Key result
Hypertensive rat plasma increases pressor responses and noradrenaline overflow, suggesting an endogenous re-uptake blocking factor.
Why the study?
Does plasma from RRM-salt hypertensive rats increase pressor responses and noradrenaline overflow in isolated mesenteric vasculature?
Does plasma from RRM-salt hypertensive rats increase pressor responses and noradrenaline overflow in isolated mesenteric vasculature?
Plasma from rats with reduced renal mass-salt hypertension contains a noradrenaline re-uptake blocking factor that increases sympathetic pressor responses.
May identify circulating sympathoexcitatory factor in rat hypertension; hypothesis-generating and leaves open human relevance.
This study was carried out to elucidate the involvement of the peripheral sympathetic nervous system in the pathogenesis of reduced renal mass (RRM)-salt hypertension in rats. Male Wistar rats underwent subtotal nephrectomy (70-80% reduction in renal mass). On the 10th postoperative day, systolic blood pressure was higher in RRM-salt rats than in RRM-water rats. Perfusion of isolated mesenteric vasculature from normotensive rats, with the deproteinized plasma from RRM-salt hypertensive rats induced significantly higher pressor responses and noradrenaline overflow with electrical stimulation than the perfusate from RRM-water normotensive rats; the responses to exogenous noradrenaline showed no significant changes. In the presence of desipramine, noradrenaline overflow did not increase following perfusion with plasma from RRM-salt hypertensive rats. These data indicate that plasma from rats with RRM-salt hypertension might contain some noradrenaline re-uptake blocking factor.
No takes yet. Share an insight, caveat, or question.
Shima et al. (1988) studied Reduced renal mass (RRM)-salt hypertension. Deproteinized plasma from RRM-salt hypertensive rats vs. Deproteinized plasma from RRM-water normotensive rats was evaluated on Pressor responses and noradrenaline overflow with electrical stimulation. Plasma from rats with reduced renal mass-salt hypertension induced significantly higher pressor responses and noradrenaline overflow, indicating a potential endogenous noradrenaline re-uptake blocking factor.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: