Interactions of sympathetic nerves with capsaicin-sensitive sensory nerves: neurogenic mechanisms for phenol-induced hypertension in the rat.

Abstract

BACKGROUND: Previous investigations have shown that norepinephrine is capable of inhibiting neurotransmission in capsaicin-sensitive sensory nerves via a prejunctional mechanism. The alteration in the activity of sympathetic or capsaicin-sensitive sensory nerves in the development of phenol-induced hypertension was observed separately in rats. METHODS: In the present study, we examined interactions of adrenergic nerves with capsaicin-sensitive sensory nerves in phenol-induced hypertensive rats. Blood pressure, the synthesis and release of calcitonin gene-related peptide (CGRP) and the content of nerve growth factor in (NGF) arteries were determined. RESULTS: Intrarenal injection of phenol caused a permanent elevation of blood pressure concomitantly with a decrease in the concentration of CGRP in plasma, the content of CGRP in dorsal root ganglia and the density of CGRP-containing nerves in the mesenteric artery, and vascular NGF content. Chronic treatment with prazosin (an alpha1-adrenoreceptor antagonist, 3 mg/kg per day) failed to alter the synthesis and release of CGRP and vascular NGF content, even though it completely normalized blood pressure. However, treatment with yohimbine (an alpha2-adrenoreceptor antagonist, 5 mg/kg per day) significantly increased CGRP level and vascular NGF content. Combined administration of prazosin and yohimbine not only significantly elevated the synthesis and release of CGRP and arterial NGF content, but also completely normalized blood pressure. CONCLUSION: These results indicate that the decreased production and release of CGRP and reduced vascular NGF content are attributed to the activation of alpha2-adrenoreceptors in phenol-induced hypertensive rats.