Altered Ion Transport in Vascular Smooth Muscle from Spontaneously Hypertensive Rats

The interaction of vascular electrolytes and early spontaneous hypertension was studied in the rat aorta. Chemical composition (FLO, Na, K, Ca, Mg, Cl, collagen, and elastin), extracellular space, and cell water content were little changed. Only uronic acid and hexosaTnine contents were significantly elevated in the spontaneously hypertensive rat. Approximately 37% of the aortic weight was cellular. Functional changes in ion transport were observed in smooth muscle from hypertensive rats; the muscle exhibited decreased ability to accumulate K and extrude Na and increased turnover of K (0.0165 ± 0.0009 vs. 0.0086 ± 0.0002 min-) and C1 (0.162 ± 0.011 vs. 0.118 ±0.003 min-). Spontaneously hypertensive rats maintained increased -K exchange after adrenalectomy and reserpinization. The bioregulants, aldosterone, norepinephrine, and angiotensin had important actions on ion exchange. After adrenalectomy, aldosterone therapy reduced -K exchange toward intact levels. Norepinephrine increased the rate of K exchange with the dose-response relation having a lower median effective dose (EDS0) for spontaneously hypertensive rats (10-° g/ml) than it did for normal Wistar rats (2 X 10-" g/ml). Angiotensin also increased K exchange with similar dose-response relations for both groups. I concluded that functional alterations observed in spontaneously hypertensive rats probably resulted from primary changes in ion transport by vascular smooth muscle rather than from secondary effects of altered regulatory systems. The decreased selectivity to K over Na and the increased turnover of ions could lead to increased reactivity to norepinephrine through effects on membrane potentials.