Stimulation of the hypothalamic paraventricular nucleus causes systemic venoconstriction

Abstract

Venous capacitance plays an important role in cardiovascular homeostasis. The anatomical loci within the central nervous system involved in modulating venous function remain to be elucidated. Stimulation of the hypothalamic paraventricular nucleus is known to increase sympathoadrenal outflow and arterial blood pressure. The present study was undertaken to determine whether electrical stimulation of the paraventricular nucleus can also affect the venous circulation. Mean circulatory filling pressure (MCFP) was used as an index of venous tone. Male Long Evans rats were initially anesthetized with pentobarbital (i.p.; 60 mg/kg) and subsequently maintained with urethane (i.v.; 600 mg/kg). Blood pressure and systemic venous pressure were monitored via catheters in the femoral artery and vein and heart rate eas derived from the pulsatile blood pressure signal. A latex tipped balloon was placed in the right atrium via the right jugular vien. Mean circulatory filling pressure was calculated from the arterial and venous plateau pressures recorded during five second balloon inflations. Arterial pressure, systemic venous pressure, heart rate and mean circulatory filling pressure were monitored before and during unilateral monopolar electrical stimulation (0.5 ms pulses at 50 Hz for a train duration of 10 s with constant current intensities of 100, 150, 200, and 300 μA) of the paraventricular nucleus. Increased graded stimulation of the paraventricular nucleus increased blood pressure by 6 ± 2, 8 ± 1, 13 ± 2 and 26 ± 5 mm Hg while heart rate changed by −22 ± 6, −18 ± 6 and −15 ± 9 bpm and+10 ± 10 bpm, respectively. Moreover, graded increases in MCFP of 0.64 ± 0.09, 1.04 ± 0.21, 1.19 ± 0.11 and 1.50 ± 0.25 mm Hg were observed concurrently. The results demonstrate, for the first time, that in addition to the documented effects on the arterial circulation, stimulation of the paraventricular nucleus induces systemic venoconstriction.