Parathyroid hormone and cardiovascular effects of dihydropyridines in chronic renal failure.

We studied the influence of parathyroid gland activity on cardiovascular response to dihydropyridines (nicardipine (NIC), 80 mg/day for 4 weeks) in 20 hypertensive patients with end-stage renal failure (ESRF). Before the treatment hyperparathyroidism (HPTH) was estimated on the basis of serum parathormone (PTH), and bone histomorphometry (osteoclastic resorption surfaces (ORS), and number of osteoclasts (NO]. NIC induced a significant decrease in systolic (SAP) and diastolic (DAP) arterial blood pressure, but did not significantly change the heart rate (HR) or the SAP X HR (myocardial oxygen consumption estimate). Changes in SAP and DAP were correlated to baseline serum PTH (P less than .001), to ORS (P less than .01) and to NO (P less than .01). Furthermore, a significant decrease in blood pressure was observed only in patients with histological signs of hyperparathyroidism (ORS greater than 1%). In this subset of patients NIC induced a significant decrease in SAP X HR (P less than .02) which was correlated to PTH and histomorphometric indexes of HPTH (P less than .01). The results of the present study show that blood pressure response to dihydropyridines in ESRF is associated with parathyroid activity as judged from serum PTH and bone histomorphometry.