Whether the vasoconstrictive actions of caffeine are enhanced in hypertensive parsons has not been demonstrated. Thus, caffeine (3.3 mg/kg) versus placebo was tested in 48 healthy men (aged 20 to 35 years) selected after screening on 2 separate occasions. Borderline hypertensive men (n = 24) were selected with screening systolic blood pressure (BP) of 140 to 160 mm Hg and/or diastolic BP 90 to 99 mm Hg. Low-risk controls (n = 24) reported no parental history of hypertension and had screening BP <130/85 mm Hg. Participants were then tested on 2 occasions after 12-hour abstinence from caffeine in each of 2 protocols; this required a total of 4 laboratory visits. Caffeine-induced changes in diastolic BP were 2 to 3 times larger in borderline subjects than in controls (+8.4 vs +3.8 mm Hg, p <0.0001), and were attributable to larger changes in impedance-derived measures of systemic vascular resistance (+135 vs +45 dynes · s · cm-5, p <0.004). These findings were consistent and reached significance in both protocols. The percentage of borderline subjects in whom diastolic BP changes exceeded the median control response was 96%. Consequently, whereas all participants exhibited normotensive levels during the resting predrug baseline, 33% of borderline subjects achieved hypertensive BP levels after caffeine ingestion. Thus, in borderline hypertensive men, exaggerated responses to caffeine were: selective for diastolic BP, consistent with greater vasoconstriction, replicated in 2 protocols, and representative of nearly all borderline hypertensives. We suspect that the potential for caffeine to stabilize high resistance states in susceptible parsons suggests that its use may facilitate their disease progression, as well as hinder accurate diagnosis and treatment.
Bibliographical noteFunding Information:
From the Veterans Affairs Medical Center (Medical Research Service & the Behavioral Sciences laboratories), University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma (Departments Psychiatry & Behavioral Sciences, Medicine, Pathology, and Coll of Pharmacy]. This study was sup averted by Grant HL32050 from?e National Heart, lung, and Bloo Instrtute, Bethesda, Maryland, and a grant from the Department of Veterans Affairs Medical Research Service, Oklahoma City, Oklahoma. Manuscript received May 15, 1995; revised manuscript received September 28, 1995, and accepted October 4. Address for reprints: Gwendolyn A. Pincomb, Sciences laboratories 15 1 A, Veterans Affairs Medical NE 13th Street, Oklahoma City, Oklahoma 73 104.