SUMMARY The net passive influx of Na + and efflux of K + (orthodirection) through the red blood cell membranes from spontaneously hypertensive rats (SHR) were observed to be significantly higher (p < 0.05) than those of three strains of normotensive rats when the measurements were made at 4°C. Similar comparative studies, carried out at 37°C, in the absence or presence of ouabain, showed no difference in these fluxes through this membrane from SHR compared to those from Wistar-Kyoto (VVKY) rats, one of the normotensive strains. A study was undertaken to determine the temperature at which the greater cation fluxes in SHR red blood cells occurred. The net fluxes of Na + and K + decreased as the temperature was reduced from 37° to 15°C, but a paradoxical increase in the fluxes was observed as the temperature was decreased from 15° to 4°C. Only with this temperature shift (15°t o 4°C) was the increase in flux significantly greater in SHR than in VVKY cells. Subsequent studies were designed to determine whether the difference in the transport systems of red blood cells of SHR and VVKY could be observed in fluxes of these cations in either direction across the membrane. For "reverse direction" flux studies, red blood cells were loaded with Na + (to 130 mEq/liter cell water) and depleted of K + (to 30 mEq/liter cell water) by incubation with the ionophore monensin. The reverse passive efflux of Na + and influx of K + at 4°C of cells from SHR were significantly greater than those of VVKY. Thus, the abnormality of the red blood cell membrane in SHR behaves as if it were just an increase in the size or number of pores through which Na + and K + diffuse freely at low temperatures. (Hypertension 6: 42-48, 1984)
The development of hypertension induced by deoxycorticosterone acetate (DOCA) in sheep was accompanied by increases in both the plasma concentration and the urinary excretion of vasopressin. The vasopressin response to an osmotic stimulus (i.v. infusion of 0.85 mol NaCl/l at 4 ml/min for 75 min) was studied before and after the development of hypertension induced by DOCA in six sheep. Before DOCA implantation, the osmotic stimulus resulted in an increase of plasma osmolality (POSM) from 290 +/- 1 to 303 +/- 1 (S.E.M.) mosmol/kg H2O and in plasma vasopressin concentration (PAVP) from 0.23 +/- 0.04 to 1.07 +/- 0.15 microunits/ml. At least 30 days after DOCA implantation when mean arterial blood pressure had risen from 81 +/- 3 to 117 +/- 5 mmHg, the same osmotic load caused an increase in POSM from 290 +/- 2 to 298 +/- 2 mosmol/kg H2O and PAVP from 0.45 +/- 0.05 to 2.02 +/- 0.27 microunits/ml. POSM and PAVP were significantly correlated in every experiment. However, the slope of the relationship increased significantly (P less than 0.01) after the animals had developed hypertension (0.185 +/- 0.026 vs 0.070 +/- 0.011 (microunits vasopressin/ml)/(mosmol/kg H2O]. The intercepts were similar. After the DOCA implant had been removed osmotic sensitivity returned to normal.
SUMMARY The influence of deoxycorticosterone acetate (DOCA) on the sodium content of the red blood cell was determined in the pig. DOCA (100 mg/kg), impregnated in Silastic, was implanted subcutaneousty (s.c.) in six male pigs; seven additional pigs received Silastic implants without the DOCA. Those receiving DOCA had an increase in mean arterial pressure (MAP) that was significant in 48 hours and reached a plateau that was 24 mm Hg greater than that of the controls after 15 days. These animals also developed hypokalemia and polydipsia over approximately the same time course. sure often varies with the amount of sodium ingested, this element is thought to play an important role in some types of experimental and clinical hypertension. The mechanism by which sodium causes this effect is not known, but it is the central theme of much research. 12Investigators studying altered electrolyte metabolism of the red blood cell in hypertension have considered the possibility that this abnormality reflects changes that may occur in other tissues such as vascular smooth muscle or the central nervous system, in which the abnormality may play a causal role in the elevated arterial pressure. MIn the current study, we have observed that the development of deoxycorticosterone acetate (DOCA) hypertension in the pig is accompanied by an increase in intracellular sodium content in the red blood cell. Additional studies were carried out to explore possible mechanisms by which DOCA may produce this increase.
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