Norepinephrine Infusion in Normal Subjects and Patients with Essential or Renal Hypertension: Effect on Blood Pressure, Heart Rate, and Plasma Catecholamine Concentrations

Abstract

Infusion of NE in seven normal subjects and 13 patients with essential or renal hypertension caused a pronounced initial rise of systolic pressure in only seven hypertensives and one normotensive. This hyperresponsiveness was not a constant finding in essential or renal hypertensives but usually occurred in patients with highest preinfusion pressures. In some of the latter, following the pronounced rise in pressure when NE infusion was started (0.05 mug/kg/min), pressure did not increase further (probably due to reflexly reduced cardiac output) despite progressively increasing the infusion rate to 0.1 and 0.2 mug/kg/min. Hyperresponsiveness could not be attributed to increased NE concentrations at receptor sites since it was not significantly correlated with elevations of NE plasma concentrations; in some essential hypertensives, mild pressure increases occurred despite marked elevations of arterial plasma NE. Since hyperresponsiveness occurred in some patients with essential and some with renal hypertension, it could not be used to differentiate these two groups of hypertensives. The mechanism for hyperresponsiveness remains unclear but may be better explained by vascular structure alterations than by hyperreactive vascular smooth muscle per se; however, a combination of these factors could participate. During NE infusion, reflex bradycardia was associated with elevated pressure and was slightly more pronounced in normotensives; this was probably related to diminished baroreflex sensitivity in essential hypertensives and due to "resetting" of their baroreceptors. During high rates of NE infusion (0.2 mu/kg/min), higher arterial plasma NE concentrations in essential hypertensives than in normotensives could result from reduction in blood flow to organs important in inactivating circulating NE; however, a defective inactivating mechanism for NE in some essential hypertensives cannot be totally excluded.

Alpha-Adrenergic Mechanisms in the Cardiovascular Hyperreactivity to Norepinephrine-Infusion in Essential Hypertension

“…With respect to HR reactivity, we did not observe reactivity differences between HT and NT to any of the infusions. In reaction to high-dose NE-infusion as applied in this study, HT and NT exhibited similar HR reactivity or bradycardia, respectively, in our study and in earlier studies (61,62). The NE-infusion-induced bradycardia as well as the PHE-infusion-induced tachycardia are supposedly mediated by the baroreceptor reflex (15,63).…”

Hemodynamic and catecholamine responses during tracheal intubation using a lightwand device (Trachlight) in elderly patients with hypertension

“…In the present study, the patients received fentanyl 2 µg ·kg Ϫ1 in addition to suitable propofol. It has been reported that patients with essential hypertension have increased activity of the sympathetic nervous system [1][2][3] and show an exaggerated hemodynamic response to the induction of anesthesia compared with normotensive patients [14]. Low et al [14] reported that there was a marked increase in NE concentration after laryngoscopy in hypertensive patients.…”

“…These hemodynamic changes are caused by increased activity of the sympathetic nervous system [1][2][3].…”

Cardiac Output Response to Norepinephrine in Postoperative Cardiac Surgery Patients

“…In fact, HR increased during NE infusion in both septic shock patients (29) and septic pigs (13). Still other studies demonstrated a NE-induced reduction in HR in healthy humans (30)(31)(32), normal and hypertensive subjects (33), and in several animal studies (14,(34)(35)(36). The HR reduction in all these studies was attributed to a baroreceptor-mediated central sympathetic withdrawal triggered by the NE-induced increased blood pressure (34,36).…”