Hypothalamus and sodium-potassium pump activity in skeletal muscles of DOCA-hypertensive rats

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 (delta [Na+]i, -14.2 +/- 2.6 and delta [K+]i, 13.9 +/- 2.6 mmol/l fiber water (FW), n = 18, P less than 0.01) or bilateral lesioning of the ventromedial hypothalamic nucleus (VMH) (delta [Na+]i, -15.5 +/- 1.5 and delta [K+]i, 17.4 +/- 4.6 mmol/l FW, n = 6, P less than 0.01 and P less than 0.05). On the other hand, the anomalous electrolyte content in EDL was counteracted by lesions of anteroventral portion of the third ventricle (AV3V) (delta [Na+]i, -8.8 +/- 1.6 and delta [K+]i, 5.2 +/- 1.2 mmol/l FW, n = 6, P less than 0.01 and P less than 0.05) or paraventricular hypothalamic nucleus (PVN) (delta [Na+]i, -6.8 +/- 0.6 and 5.7 +/- 1.2 mmol/l FW, n = 6, P less than 0.01 and P less than 0.05), but aggravated by denervation (delta [Na+]i, 13.4 +/- 1.8 and delta [K+]i, -9.6 +/- 1.8 mmol/l FW, n = 18, P less than 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.