Presynaptic ?2-adrenoceptor-mediated modulation of norepinephrine release from vascular adrenergic neurons in reduced renal mass salt hypertensive rats
Autor: | Keizo Kimura, Kazushi Tsuda, Hiroki Shima, Yoshiaki Masuyama, Ichiro Nishio |
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Rok vydání: | 1992 |
Předmět: |
medicine.medical_specialty
Hypertension Renal Sympathetic Nervous System Epinephrine Physiology Blood Pressure Sodium Chloride Adrenergic Neurons Pathogenesis Norepinephrine (medication) Norepinephrine Physiology (medical) Internal medicine Renal mass Animals Medicine Nerve Endings Neurons Pharmacology business.industry Antagonist Yohimbine Rats Inbred Strains Receptors Adrenergic alpha Pathophysiology Mesenteric Arteries Rats medicine.anatomical_structure Endocrinology Synapses business medicine.drug Blood vessel |
Zdroj: | Clinical and Experimental Pharmacology and Physiology. 19:531-535 |
ISSN: | 1440-1681 0305-1870 |
Popis: | SUMMARY The present study was designed to investigate the presynaptic α2-adrenoceptor function to inhibit norepinephrine (NE) release in blood vessels of reduced renal mass salt hypertensive rats (Na-loaded HT). Isolated perfused mesenteric vasculatures were prepared from Na-loaded HT and normotensive control rats (NT-control), and the NE release and vascular responsiveness were examined. Periarterial nerve stimulation caused a significantly greater release of NE and pressor responses in Na-loaded HT than in NT-control. Yohimbine, a potent α-adrenoceptor antagonist, demonstrated the facilitatory effects on NE release during nerve stimulation. The effects were significantly attenuated in Na-loaded HT compared with NT-control. These results demonstrate that vascular sympathetic nervous activity might be enhanced in Na-loaded HT. Furthermore, the increased NE release from vascular adrenergic neurons in Na-loaded HT could partially depend on impaired presynaptic α2-adrenoceptor-mediated modulation, which might contribute to the pathogenesis and maintenance of this form of salt-dependent hypertension. |
Databáze: | OpenAIRE |
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