It has been feared that lowering the blood pressure (BP) of elderly patients with systolic hypertension (SH) may compromise cerebral perfusion. To test this hypothesis, BP, cerebral blood flow (CBF), plasma renin activity (PRA), blood counts, urinary and serum electrolytes and other blood chemistries were measured in fifteen elderly patients (ages 61-76 years) with SH (systolic BP greater than 170 and diastolic BP less than 100 mmHg). Gray matter flow (Fg) was calculated from clearance curves of inhaled 133-Xenon. All subjects were studied while untreated, as well as during long-term treatment (average 15 weeks) with hydrochlorothiazide. BP fell during treatment from 186/90 to 160/86 while average Fg and cerebrovascular resistance (CVR) were not significantly changed. There was some suggestion, however, that in patients who became normotensive the CVR decreased (p less than 0.05) while in those who did not Fg fell (p less than 0.05). Cerebrovascular response to 5% CO2 inhalation was impaired during both the treated and untreated states. Individual changes in Fg and CVR did not correlate with changes in BP or with changes in PRA, electrolytes or other chemistries. In general, cautious, gradual reduction of BP with a thiazide diuretic in SH of the elderly seems not to impair cerebral perfusion, but individual differences exist and further studies are needed to characterize them.
Eighteen patients with essential hypertension were treated in a single-blind, crossover study with pindolol and with propranolol. The two drugs were compared because of known differences between them on renin secretion. We noted that plasma renin activity and plasma aldosterone concentration were suppressed by propranolol but not by pindolol. Blood pressure was reduced about equally by both drugs. Serum potassium levels rose in 17 patients on pindolol (p < 0.001) and in 14 patients on propranolol (p = 0.08). Our data suggest that serum potassium elevations induced by beta blockade do not depend on the renin-angiotensin-aldosterone system. Alternative possibilities are discussed.
A patient with polycystic kidneys is presented, in whom obliteration of a renal artery led to the development of high renin malignant hypertension. During chronic hemodialysis 3 years later the patient had normal renin values and the blood pressure became volume-dependent. It is concluded that the occurrence of malignant hypertension and/or elevated renin values in patients with polycystic kidney disease should lead to the search for a coexisting renal artery stenosis or occlusion.
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