Abstract
Abstract
It has been suggested that the cell membrane of vascular smooth muscle in one-kidney, one-clip hypertension, and other forms of volume-dependent, low-renin hypertension, is partially depolarized due to the effects of a circulating ouabain-like factor, and that this depolarization is an important mechanism of the hypertension. Levels of circulating ouabain-like factors in early stages of volume-dependent hypertension are reported equal to, or greater than, those in chronic hypertension. Therefore, we measured intracellular membrane potentials (E m ) in vitro (37 °C, physiological salt solution) in vascular smooth muscle of the caudal artery from normotensive control rats (1K) and rats in the early and chronic stages of one-kidney, one-clip hypertension (1K1C). In 20 chronic 1K1C (4-6 weeks of systolic pressure > 140 mm Hg) the resting E m's (M ± SEM) were −46.7 ± 0.7 mV, compared to −50.9 ± 0.6 for 20 1K (P < 0.01). The ΔE m due to 1 mM ouabain was attenuated in 10 1K1C compared to 11 1K (+5.4 ± 0.9 and +10.0 ± 0.7 mV, respectively; P < 0.01). The E m's of the two groups after ouabain were the same. In contrast, in 16 early 1K1C rats (<7 days hypertension, average 3 days) compared to 15 appropriate 1K, there were no significant alterations in resting E m (-50.1 ± 0.4 mV, compared to −50.5 ± 0.5, respectively) and there were no differences in ouabain response. These results suggest a temporal dissociation between levels of humoral inhibitors and depolarization, and between depolarization and hypertension, and thus fail to support the hypotheses that there are causal relationships between these variables in volume-dependent, low-renin hypertension.
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