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Does excessive activity of the sympathetic nervous system (SNS) contribute to the development and persistence of abnormal arterial pressure in patients with primary hypertension? Many investigators have tried to answer this question during the last four decades, but, because of conceptual and methodologic problems, no firm conclusions have been reached.1 , 2 "Overactivity" of the SNS in hypertension is a problematical concept. In normotensive persons, the intensity of sympathetic stimulation of the heart and blood vessels varies greatly with posture, activity, emotional state, physical conditioning and cardiovascular health. It influences venous capacitance, heart rate, myocardial contractility, as well as cardiac output and . . .
Jan Koch‐Weser (Thu,) studied this question.
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