No abstract

Renal and systemic hemodynamics, plasma arginine vasopressin, plasma renin activity, plasma norepinephrine, blood volume and water loading test were studied in 10 patients with falciparum malaria without renal failure. Six patients responded to water load normally, while 4 patients had a decreased response to water load. The patients with a normal water load response had normal renal and systemic hemodynamics and a normal hormonal profile. The patients with a decreased response to water load had hyponatremia, hypervolemia, high cardiac index, low systemic vascular resistance, high plasma arginine vasopressin, high plasma renin activity, high plasma norepinephrine, low creatinine and p·aminohippurate clearances, low urine sodium and high urine osmolality. They had a lower mean arterial pressure during the acute phase of the disease than during the recovery phase. The findings suggest that a decreased response to water load is due to peripheral vasodilatation which results in a decreased effective blood volume leading to the release of vasopressin and norepinephrine, increased renin activity and decreased renal hemodynamics.

Effects of L-arginine (ARG) infusion on renal and systemic hemodynamics were studied in 12 anesthetized dogs. The experiment was performed in two groups of dogs. The dogs of group 1 (n = 6) received intravenous ARG at 2.5 mmol/kg followed by indomethacin (IND) injection (10 mg/kg) and were rechallenged with ARG at the same amount. The dogs of group 2 (n = 6) received intravenous ARG at 5 mmol/kg followed by IND injection (10 mg/kg) and were later infused with ARG at the same dose. In group 1, the first ARG infusion caused no significant changes in renal and systemic hemodynamics. During the second ARG infusion, glomerular filtration rate (GFR) and renal plasma flow (RPF) were significantly increased when compared with the IND-treated period. In group 2, the first ARG infusion increased cardiac output (CO) and decreased total peripheral resistance (TPR) without significant changes in GFR and RPF. The second ARG infusion induced acute rise of both GFR and RPF approximately twofold, compared with the IND-treated period. CO was also increased significantly. Plasma glucagon levels determined in 2 dogs showed an increase following both ARG infusions. These results indicate that an acute ARG loading induces renal and systemic vasodilatation in a dose-dependent manner despite IND effect, and would indicate that increased renal hemodynamics are not prostaglandin-mediated.

The sorbitol permease enables the efflux of sorbitol from cultured rabbit papillary cells (PAP-HT25) in response to a reduction in osmolality. The anion transport inhibitor 5-nitro-2-(3-phenylpropylamino)benzoate (100 microM) inhibited efflux by 92%, and 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (0.5 mM) reduced efflux by 40%. 2,4-Dinitrobenzenesulfonate and p-chloromercuriphenylsulfonic acid had no effect. The protease trypsin (0.05 mg/ml) reduced sorbitol efflux by 53%, pronase (0.01 mg/ml) by 47%, and papain (0.1 mg/ml) by 49%; chymotrypsin had no effect. Sugars and sugar alcohols at different concentrations (10-200 mM) in the bathing solution did not influence sorbitol efflux. Determination of the osmotically induced influx of sugar alcohols showed that xylitol uptake was faster than that of sorbitol; 6-deoxysorbitol was slower; L-sorbitol, arabitol, galactitol, and 2-deoxysorbitol entered at the same rate as sorbitol; and maltitol did not enter the cells. Sorbitol and 6-deoxysorbitol at 9 mM competitively inhibited [14C]sorbitol influx by 24 and 32%, respectively, whereas xylitol, taurine, betaine, and myo-inositol showed no inhibition. We conclude that 1) a specific inhibitor of the permease was not found, 2) the sorbitol permease or associated regulator is a protein, and 3) the C-6 atom of sorbitol is important in the selectivity of the permease.