Potassium preserves endothelial function and enhances aortic compliance in Dahl rats.

Abstract

It has recently been proposed that in rat models of genetic hypertension, supplemental dietary potassium preserves release of endothelium-derived relaxing factor independently of its capacity to either attenuate hypertension or increase plasma potassium. To test this hypothesis in Dahl salt-sensitive rats given sodium chloride (4%) for 3 weeks, we supplemented dietary potassium (2.1%) with either KCI (n=16) or KHCO 3 (n=16). Compared with unsupplemented rats (n=16), rats supplemented with either potassium salt had a lower mean arterial pressure and a greater release of endothelium-derived relaxing factor, as assessed from acetylcholine-induced relaxation of precontracted aortic rings. However, the maximum relaxation response to acetylcholine correlated inversely with blood pressure (r=-.82, P<.001), not only in the KCI (r=-.68, J><.002) and KHCO 3 (r=-.77, P<Ml) groups but also in unsupplemented rats (r=-.86, P<.001). With potassium supplementation, plasma potassium concentrations measured between 4 and 6 PM did not increase, but those measured between 4 and 6 AM did increase (P<.05). In isolated ring segments, aortic compliance was greater in both the KCI and KHCO 3 groups than in unsupplemented rats (0.015 and 0.017 vs 0.009 mm 2 /mm Hg) (P<.01). This greater compliance could not be related to differences in blood pressure, plasma potassium, or collagen or elastin content of the aortic wall. In salt-loaded Dahl salt-sensitive rats in which supplemental dietary potassium attenuates hypertension, (1) the extent to which release of endothelium-derived relaxing factor is preserved is directly related to the extent to which potassium restricts the salt-induced rise in blood pressure, (2) nocturnal but not diurnal plasma potassium is increased, and (3) aortic compliance is enhanced. (Hypertension. 1993;22:315-322.)

Chloride-Dominant Salt Sensitivity in the Stroke-Prone Spontaneously Hypertensive Rat

“…In sharp contrast to the current observations, it has been repeatedly observed that KCl-loading attenuates salt-sensitive hypertension in its archetypal genetic model, the Dahl S rat, 7,23 and in its archetypal acquired model, that induced by desoxycorticosterone. 24,25 K ϩ loading induces natriuresis by directly reducing renal tubular reclamation of Na ϩ .…”

Effect of potassium on vasodilation to acetylcholine in essential hypertension.

“…It is important to observe that our results were obtained with acute potassium infusion, whereas the above-reported data were obtained with chronic dietary potassium supplementation. However, Sudhir and colleagues 13 demonstrated that chronic potassium administration led to an increment in nocturnal plasma potassium concentrations comparable to that obtained with our acute infusion of potassium chloride.…”

“…Earlier work had determined the sensitivity and reproducibility of the method. 13 Forearm volume was measured by the water displacement method, and drug infusion rates were normalized to 100 mL of tissue by altering the drug concentration in the solvent but not the speed of infusion. Drugs used were infused through separate ports via three-way stopcocks at concentrations that had no systemic effects.…”

Effects of Potassium Chloride and Potassium Bicarbonate on Endothelial Function, Cardiovascular Risk Factors, and Bone Turnover in Mild Hypertensives

“…20 Our finding of an improvement of large elastic artery compliance would suggest a potential beneficial effect of potassium on the cardiovascular system in the long term. Studies in Dahl salt-sensitive rats demonstrated that potassium supplementation enhanced aortic compliance 21 and protected against the development of vascular damage induced by salt loading, possibly through suppression of salt-induced oxidative stress. 22 Urinary albumin excretion has been shown to be an important, independent, and continuous risk factor for the development and progression of renal disease and also for cardiovascular disease.…”