Key result
Ouabain and partially purified plasma from salt-induced hypertensive rats increased stimulation-evoked pressor responses and norepinephrine overflow, with effects more prominent in hypertensive rats.
Na+,K+-ATPase on vascular adrenergic neurons plays an important role in regulating neurotransmitter release, and its enhanced activity may contribute to the pathophysiology of hypertension.
No immediate clinical implications; leaves open whether Na+,K+-ATPase modulation could treat human hypertension.
The purpose of the present study was to examine the role of Na+,K+-ATPase activity in vascular adrenergic transmission of hypertension. In isolated perfused mesenteric vasculatures of spontaneously hypertensive rats (SHR, Okamoto and Aoki strain, seven- to ten-weeks-old) and age-matched Wistar Kyoto rats (WKY), the effects of ouabain, a potent Na+,K+-ATPase inhibitor, or partially purified plasma obtained from salt-induced hypertension on pressor responses and norepinephrine overflow were investigated. Pressor responses and norepinephrine overflow during electrical nerve stimulation were significantly greater in SHR than in WKY. Ouabain increased the stimulation-evoked pressor responses and norepinephrine overflow. This facilitation was more prominent in SHR than in WKY. Partially purified plasma obtained from reduced renal mass-salt hypertensive rats, which had a crossimmunoreactivity with digoxin, also increased the pressor responses and norepinephrine overflow during electrical nerve stimulation, and the effects were greater in SHR than in WKY. These results suggest that Na+,K+-ATPase on vascular adrenergic neurons has an important role in the regulation of neurotransmitter release, and that its activity might be enhanced in SHR.
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Tsuda et al. (1989) studied Hypertension. Ouabain or partially purified plasma from salt-induced hypertension vs. Wistar Kyoto rats (normotensive controls) was evaluated on Pressor responses and norepinephrine overflow during electrical nerve stimulation. Ouabain and partially purified plasma from salt-induced hypertensive rats increased stimulation-evoked pressor responses and norepinephrine overflow, with effects more prominent in hypertensive rats.
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