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Urinary output, urinary sodium and potassium excretion, plasma electrolyte concentrations and osmolality, plasma renin activity (PRA), and plasma aldosterone and arginine-vasopressin (AVP) concentrations were determined in eight camels in Tadla (Morocco). After administration of furosemide (2 mg.kg-1 body wt) urinary water, sodium and potassium excretions increased, inducing hypovolemia (as reflected by 14.6% increase in hematocrit), hyponatremia (142 +/- 1.0 vs 150 +/- 2.1 mmol.liter-1 in controls; P < 0.05), plasma hypo-osmolality (287.5 +/- 11.5 vs 307 +/- 1.4 mOsm.kg-1 H2O in controls; P < 0.05), and hypokalemia (3.7 +/- 0.2 vs 4.6 +/- 0.1 mmol.liter-1 in controls; P < 0.05). Such body fluid volume and composition changes were associated with parallel increases in PRA and plasma aldosterone concentrations (5.9 +/- 0.6 vs 0.9 +/- 0.2 ng AI.ml-1.hr-1 and 132.4 +/- 35.5 vs 25.1 +/- 6.5 pg.ml-1 in controls, respectively; P < 0.05). They were also associated with a fourfold increase in plasma arginine-vasopressin concentrations (0.8 +/- 0.2 vs 0.2 +/- 0.1 pg.ml-1; P < 0.05). In furosemide-treated animals, plasma aldosterone concentrations correlated positively with PRA (r = 0.85; n = 64; P < 0.01) and negatively with plasma sodium concentrations (r = -0.80; n = 64; P < 0.01), suggesting that in sodium-depleted camels the nexus between the renin-angiotensin system and aldosterone was restored.

The pharmacokinetics of sulfamethoxypyridazine (SMPD) were investigated in the camel after intravenous and oral administration. After intravenous injection, the plasma concentration of the drug followed the kinetics of a two-compartment model. The steady-state volume of distribution (Vss) of 0.47 l/kg suggested that sulfamethoxypyridazine was mostly distributed within the vascular compartment and the strongly vascularized tissues. The elimination from the body was rather slow, with a biological half-life [t1/2(beta)] and a total plasma clearance of about 9.5 h and 0.037 l/kg.h, respectively. Oral treatment showed that the maximum plasma concentration was reached 17 hours post drug administration and that the bioavailability ranged around 57%. Study of the plasma protein binding showed that the percentage of SMPD binding to plasma proteins varied from 47 to 72% and seemed to be concentration-dependent. The total binding capacity and the dissociation constant at equilibrium were 196 micrograms/ml and 335 micrograms/ml, respectively.

Eight dromedary camels were studied for 24 days under control conditions (3 days), and during water deprivation (14 days) and rehydration (7 days) in Tadla (Morocco), during the summer. During dehydration, food intake gradually fell and was zero on the last day and animals lost about 30% of their body weight. However, most of this reduction in weight was attributed to water loss, since body weight of the animals returned to control values following rehydration. Dehydration was associated with a decrease in plasma volume (-42 +/- 3%) and a concomitant rise in plasma Na concentration (from 154 +/- 2 to 191 +/- 3 mM). These changes were accompanied by increased plasma arginine-vasopressin (from 0.2 +/- 0.1 to 5.7 +/- 2.2 pg ml-1) and plasma renin activity (from 1.2 +/- 0.2 to 20.0 +/- 5.2 ng Al ml-1 hr-1), without significantly changed plasma concentrations of aldosterone and atrial natriuretic peptide. Dehydration was associated with increased urine osmolality (from 952 +/- 515 to 1963 +/- 498 mosm kg-1 H2O), reduced urine production (from 4565 +/- 2230 to 817 +/- 178 ml day-1), and increased Na excretion. Most of these parameters returned to control values during initial rehydration, except for plasma renin activity, which remained elevated for 7 days, and diuresis, which rose to 12773 +/- 6707 ml day-1 on Day 7 of rehydration.