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ALTERED BASAL RELEASE AND DEPRESSOR EFFECT OF L‐DOPA IN THE NUCLEUS TRACTUS SOLITARII OF SPONTANEOUSLY HYPERTENSIVE RATS
Author(s) -
Misu Yoshimi,
Yue JinLiang,
Okumura Yoko,
Miyamae Takeaki,
Ueda Hiroshi
Publication year - 1995
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1995.tb02946.x
Subject(s) - endocrinology , medicine , tetrodotoxin , solitary nucleus , baroreceptor , tonic (physiology) , chemistry , glutamate receptor , neurotransmitter , microdialysis , spontaneously hypertensive rat , dopamine , central nervous system , heart rate , receptor , blood pressure
Summary 1. L‐DOPA as a probable neurotransmitter of baroreceptor afferents functions as a tonic to mediate cardiodepressor control in the nucleus tractus solitarii (NTS). We attempted to clarify further whether a transmitter‐like L‐DOPA system is altered in NTS of adult spontaneously hypertensive rats (SHR). 2. By microdialysis of left NTS area, the basal L‐DOPA release was lower in SHR than in Wistar‐Kyoto (WKY) rats. This release was partially inhibited by tetrodotoxin (TTX, 1 μmol/L) to a similar degree in both strains. TTX‐sensitive L‐DOPA release was lower in SHR than in WKY. 3. L‐DOPA (10–300 ng) and L‐glutamate (3–100 ng) micro‐injected into left NTS produced dose‐dependent hypotension and bradycardia. No difference of responses to L‐glutamate was seen in either strain. However, depressor but not bradycardic responses to L‐DOPA at higher doses were slightly greater in SHR than in WKY. 4. In caudal dorsomedial medulla including NTS, tyrosine hydroxylase activity was increased in SHR compared to WKY, while there was no difference in either strain of L‐aromatic amino acid decarboxylase activity. 5. Impaired tonic neuronal activity to release L‐DOPA in NTS may be involved in the maintenance of hypertension in SHR. An increase in sensitivity of a recognition site for L‐DOPA seems to occur as a compensatory mechanism for impairment of the neuronal activity.