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Michael A. Weber, Elmar Weiler, Harvey C. Gonick, Bruce A. Prins, Ralph E. Purdy, Effects of a Human-Derived Sodium Transport Inhibitor on In Vitro Vascular Reactivity, American Journal of Hypertension, Volume 2, Issue 10, October 1989, Pages 754–761, https://doi.org/10.1093/ajh/2.10.754
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Abstract
Concentrations of sodium-transport inhibitors (STI) which block the sodium-potassium-ATPase pump are increased in the plasma and urine of volumeexpanded and low-renin hypertensive humans and animals. To evaluate the physiologic relevance of STI to blood-pressure-raising mechanisms, we have examined the in vitro properties of STI extracted from the urine of human subjects. STI produced a significant (by ANOVA: P < .01) dose-contraction response in the isolated rabbit femoral artery. Moreover, small noncontractile doses of STI in this in vitro preparation produced a fivefold leftward shift in the contraction dose-response curve of norepinephrine (P < .01) and a threefold shift for angiotensin II (P < .01); at lower, physiologic, concentrations of these vasoconstrictor hormones the amplifications in contraction caused b y STI ranged from 100% to 500%. In studies in calciumfree tissue bath solutions, the direct contractile action of S T I was abolished; however, its amplification of responses to norepinephrine remained, suggesting that this latter effect of STI is not entirely dependent upon calcium influx into vascular smooth muscle cells. The glycoside ouabain produced effects identical to those of STI in arteries, but its actions on a rabbit atrium preparation were different: ouabain stimulated powerful inotropic effects, whereas human STI failed to cause myocardial contractions even though the amounts of STI administered had the same sodium-transport inhibitory capacity as t h e ouabain. Thus, the actions of human STI are primarily in the peripheral circulation, where they directly produce arterial contractions and also enhance contractile responses to other pressor hormones, suggesting that they may have a role in regulating systemic blood pressure. Am J Hypertens 1989;2:754–761.
- norepinephrine
- cardiac glycosides
- hypertension
- vasoconstrictor agents
- renin
- myocardial contraction
- angiotensin ii
- atrium
- peripheral circulation
- calcium
- muscle, smooth, vascular
- hormones
- dose-response relationship, drug
- femoral artery
- glycosides
- muscle contraction
- na(+)-k(+)-exchanging atpase
- plasma
- oryctolagus cuniculus
- bathing
- arterial pressure
- ouabain
- urine
- inotropic agents
- amplification
- sodium ion transport
