Antihypertensive and renal haemodynamic effects of atenolol and nadolol in elderly hypertensive patients.

As little is known of the antihypertensive efficacy or renal haemodynamic effects of beta-adrenoceptor blocking drugs in the elderly we studied two such drugs, atenolol and nadolol, in elderly hypertensive patients. Ten patients took part in a placebo-controlled double-blind study of atenolol and 10 received nadolol in a single-blind placebo-controlled study. Treatment phases lasted 12 weeks for atenolol or 10 weeks for nadolol. Blood pressure, effective renal blood flow and glomerular filtration rate data obtained at the end of each treatment phase were analysed. Atenolol lowered mean arterial pressure (mean +/- s.e. mean) from 129.9 +/- 1.5 to 108.2 +/- 2.3 mm Hg (P less than 0.01) while it increased mean effective renal blood flow 512.5 +/- 86.6 to 646.0 +/- 116.1 ml min-1 1.73 m-2 (P less than 0.05). Nadolol reduced mean arterial pressure from 133.2 +/- 2.0 to 113.5 +/- 3 mm Hg (P less than 0.001) but reduced mean effective renal blood flow from 558.8 +/- 32.2 to 446.0 +/- 26.9 ml min-1 1.73 m-2 (P less than 0.05). Glomerular filtration did not alter significantly with either drug. We conclude that beta-adrenoceptor blocking drugs are effective antihypertensive agents in the elderly but have disparate effects on effective renal blood flow perhaps because of differences in cardioselectivity. These data suggest that comparative studies with thiazide diuretics and beta-adrenoceptor blocking drugs are warranted in elderly hypertensives.     

Release of platelet constituents by monosodium urate crystals.

The release of human platelet constituents by the etiologic agent of gout, the monosodium urate crystal, is described here. In suspensions of washed platelets, response to urate crystals proceeded in two phases: A secretory phase involved the rapid active release of serotonin, ATP, and ADP with little loss of lactic dehydrogenase or beta-glucuronidase. A lytic phase involved the slower loss of all platelet constituents. Both phases were inhibited by iodoacetate plus dinitrophenol, suggesting an energy requirement. In ultrastructural studies, lysis of washed platelets which appeared to contain crystals was seen. Urate crystals were also shown to induce serotonin release and platelet lysis in citrated platelet-rich plasma. Since urate crystals are deposited at a variety of sites, urate crystal-platelet interaction in vivo is a possibility. Such interactions, leading to release of platelet constituents, might contribute to gouty inflammation or to enhanced atherogenesis.