into SHR; SHR-RAM, 1 mg/kg/d; SHR-AT, 100 mg/kg/d; and WKY rats. After 6 months, the animals were sacrificed and CG and AG were processed by hematoxylin and eosin (H&E) and Masson's trichrome and immunohistochemistry (transforming growth factor-beta(1) and plasminogen activator inhibitor-1). RESULTS: At the end of the experiment, SHR-AT and SHR-RAM showed a similar control in BP compared with SHR. However, SHR-RAM presented a significant reduction in ECM expansion in CG, AG, and autonomic nerves. Moreover, the number of neurons in AG was preserved with AT and even more with RAM, when compared with SHR group. Transforming growth factor-beta(1) and plasminogen activator inhibitor-1 were increased in CG and AG in SHR and in SHR-AT, whereas SHR-RAM showed a similar expression to the WKY group. CONCLUSIONS: According to these results, RAM but not AT provided a significant protective role against structural changes in CG as well as in AG caused by arterial hypertension in SHR. This effect seems to be independent of BP reduction.