Effects of histamine H₂‐receptor blockade on the cardiovascular reflex response to lower‐body negative pressure in man

Abstract

The role of histamine H2-receptors in cardiovascular control is unknown. In seven healthy volunteers, we studied how histamine H2-receptor blockade affected the reflex response to hypovolaemia induced by lower-body negative pressure (LBNP). In placebo-treated individuals, LBNP down to -40 mmHg did not change systolic pressure but increased diastolic pressure, heart rate, forearm vascular resistance, plasma noradrenaline concentration and plasma renin activity. After pretreatment with ranitidine, a specific histamine H2-receptor antagonist, the diastolic pressure rise no longer sufficed to maintain a constant systolic pressure during LBNP. Ranitidine pretreatment also attenuated the heart rate response and the rise in plasma renin activity induced by LBNP, but did not significantly change the reflex forearm vasoconstriction or the forearm plasma noradrenaline response. The results suggest that histamine H2-receptor blockade attenuates the reflex vasoconstrictor response to lower-body negative pressure. The mechanism behind this effect remains unknown, but the data do not support the idea that the effect is exerted in the skeletal muscle vascular bed.

Intestinal nitric oxide output during reduced mucosal blood flow in healthy volunteers

“…The subjects' legs were positioned inside a specially constructed air-tight box sealed around the hips with a rubber membrane. The intrabox pressure was lowered between 30 and 50 mm Hg by use of a conventional vacuum cleaner regulated by a variostat (26).…”