The effects of hypothalamic lesions on Na+ and K+ content ([Na+](i) and [K+](i)) in both slow tonic muscle [soleus (SOL)] and fast-twitch muscle [extensor digitorum longus (EDL)] were investigated in deoxycorticosterone acetate (DOCA)-salt hypertensive rats. In DOCA-treated rats, [Na+](i) was increased and [K+](i) decreased in both SOL and EDL muscles compared with controls. Cellular K+ loss and Na+ accumulation in SOL were restored after tibial nerve sectioning (Δ[Na+](i), -14.2 ± 2.6 and Δ[K+](i), 13.9 ± 2.6 mmol/l fiber water (FW), n = 18, P < 0.01) or bilateral lesioning of the ventromedial hypothalamic nucleus (VMH) (Δ[Na+](i), - 15.5 ±1.5 and Δ[K+](i), 17.4 ± 4.6 mmol/l FW, n = 6, P < 0.01 and P < 0.05). On the other hand, the anomalous electrolyte content in EDL was counteracted by lesions of anteroventral portion of the third ventricle (AV3V) (Δ[Na+](i), - 8.8 ± 1.6 and Δ[K+](i), 5.2 ± 1.2 mmol/l FW, n = 6, P < 0.01 and P < 0.05) or paraventricular hypothalamic nucleus (PVN) (Δ[Na+](i), - 6.8 ± 0.6 and 5.7 ± 1.2 mmol/l FW, n = 6, P < 0.01 and P < 0.05), but aggravated by denervation (Δ[Na+](i), 13.4 ± 1.8 and Δ[K+](i), - 9.6 ± 1.8 mmol/l Fw, n = 18, P < 0.01). These results suggest that there are at least two hypothalamic mechanisms of suppression of muscle Na-K pump activity in DOCA-hypertensive rats; i.e., neurally mediated inhibition in SOL by the VMH and, presumably, humorally mediated inhibition originating from the AV3V or PVN with greater influence in EDL.
|ジャーナル||American Journal of Physiology - Regulatory Integrative and Comparative Physiology|
|出版ステータス||出版済み - 12 1 1987|
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