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Practical clinical aspects of the evaluation and treatment of essential hypertension are reviewed. Drug therapy discussed includes diuretics, and as adjunctive therapy, sympathoplegic agents, peripheral vasodilators and beta blockers. Also covered are treatment of less common forms of essential hypertension, other forms of antihypertensive therapy, and the use of fixed combinations of antihypertensive drugs.
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We evaluated the hypothesis that thiazide-induced hypercalcemia reflects potentiation of the cAMP response to parathyroid hormone (PTH) consequent to inhibition of phosphodiesterase in bone and kidney. A panel of thiazide diuretics did inhibit low-Km phosphodiesterase activity from bone homogenates. However, furosemide, a nonthiazide diuretic that does not promote calcium retention, was more potent a phosphodiesterase inhibitor than either chloro- or hydrochlorothiazide (CTZ, HCTZ). Thiazides did not influence basal or PTH-stimulated cAMP levels in incubated calvaria or renal cortical slices. Administration of CTZ or HCTZ to rats for 4 days did not affect basal cAMP, nor did such treatment potentiate the cAMP response in Calvaria to infusion of parathyroid extract in vivo. CTZ, HCTZ, and furosemide increased basal adenylate cyclase from renal cortex but did not affect PTH-stimulated activity. Adenylate cyclase from bone was not affected by thiazides but was inhibited by furosemide. Thiazide treatment potentiated the calcemic response to parathyroid extract in vivo but did not affect the calcemic response to dibutyryl cAMP. We conclude that potentiation of the cAMP response to PTH does not underlie the unique effects of thiazides on calcium metabolism.
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Adequate treatment of hypertension requires that the physician understand the pharmacologic actions of antihypertensive agents. Although no drug is without adverse reactions, it should be possible to choose an agent or combination of agents which can effectively lower blood pressure and be tolerated by the patient. The indications, proposed mechanisms of actions and adverse effects of the following antihypertensive drugs are discussed: thiazide diuretics, spironolactone, triamterene, trimethaphan, Rauwolfia alkaloids. guanethidine, bethanidine, methyldopa, clonidine, pargyline, propranolol, hydrazaline, minoxidil, guancydine, diazoxide and sodium nitroprusside.
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Dietary and drug treatments of calcium nephrolithiasis depend mainly on the mineral composition of renal stones: calcium oxalate, phosphate or mixed stones. The association with an hypercalciuria is an important factor which must be taken into account because oxalates and phosphates precipitate as calcium crystals in case of urinnary oversaturation. Despite many therapies have been proposed, their efficiency seems to be rather small when they are used alone. Usually, it is necessary to act on several factors with a combination of therapeutic methods. Absorptive hypercalciuria are improved with both low calcium diets and inhibitors of calcium absorption. In renal hypercalciuria, the treatment is based on the administration of thiazide diuretics which enhance calcium renal tubular reabsorption. The other therapeutic methods depend on the nature of renal stones: urinary acidification for calcium phosphate; administration of succinimide, oral phosphate or organic phosphonates for calcium oxalate stones; association with purine biosynthesis inhibitors in case of the presence of urates in renal calculi.
Rapid evaporation of urine to osmolarity 1200 results in a high incidence of envelope Wedellite and calcium phosphate crystals. The Wedellite crystals closely resemble those seen in untreated urine samples of stone formers. The incidence of crystalluria produced by these tests is higher in the stone formers than in the normal subjects, reduced by thiazides and increased by cellulose phosphate; combined thiazide and cellulose phosphate therapy was most effective in reducing crystalluria. Simple calcium and oxalate concentration products were calculated and did not correlate well with incidence of calcium oxalate crystalluria. Although the product is important, inhibitors of crystal formation must be equally important. It is postulated, but not proven, that the evaporation tests may indicate normal subjects at risk to stone formation when exposed to chronic dehydration and whether a stone former is still metabolically active.
The stone-forming process includes crystal formation, crystal aggregation, and retention time to allow growth. The crystal-forming process, in turn, is influenced by the pH of the urine, the solute load, and inhibitors of crystallization. Idiopathic stone disease is characterized by recurrent formation of calcium oxalate, calcium phosphate, and hydroxyapatite stones without an apparent underlying cause. Treatment of idiopathic stone disease has been aimed at decreasing the solute concentration, increasing the solubility of calcium phosphate, or interfering with extension of the crystal lattice.
1 Daily treatment of two-kidney clipped renal hypertensive rats with hydrallazine, hydrochlorothiazide (HCTZ) and a new orally active inhibitor of the angiotensin-converting enzyme, captopril (SQ14,225), was correlated with survival rates for up to 9 months. 2 The groups of rats given captopril alone or captopril plus intermittent or chronic HCTZ had the best survival rate, whereas HCTZ alone or hydrallazine did not benefically affect survival. 3 Survival rates correlated well with control of BP in these animals.
Twenty patients being treated with thiazides were found among 95 subjects (21%) with hyercalcemia verified in repeated determinations in a health screening of 15,903 persons. There were 1,034 patients treated with thiazides in this total health screening. The prevalence of hypercalcemia in the patients treated with thiazides in this total health screening. The prevalence of hypercalcemia in the patients treated with thiazide (1.9%) was considerably higher than the prevalence of hypercalcemia found in the entire health-screened population (0.6%). The thiazide treatment was withdrawn in the 20 hypercalcemic subjects after an examination, and the patients were observed at intervals during a follow-up period of one year. The necks of 14 were explored during or after the follow-up period because of an initial serum calcium level greater than 3.0 mmole/liter or persistent hypercalcemia. Parathyroid adenomas were seen in all patients receiving surgery. Single adenomas predominated in surgical findings. The finding of the present high number of patients with primary hyperparathyroidism may be associated with elevated blood pressure resulting in thiazide treatment after detection.
Twenty-one of a total of 72 patients with acute pancreatitis admitted to a university hospital over a three-year period were found to have "idiopathic" pancreatitis. Of these, six nonalcoholic patients without gallbladder disease were receiving one of the thiazide diuretics prior to the onset of pancreatitis. Three patients taken from an earlier series likewise had pancreatitis associated with thiazide administration and at the time of autopsy harbored parathyroid hyperplasia. It is suggested that both the parathyroids and the pancreas may be affected by thiazide administration, and that a history of ingestion of these drugs should be sought in patients who have idiopathic pancreatitis.