Renal lithium clearance in the different stages of hypertension.

This study investigated whether fractional lithium excretion (FELi), used as a marker of proximal fluid delivery, changes during different phases of essential hypertension. Forty-eight subjects were studied: 12 essential hypertensives (EH); 12 borderline hypertensives (BL); 12 normotensives with a positive family history of essential hypertension (NH) and 12 normotensives without a family history of essential hypertension (NN). Measurements were performed in the recumbent position, both in basal conditions and after a saline load (2% body weight in 1 h; 0.333 ml/min per kg body weight). In basal conditions, a moderate extracellular volume expansion was already present in the subjects. In these conditions, FELi of EH was significantly higher than that of all the other groups (P less than 0.01). After the saline load, fractional sodium excretion increased in all the groups (P less than 0.01), but to a significantly greater extent in EH (P less than 0.01). FELi rose significantly only in BL (P less than 0.05). The change in FELi of BL correlated positively (P less than 0.02) with the change in blood pressure in 10 of these subjects 3 years after this study. Moderate extracellular volume expansion may be able to either reveal or stimulate an increase of FELi in subjects with established hypertension. When a greater degree of extracellular volume expansion is induced, this increases FELi in BL and this effect may be related to the subsequent development of hypertension.

Predicting interindividual variations in antihypertensive therapy: the role of sodium transport systems and renin.

The efficacy of captopril at 75 mg/day, atenolol at 100 mg/day and canrenoate potassium at 200 mg/day was compared in 42 essential hypertensive patients in randomly assigned sequences. All the drugs lowered blood pressure significantly but variations were found in the individual response. Patients who were more responsive to captopril also seemed to be more responsive to atenolol and vice versa (r = 0.75; P less than 0.0001), while the relationship between mean blood pressure reached after canrenoate potassium and that reached after atenolol or captopril was much weaker. The patients who were responsive to atenolol and captopril were considered as one group (n = 22) and compared with the 12 patients more responsive to canrenoate potassium. Before treatment, the former group had higher plasma renin activity (PRA) and lower Na,K cotransport activity across the erythrocyte membrane than the latter. These two variables, considered together as a discriminant function, correctly classified 92% of cases in the canrenoate potassium responder group and 73% of cases in the atenolol-captopril responders. These results raise the problem of individual assessment to obtain the most effective antihypertensive therapy and suggest that PRA and Na,K cotransport may be useful in predicting the individual response to antihypertensive drugs.

Antihypertensive effect of captopril, canrenoate potassium, and atenolol. Relations with red blood cell sodium transport and renin.

We compared the antihypertensive efficacy of atenolol (100 mg/d), canrenoate potassium (200 mg/d), and captopril (75 mg/d) in 30 essential hypertensives. The three drugs were administered in a randomized change-over sequence for four-months each. The main variables associated with blood pressure regulation were measured in the basal condition and at the end of each treatment period. The erythrocyte Na transport systems were measured only in the basal condition and at the end of the first treatment period. The average blood pressure reduction was similar for each drug. Mean blood pressure levels after captopril correlated positively with those after atenolol in the individual patients (P less than 0.0001); mean blood pressure levels after canrenoate potassium, on the contrary, did not correlate with those after the other two drugs. Captopril and canrenoate potassium treatment reduced intraerythrocyte Na content (P less than 0.02), canrenoate potassium increased Na-K pump (P0.05), atenolol did not change any erythrocyte membrane Na transport parameters. The ouabain-resistant Na transport systems were not modified by any drug. The patients were divided in three groups according to their antihypertensive response: nonresponders (six patients), canrenoate potassium responders (nine patients) and captopril-atenolol responders (15 patients, equally responsive to both drugs). Nonresponders had the lowest basal Na pump (P less than 0.02). Canrenoate potassium responders had higher basal Na-K cotransport than captopril-atenolol responders (P less than 0.02). Atenolol-captopril responders had the highest basal plasma renin activity (PRA, P less than 0.02). The blood pressure reduction after atenolol correlated with the induced fall in PRA (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)