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Research Article Free access | 10.1172/JCI107605
Department of Physiology, Michigan State University, East Lansing, Michigan 48823
Department of Medicine, Michigan State University, East Lansing, Michigan 48823
Veterans Administration Hospital, Saginaw, Michigan 48602
Find articles by Overbeck, H. in: JCI | PubMed | Google Scholar
Department of Physiology, Michigan State University, East Lansing, Michigan 48823
Department of Medicine, Michigan State University, East Lansing, Michigan 48823
Veterans Administration Hospital, Saginaw, Michigan 48602
Find articles by Derifield, R. in: JCI | PubMed | Google Scholar
Department of Physiology, Michigan State University, East Lansing, Michigan 48823
Department of Medicine, Michigan State University, East Lansing, Michigan 48823
Veterans Administration Hospital, Saginaw, Michigan 48602
Find articles by Pamnani, M. in: JCI | PubMed | Google Scholar
Department of Physiology, Michigan State University, East Lansing, Michigan 48823
Department of Medicine, Michigan State University, East Lansing, Michigan 48823
Veterans Administration Hospital, Saginaw, Michigan 48602
Find articles by Sözen, T. in: JCI | PubMed | Google Scholar
Published March 1, 1974 - More info
To study limb vascular responses to K+ in man, paired intrabrachial arterial infusions of isosmolar NaCl (control) and isosmolar KCl (0.077, 0.154, and 0.307 meq K+/min) in isosmolar NaCl were made in 20 normotensive men and 20 men with essential hypertension of mild to moderate severity. Limb blood pressures were monitored, limb blood flow was measured by indicator-dilution, and limb vascular resistance was calculated as mm Hg/ml flow/min/100 cm3 limb volume. Measured concentrations of K+ in limb venous plasma during infusion of 0.307 meq K+/min ranged from 4.8 to 9.0 meq/liter. Changes in limb venous hematocrit, sodium, calcium, magnesium, and osmolality were similar during control and KCl infusions. The infusions did not significantly change systemic blood K+ concentration or blood pressures. Compared to NaCl, KCl decreased limb resistance (P < 0.05) in both normotensives and hypertensives, in a dose-related manner. Resting limb vascular resistances (IR) in hypertensives were greater (P < 0.05) than those in normotensives. Despite a positive correlation (P < 0.05) between IR and magnitude of response to K+, responses in hypertensives to K+ were not greater than those in normotensives. Further, analysis of covariance indicated that responses to 0.307 meq K+/min in hypertensives as a group were, in fact, less (P = 0.02) than those in normotensives. These results indicate that the vasodilator response to K+ may be attenuated in a significant proportion of essential hypertensive men, as it is in renal hypertensive animals. These abnormal responses to K+ in hypertensives may indicate an underlying defect in vascular K+ metabolism.