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Hemodynamic changes during long‐term thiazide treatment of essential hypertension in responders and nonresponders
Author(s) -
Brummelen Peter,
Man In 't Veld Arie J,
Schalekamp Maarten A D H
Publication year - 1980
Publication title -
clinical pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.941
H-Index - 188
eISSN - 1532-6535
pISSN - 0009-9236
DOI - 10.1038/clpt.1980.44
Subject(s) - aldosterone , hydrochlorothiazide , plasma renin activity , medicine , thiazide , cardiac output , hemodynamics , blood pressure , placebo , essential hypertension , mean arterial pressure , heart rate , vascular resistance , cardiology , stroke volume , renin–angiotensin system , endocrinology , anesthesia , alternative medicine , pathology
Blood pressure, cardiac output, plasma volume, renin, and aldosterone were measured in 13 patients with essential hypertension on placebo and after 1, 4, and 12 wk on hydrochlorothiazide 100 mg daily. In 9 patients the same variables were also measured after 24 and 36 wk. Hydrochlorothiazide lowered mean arterial pressure (p < 0.01). Cardiac output was reduced after 4 and 12 wk of treatment, followed by a return to placebo levels. Stroke volume changed in the same way but heart rate and total peripheral resistance did not differ from placebo values. Plasma volume was reduced after 1 and 24 wk. Renin was permanently elevated (p < 0.01), but aldosterone rose only during the first 12 wk of treatment. A comparison between responders (>10% fall in mean arterial pressure) and nonresponders (<10% fall) revealed different hemodynamic patterns. In responders the initial fall in cardiac output was followed by a return to pretreatment levels, whereas in nonresponders it was permanently reduced. Consequently, total peripheral resistance was lowered only in responders. Nonresponders tended to show a greater degree of plasma volume depletion and greater stimulation of renin and aldosterone, which probably contributed to elevated peripheral resistance. It is concluded that changes in cardiac output are unlikely to be of decisive importance in the ultimate reduction of peripheral resistance in responders to thiazide therapy. Clinical Pharmacology and Therapeutics (1980) 27, 328–336; doi: 10.1038/clpt.1980.44